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Hypertension (Case 7)

Published on 24/06/2015 by admin

Filed under Internal Medicine

Last modified 24/06/2015

This article have been viewed 6306 times

Elie R. Chemaly MD, MSc and Michael Kim MD

Case: A 59-year-old African-American woman is referred by her primary physician. She has had a history of severe hypertension for 38 years. She complains of dizziness, occipital headaches with blurred vision, and palpitations correlated with high BP sometimes reaching 200 mm Hg systolic and 120 mm Hg diastolic. She also has claudication of the legs and thighs upon walking four street blocks. She has a history of thyroid disease and is presently hypothyroid. Her medications on presentation were valsartan/hydrochlorothiazide 320 mg/25 mg (one tablet daily in the morning), clonidine 0.3 mg (one tablet daily in the evening), verapamil SR 240 mg (one tablet twice a day), and levothyroxine 0.1 mg (one tablet daily). Although she takes her medications each day as directed, she confides to you that she is concerned that they are becoming increasingly difficult for her to afford on a limited budget. She has an extensive family history of hypertension, and her father died at the age of 57 years in his sleep. On examination she weighs 68 kg, her pulse is 60 bpm, and her BP is 148/88 mm Hg. Her examination is remarkable for bilateral femoral bruits.

Differential Diagnosis

Speaking Intelligently

The first assessment when approaching the hypertensive patient is to classify the patient based on the following:

1. The arterial BP measurements

2. The acuteness of the problem

3. The status of the patient in terms of antihypertensive therapy

4. The cause of hypertension in the patient: essential vs. secondary. In acute settings, BP elevation may be an appropriate response to stress such as hypoxia, hypercapnia, hypoxemia, or even intracranial hypertension (the Cushing response of hypertension and bradycardia).

PATIENT CARE

Clinical thinking.

• The definition of hypertension is an operational definition, which means that a BP is considered to be in the hypertensive range when it requires treatment to lower it, not just when it is above the number considered to be normal, and such treatment is required when the benefit of therapy outweighs the risk of therapy. This explains the changes in the definition of hypertension over the course of the years, motivated by treatment availability and data on treatment benefit and treatment targets.

• The seventh report of the Joint National Committee (JNC 7), published in 2003, has issued those definitions. 1 Based upon the average of two or more BP readings at each of two or more visits after an initial screen, the following classification is used:

• Normal blood pressure: systolic less than 120 mm Hg and diastolic less than 80 mm Hg

• Prehypertension: systolic 120 to 139 mm Hg or diastolic 80 to 89 mm Hg

• Hypertension:

Stage 1: systolic 140 to 159 mm Hg or diastolic 90 to 99 mm Hg

Stage 2: systolic ≥160 mm Hg or diastolic ≥100 mm Hg

• It is not the same thing to have hypertension and to have a BP that is not normal. The normal BP definition comes from studies recognizing a continuous rise in the risk of hypertension complications starting at a BP over 110/75 mm Hg (mainly cardiovascular morbidity and mortality).

• These definitions apply to adults on no antihypertensive medications and who are not acutely ill. If there is a disparity in category between the systolic and diastolic pressures, the higher value determines the severity of the hypertension. The systolic pressure is the greater predictor of risk in patients over the age of 50 to 60 years. Also, systolic blood pressure (SBP) is measured more reliably than diastolic blood pressure (DBP) and classifies most patients. Isolated systolic hypertension is common in elderly patients; younger hypertensive patients tend to have elevations of both SBP and DBP. An isolated elevation of the DBP is much less common.

• I need to know if the patient, especially in the acute setting, is presenting with malignant hypertension, hypertensive emergency, or hypertensive urgency.

• If the patient is already receiving antihypertensive therapy, the diagnosis of hypertension is made. I need to assess the particular therapeutic goal for the BP of this patient, since BP treatment goals vary from patient to patient (see JNC 7 report 1 ) and the appropriateness of the treatment.

• The decision to search for a secondary cause of hypertension and/or poor BP control is made on a case-by-case basis.

The history should search for precipitating or aggravating factors as well as an identifiable cause (secondary hypertension), establish the course of the disease, assess the extent of target organ damage, and look for other risk factors for cardiovascular disease.

• Duration and course of the disease

• Prior treatment, response, tolerance, and compliance. Noncompliance with treatment is an important cause of poor BP control.

• Medications, diet, and social history: Drugs that may aggravate or cause hypertension include sympathomimetics, steroids, NSAIDs, and estrogens; psychiatric medications causing a serotonin syndrome; cocaine and alcohol abuse. Withdrawal syndromes and rebound effects also need to be considered: alcohol, benzodiazepines, β-blockers, and clonidine.

• Family history

• Comorbidities, especially diabetes; diseases that can be secondary causes of hypertension (e.g., kidney disease); other cardiovascular risk factors (e.g., tobacco).

• Symptoms of sleep apnea: early-morning headaches, daytime somnolence, snoring, erratic sleep.

• Symptoms of severe hypertension, end-organ damage, or volume overload: epistaxis, headache, visual disturbances, neurologic deficits, dyspnea, chest pain, syncope, claudication.

• Symptoms suggestive of a secondary cause: headaches, sweating, tremor, tachycardia/palpitations, muscle weakness, and skin symptoms.

Physical Examination

• Proper measurement of BP: Away from stressors, with an appropriate cuff size, use Korotkoff phase V for auscultatory DBP. Korotkoff phase V is when the sounds disappear; one can use phase IV when they muffle if they do not disappear until a BP of 0 mm Hg. SBP, measured by auscultation, can and should also be measured through the radial pulse: when the cuff is inflated above the SBP, the radial pulse disappears. This maneuver allows the assessment of auscultatory gap (a stiff artery that does not oscillate and leads to an auscultatory underestimation of SBP) and pseudo-hypertension (a stiff artery not compressed by the cuff; SBP is overestimated). In selected settings, BP should be measured in both arms (especially in the younger patient to assess for coarctation of the aorta). Measurements should be repeated at different visits, unless BP is markedly elevated, before treatment.

• Vital signs , in particular heart rate in relationship to BP and treatments already taken. It may be important, especially in the acute setting, to know if the patient is febrile or hypoxic. Mental status is an important vital sign in the acute setting (hypertensive emergencies and urgencies).

• General appearance: body fat, skin (cutaneous manifestations of endocrinopathies causing secondary hypertension).

• Funduscopic examination to evaluate retinal complications.

• Thyroid examination.

• Cardiac auscultation (for murmurs and abnormal sounds: An S 4 gallop may indicate the stiff left ventricle of hypertensive heart disease).

• Vascular auscultation (carotid bruits, renal bruits, pulses): to assess atherosclerotic status and the presence of renal artery stenosis; the relationship between carotid artery disease, its treatment, and hypertension is not well understood.

• Abdominal examination , especially of the aorta and the kidneys.

• Neurologic examination , if applicable.

Tests for Consideration

IMAGING CONSIDERATIONS

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Patient Case Presentation

Mr. E.A. is a 40-year-old black male who presented to his Primary Care Provider for a diabetes follow up on October 14th, 2019. The patient complains of a general constant headache that has lasted the past week, with no relieving factors. He also reports an unusual increase in fatigue and general muscle ache without any change in his daily routine. Patient also reports occasional numbness and tingling of face and arms. He is concerned that these symptoms could potentially be a result of his new diabetes medication that he began roughly a week ago. Patient states that he has not had any caffeine or smoked tobacco in the last thirty minutes. During assessment vital signs read BP 165/87, Temp 97.5 , RR 16, O 98%, and HR 86. E.A states he has not lost or gained any weight. After 10 mins, the vital signs were retaken BP 170/90, Temp 97.8, RR 15, O 99% and HR 82. Hg A1c 7.8%, three months prior Hg A1c was 8.0%. Glucose 180 mg/dL (fasting). FAST test done; negative for stroke. CT test, Chem 7 and CBC have been ordered.

Past medical history

Diagnosed with diabetes (type 2) at 32 years old

Overweight, BMI of 31

Had a cholecystomy at 38 years old

Diagnosed with dyslipidemia at 32 years old

Past family history

Mother alive, diagnosed diabetic at 42 years old

Father alive with Hypertension diagnosed at 55 years old

Brother alive and well at 45 years old

Sister alive and obese at 34 years old

Pertinent social history

Social drinker on occasion

Smokes a pack of cigarettes per day

Works full time as an IT technician and is in graduate school

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Patient Management in the Telemetry/Cardiac Step-Down Unit: A Case-Based Approach

Chapter 6: 10 Real Cases on Hypertensive Emergency and Pericardial Disease: Diagnosis, Management, and Follow-Up

Niel Shah; Fareeha S. Alavi; Muhammad Saad

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Case review, case discussion.

Clinical Symptoms
Diagnostic Evaluation
Full Chapter
Supplementary Content

Case 1: Management of Hypertensive Encephalopathy

A 45-year-old man with a 2-month history of progressive headache presented to the emergency department with nausea, vomiting, visual disturbance, and confusion for 1 day. He denied fever, weakness, numbness, shortness of breath, and flulike symptoms. He had significant medical history of hypertension and was on a β-blocker in the past, but a year ago, he stopped taking medication due to an unspecified reason. The patient denied any history of tobacco smoking, alcoholism, and recreational drug use. The patient had a significant family history of hypertension in both his father and mother. Physical examination was unremarkable, and at the time of triage, his blood pressure (BP) was noted as 195/123 mm Hg, equal in both arms. The patient was promptly started on intravenous labetalol with the goal to reduce BP by 15% to 20% in the first hour. The BP was rechecked after an hour of starting labetalol and was 165/100 mm Hg. MRI of the brain was performed in the emergency department and demonstrated multiple scattered areas of increased signal intensity on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images in both the occipital and posterior parietal lobes. There were also similar lesions in both hemispheres of the cerebellum (especially the cerebellar white matter on the left) as well as in the medulla oblongata. The lesions were not associated with mass effect, and after contrast administration, there was no evidence of abnormal enhancement. In the emergency department, his BP decreased to 160/95 mm Hg, and he was transitioned from drip to oral medications and transferred to the telemetry floor. How would you manage this case?

The patient initially presented with headache, nausea, vomiting, blurred vision, and confusion. The patient’s BP was found to be 195/123 mm Hg, and MRI of the brain demonstrated scattered lesions with increased intensity in the occipital and posterior parietal lobes, as well as in cerebellum and medulla oblongata. The clinical presentation, elevated BP, and brain MRI findings were suggestive of hypertensive emergency, more specifically hypertensive encephalopathy. These MRI changes can be seen particularly in posterior reversible encephalopathy syndrome (PRES), a sequela of hypertensive encephalopathy. BP was initially controlled by labetalol, and after satisfactory control of BP, the patient was switched to oral antihypertensive medications.

Hypertensive emergency refers to the elevation of systolic BP >180 mm Hg and/or diastolic BP >120 mm Hg that is associated with end-organ damage; however, in some conditions such as pregnancy, more modest BP elevation can constitute an emergency. An equal degree of hypertension but without end-organ damage constitutes a hypertensive urgency, the treatment of which requires gradual BP reduction over several hours. Patients with hypertensive emergency require rapid, tightly controlled reductions in BP that avoid overcorrection. Management typically occurs in an intensive care setting with continuous arterial BP monitoring and continuous infusion of antihypertensive agents.

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PICO: Form a Focused Clinical Question

1. Ask: PICO(T) Question
2. Align: Levels of Evidence
3a. Acquire: Resource Types
3b. Acquire: Searching
4. Appraise
Primary vs. Secondary Sources
Case Study Example
Practice PICO

Formulate a Clinical Question from a Case Study

Case: Hypertension

I: Intervention

C: comparison.

PICO: Putting It Together

Clinical Scenario

A 68-year-old female patient has recently been diagnosed with high blood pressure. She is otherwise healthy and active. You need to decide whether to prescribe her a beta-blocker or an ACE inhibiter.

Image: "Blood pressure measuring. Doctor and patient. Health care." by agilemktg1 is marked with CC PDM 1.0

► Click on the P: Patient tab to proceed in developing a clinical question.

(Case study from EBM Librarian: Teaching Tools: Scenarios .)

Consider when choosing your patient/problem:

What are the most important characteristics?
Relevant demographic factors
The setting

Patient: adult hypertensive female

Image: "Nurse measuring blood pressure of senior woman at home. Looking at camera, smiling.?" by agilemktg1 is marked with CC PDM 1.0

► Click on the I: Intervention tab to proceed in developing a clinical question.

Consider for your intervention:

What is the main intervention, treatment, diagnostic test, procedure, or exposure?
Think of dosage, frequency, duration, and mode of delivery

Intervention: beta-blocker

Image: "Atenolol Blood Pressure Tablets Image 4" by Doctor4U_UK is licensed under CC BY 2.0

► Click on the C: Comparison tab to proceed in developing a clinical question.

Consider for your comparison:

Inactive control intervention: Placebo, standard care, no treatment
Active control intervention: A different drug, dose, or kind of therapy

Comparison: ACE inhibiter

Image: "Ramipril Blood Pressure Capsules Image 5" by Doctor4U_UK is licensed under CC BY 2.0

► Click on the O: Outcome tab to proceed in developing a clinical question.

Consider for your outcome:

Be specific and make it measurable
It can be something objective or subjective

Outcome: relief of symptoms; controlled blood pressure

Image: "File:BP B6 Connect blood pressure monitor.png" by 百略醫學 is licensed under CC BY-SA 4.0

► Click on the PICO: Putting It Together tab to proceed in developing a clinical question.

Formulate a PICO Question

Answerable PICO Question: In middle-aged adult females with hypertension, are beta blockers more effective than ACE inhibiters in controlling blood pressure?

Image: "Dagstuhl 2008-02-01 - 37" by Nic's events is licensed under CC BY-SA 2.0

Suggested MeSH Terms: Adrenergic beta-Antagonists/therapeutic use; Angiotensin-Converting Enzyme Inhibitors/therapeutic use; hypertension/drug therapy

Tip: Incorporating sex into the search may not be necessary unless there is a significant difference between males and females in relevant studies.

Click "Next" below to practice formulating clinical questions using PICO format.

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Newly diagnosed hypertension: case study

Angela Brown

Trainee Advanced Nurse Practitioner, East Belfast GP Federation, Northern Ireland

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The role of an advanced nurse practitioner encompasses the assessment, diagnosis and treatment of a range of conditions. This case study presents a patient with newly diagnosed hypertension. It demonstrates effective history taking, physical examination, differential diagnoses and the shared decision making which occurred between the patient and the professional. It is widely acknowledged that adherence to medications is poor in long-term conditions, such as hypertension, but using a concordant approach in practice can optimise patient outcomes. This case study outlines a concordant approach to consultations in clinical practice which can enhance adherence in long-term conditions.

Hypertension is a worldwide problem with substantial consequences ( Fisher and Curfman, 2018 ). It is a progressive condition ( Jamison, 2006 ) requiring lifelong management with pharmacological treatments and lifestyle adjustments. However, adopting these lifestyle changes can be notoriously difficult to implement and sustain ( Fisher and Curfman, 2018 ) and non-adherence to chronic medication regimens is extremely common ( Abegaz et al, 2017 ). This is also recognised by the National Institute for Health and Care Excellence (NICE) (2009) which estimates that between 33.3% and 50% of medications are not taken as recommended. Abegaz et al (2017) furthered this by claiming 83.7% of people with uncontrolled hypertension do not take medications as prescribed. However, leaving hypertension untreated or uncontrolled is the single largest cause of cardiovascular disease ( Fisher and Curfman, 2018 ). Therefore, better adherence to medications is associated with better outcomes ( World Health Organization, 2003 ) in terms of reducing the financial burden associated with the disease process on the health service, improving outcomes for patients ( Chakrabarti, 2014 ) and increasing job satisfaction for professionals ( McKinnon, 2013 ). Therefore, at a time when growing numbers of patients are presenting with hypertension, health professionals must adopt a concordant approach from the initial consultation to optimise adherence.

Great emphasis is placed on optimising adherence to medications ( NICE, 2009 ), but the meaning of the term ‘adherence’ is not clear and it is sometimes used interchangeably with compliance and concordance ( De Mauri et al, 2022 ), although they are not synonyms. Compliance is an outdated term alluding to paternalism, obedience and passivity from the patient ( Rae, 2021 ), whereby the patient's behaviour must conform to the health professional's recommendations. Adherence is defined as ‘the extent to which a person's behaviour, taking medication, following a diet and/or executing lifestyle changes, corresponds with agreed recommendations from a health care provider’ ( Chakrabarti, 2014 ). This term is preferred over compliance as it is less paternalistic ( Rae, 2021 ), as the patient is included in the decision-making process and has agreed to the treatment plan. While it is not yet widely embraced or used in practice ( Fawcett, 2020 ), concordance is recognised, not as a behaviour ( Rae, 2021 ) but more an approach or method which focuses on the equal partnership between patient and professional ( McKinnon, 2013 ) and enables effective and agreed treatment plans.

NICE last reviewed its guidance on medication adherence in 2019 and did not replace adherence with concordance within this. This supports the theory that adherence is an outcome of good concordance and the two are not synonyms. NICE (2009) guidelines, which are still valid, show evidence of concordant principles to maximise adherence. Integrating the theoretical principles of concordance into this case study demonstrates how the trainee advanced nurse practitioner aimed to individualise patient-centred care and improve health outcomes through optimising adherence.

Patient introduction and assessment

Jane (a pseudonym has been used to protect the patient's anonymity; Nursing and Midwifery Council (NMC) 2018 ), is a 45-year-old woman who had been referred to the surgery following an attendance at an emergency department. Jane had been role-playing as a patient as part of a teaching session for health professionals when it was noted that her blood pressure was significantly elevated at 170/88 mmHg. She had no other symptoms. Following an initial assessment at the emergency department, Jane was advised to contact her GP surgery for review and follow up. Nazarko (2021) recognised that it is common for individuals with high blood pressure to be asymptomatic, contributing to this being referred to as the ‘silent killer’. Hypertension is generally only detected through opportunistic checking of blood pressure, as seen in Jane's case, which is why adults over the age of 40 years are offered a blood pressure check every 5 years ( Bostock-Cox, 2013 ).

Consultation

Jane presented for a consultation at the surgery. Green (2015) advocates using a model to provide a structured approach to consultations which ensures quality and safety, and improves time management. Young et al (2009) claimed that no single consultation model is perfect, and Diamond-Fox (2021) suggested that, with experience, professionals can combine models to optimise consultation outcomes. Therefore, to effectively consult with Jane and to adapt to her individual personality, different models were intertwined to provide better person-centred care.

The Calgary–Cambridge model is the only consultation model that places emphasis on initiating the session, despite it being recognised that if a consultation gets off to a bad start this can interfere throughout ( Young et al, 2009 ). Being prepared for the consultation is key. Before Jane's consultation, the environment was checked to minimise interruptions, ensuring privacy and dignity ( Green, 2015 ; NMC, 2018 ), the seating arrangements optimised to aid good body language and communication ( Diamond-Fox, 2021 ) and her records were viewed to give some background information to help set the scene and develop a rapport ( Young et al, 2009 ). Being adequately prepared builds the patient's trust and confidence in the professional ( Donnelly and Martin, 2016 ) but equally viewing patient information can lead to the professional forming preconceived ideas ( Donnelly and Martin, 2016 ). Therefore, care was taken by the trainee advanced nurse practitioner to remain open-minded.

During Jane's consultation, a thorough clinical history was taken ( Table 1 ). History taking is common to all consultation models and involves gathering important information ( Diamond-Fox, 2021 ). History-taking needs to be an effective ( Bostock-Cox, 2019 ), holistic process ( Harper and Ajao, 2010 ) in order to be thorough, safe ( Diamond-Fox, 2021 ) and aid in an accurate diagnosis. The key skill for taking history is listening and observing the patient ( Harper and Ajao, 2010 ). Sir William Osler said:‘listen to the patient as they are telling you the diagnosis’, but Knott and Tidy (2021) suggested that patients are barely given 20 seconds before being interrupted, after which they withdraw and do not offer any new information ( Demosthenous, 2017 ). Using this guidance, Jane was given the ‘golden minute’ allowing her to tell her ‘story’ without being interrupted ( Green, 2015 ). This not only showed respect ( Ingram, 2017 ) but interest in the patient and their concerns.

Once Jane shared her story, it was important for the trainee advanced nurse practitioner to guide the questioning ( Green 2015 ). This was achieved using a structured approach to take Jane's history, which optimised efficiency and effectiveness, and ensured that pertinent information was not omitted ( Young et al, 2009 ). Thomas and Monaghan (2014) set out clear headings for this purpose. These included:

The presenting complaint
Past medical history
Drug history
Social history
Family history.

McPhillips et al (2021) also emphasised a need for a systemic enquiry of the other body systems to ensure nothing is missed. From taking this history it was discovered that Jane had been feeling well with no associated symptoms or red flags. A blood pressure reading showed that her blood pressure was elevated. Jane had no past medical history or allergies. She was not taking any medications, including prescribed, over the counter, herbal or recreational. Jane confirmed that she did not drink alcohol or smoke. There was no family history to note, which is important to clarify as a genetic link to hypertension could account for 30–50% of cases ( Nazarko, 2021 ). The information gathered was summarised back to Jane, showing good practice ( McPhillips et al, 2021 ), and Jane was able to clarify salient or missing points. Green (2015) suggested that optimising the patient's involvement in this way in the consultation makes her feel listened to which enhances patient satisfaction, develops a therapeutic relationship and demonstrates concordance.

During history taking it is important to explore the patient's ideas, concerns and expectations. Moulton (2007) refers to these as the ‘holy trinity’ and central to upholding person-centredness ( Matthys et al, 2009 ). Giving Jane time to discuss her ideas, concerns and expectations allowed the trainee advanced nurse practitioner to understand that she was concerned about her risk of a stroke and heart attack, and worried about the implications of hypertension on her already stressful job. Using ideas, concerns and expectations helped to understand Jane's experience, attitudes and perceptions, which ultimately will impact on her health behaviours and whether engagement in treatment options is likely ( James and Holloway, 2020 ). Establishing Jane's views demonstrated that she was eager to engage and manage her blood pressure more effectively.

Vincer and Kaufman (2017) demonstrated, through their case study, that a failure to ask their patient's viewpoint at the initial consultation meant a delay in engagement with treatment. They recognised that this delay could have been avoided with the use of additional strategies had ideas, concerns and expectations been implemented. Failure to implement ideas, concerns and expectations is also associated with reattendance or the patient seeking second opinions ( Green, 2015 ) but more positively, when ideas, concerns and expectations is implemented, it can reduce the number of prescriptions while sustaining patient satisfaction ( Matthys et al, 2009 ).

Physical examination

Once a comprehensive history was taken, a physical examination was undertaken to supplement this information ( Nuttall and Rutt-Howard, 2016 ). A physical examination of all the body systems is not required ( Diamond-Fox, 2021 ) as this would be extremely time consuming, but the trainee advanced nurse practitioner needed to carefully select which systems to examine and use good examination technique to yield a correct diagnosis ( Knott and Tidy, 2021 ). With informed consent, clinical observations were recorded along with a full cardiovascular examination. The only abnormality discovered was Jane's blood pressure which was 164/90 mmHg, which could suggest stage 2 hypertension ( NICE, 2019 ; 2022 ). However, it is the trainee advanced nurse practitioner's role to use a hypothetico-deductive approach to arrive at a diagnosis. This requires synthesising all the information from the history taking and physical examination to formulate differential diagnoses ( Green, 2015 ) from which to confirm or refute before arriving at a final diagnosis ( Barratt, 2018 ).

Differential diagnosis

Hypertension can be triggered by secondary causes such as certain drugs (non-steroidal anti-inflammatory drugs, steroids, decongestants, sodium-containing medications or combined oral contraception), foods (liquorice, alcohol or caffeine; Jamison, 2006 ), physiological response (pain, anxiety or stress) or pre-eclampsia ( Jamison, 2006 ; Schroeder, 2017 ). However, Jane had clarified that these were not contributing factors. Other potential differentials which could not be ruled out were the white-coat syndrome, renal disease or hyperthyroidism ( Schroeder, 2017 ). Further tests were required, which included bloods, urine albumin creatinine ratio, electrocardiogram and home blood pressure monitoring, to ensure a correct diagnosis and identify any target organ damage.

Joint decision making

At this point, the trainee advanced nurse practitioner needed to share their knowledge in a meaningful way to enable the patient to participate with and be involved in making decisions about their care ( Rostoft et al, 2021 ). Not all patients wish to be involved in decision making ( Hobden, 2006 ) and this must be respected ( NMC, 2018 ). However, engaging patients in partnership working improves health outcomes ( McKinnon, 2013 ). Explaining the options available requires skill so as not to make the professional seem incompetent and to ensure the patient continues to feel safe ( Rostoft et al, 2021 ).

Information supported by the NICE guidelines was shared with Jane. These guidelines advocated that in order to confirm a diagnosis of hypertension, a clinic blood pressure reading of 140/90 mmHg or higher was required, with either an ambulatory or home blood pressure monitoring result of 135/85 mmHg or higher ( NICE, 2019 ; 2022 ). However, the results from a new retrospective study suggested that the use of home blood pressure monitoring is failing to detect ‘non-dippers’ or ‘reverse dippers’ ( Armitage et al, 2023 ). These are patients whose blood pressure fails to fall during their nighttime sleep. This places them at greater risk of cardiovascular disease and misdiagnosis if home blood pressure monitors are used, but ambulatory blood pressure monitors are less frequently used in primary care and therefore home blood pressure monitors appear to be the new norm ( Armitage et al, 2023 ).

Having discussed this with Jane she was keen to engage with home blood pressure monitoring in order to confirm the potential diagnosis, as starting a medication without a true diagnosis of hypertension could potentially cause harm ( Jamison, 2006 ). An accurate blood pressure measurement is needed to prevent misdiagnosis and unnecessary therapy ( Jamison, 2006 ) and this is dependent on reliable and calibrated equipment and competency in performing the task ( Bostock-Cox, 2013 ). Therefore, Jane was given education and training to ensure the validity and reliability of her blood pressure readings.

For Jane, this consultation was the ideal time to offer health promotion advice ( Green, 2015 ) as she was particularly worried about her elevated blood pressure. Offering health promotion advice is a way of caring, showing support and empowerment ( Ingram, 2017 ). Therefore, Jane was provided with information on a healthy diet, the reduction of salt intake, weight loss, exercise and continuing to abstain from smoking and alcohol ( Williams, 2013 ). These were all modifiable factors which Jane could implement straight away to reduce her blood pressure.

Safety netting

The final stage and bringing this consultation to a close was based on the fourth stage of Neighbour's (1987) model, which is safety netting. Safety netting identifies appropriate follow up and gives details to the patient on what to do if their condition changes ( Weiss, 2019 ). It is important that the patient knows who to contact and when ( Young et al, 2009 ). Therefore, Jane was advised that, should she develop chest pains, shortness of breath, peripheral oedema, reduced urinary output, headaches, visual disturbances or retinal haemorrhages ( Schroeder, 2017 ), she should present immediately to the emergency department, otherwise she would be reviewed in the surgery in 1 week.

Jane was followed up in a second consultation 1 week later with her home blood pressure readings. The average reading from the previous 6 days was calculated ( Bostock-Cox, 2013 ) and Jane's home blood pressure reading was 158/82 mmHg. This reading ruled out white-coat syndrome as Jane's blood pressure remained elevated outside clinic conditions (white-coat syndrome is defined as a difference of more than 20/10 mmHg between clinic blood pressure readings and the average home blood pressure reading; NICE, 2019 ; 2022 ). Subsequently, Jane was diagnosed with stage 2 essential (or primary) hypertension. Stage 2 is defined as a clinic blood pressure of 160/100 mmHg or higher or a home blood pressure of 150/95 mmHg or higher ( NICE, 2019 ; 2022 ).

A diagnosis of hypertension can be difficult for patients as they obtain a ‘sick label’ despite feeling well ( Jamison, 2006 ). This is recognised as a deterrent for their motivation to initiate drug treatment and lifestyle changes ( Williams, 2013 ), presenting a greater challenge to health professionals, which can be addressed through concordance strategies. However, having taken Jane's bloods, electrocardiogram and urine albumin:creatinine ratio in the first consultation, it was evident that there was no target organ damage and her Qrisk3 score was calculated as 3.4%. These results provided reassurance for Jane, but she was keen to engage and prevent any potential complications.

Agreeing treatment

Concordance is only truly practised when the patient's perspectives are valued, shared and used to inform planning ( McKinnon, 2013 ). The trainee advanced nurse practitioner now needed to use the information gained from the consultations to formulate a co-produced and meaningful treatment plan based on the best available evidence ( Diamond-Fox and Bone, 2021 ). Jane understood the risk associated with high blood pressure and was keen to begin medication as soon as possible. NICE guidelines ( 2019 ; 2022 ) advocate the use of an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blockers in patients under 55 years of age and not of Black African or African-Caribbean origin. However, ACE inhibitors seem to be used as the first-line treatment for hypertensive patients under the age of 55 years ( O'Donovan, 2019 ).

ACE inhibitors directly affect the renin–angiotensin-aldosterone system which plays a central role in regulation of blood pressure ( Porth, 2015 ). Renin is secreted by the juxtaglomerular cells, in the kidneys' nephrons, when there is a decrease in renal perfusion and stimulation of the sympathetic nervous system ( O'Donovan, 2018 ). Renin then combines with angiotensinogen, a circulating plasma globulin from the liver, to form angiotensin I ( Kumar and Clark, 2017 ). Angiotensin I is inactive but, through ACE, an enzyme present in the endothelium of the lungs, it is transformed into angiotensin II ( Kumar and Clark, 2017 ). Angiotensin II is a vasoconstrictor which increases vascular resistance and in turn blood pressure ( Porth, 2015 ) while also stimulating the adrenal gland to produce aldosterone. Aldosterone reduces sodium excretion in the kidneys, thus increasing water reabsorption and therefore blood volume ( Porth, 2015 ). Using an ACE inhibitor prevents angiotensin II formation, which prevents vasoconstriction and stops reabsorption of sodium and water, thus reducing blood pressure.

When any new medication is being considered, providing education is key. This must include what the medication is for, the importance of taking it, any contraindications or interactions with the current medications being taken by the patient and the potential risk of adverse effects ( O'Donovan, 2018 ). Sharing this information with Jane allowed her to weigh up the pros and cons and make an informed choice leading to the creation of an individualised treatment plan.

Jamison (2006) placed great emphasis on sharing information about adverse effects, because patients with hypertension feel well before commencing medications, but taking medication has the potential to cause side effects which can affect adherence. Therefore, the range of side effects were discussed with Jane. These include a persistent, dry non-productive cough, hypotension, hypersensitivity, angioedema and renal impairment with hyperkalaemia ( Hitchings et al, 2019 ). ACE inhibitors have a range of adverse effects and most resolve when treatment is stopped ( Waterfield, 2008 ).

Following discussion with Jane, she proceeded with taking an ACE inhibitor and was encouraged to report any side effects in order to find another more suitable medication and to prevent her hypertension from going untreated. This information was provided verbally and written which is seen as good practice ( Green, 2015 ). Jane was followed up with fortnightly blood pressure recordings and urea and electrolyte checks and her dose of ramipril was increased fortnightly until her blood pressure was under 140/90 mmHg ( NICE, 2019 ; 2022 ).

Conclusions

Adherence to medications can be difficult to establish and maintain, especially for patients with long-term conditions. This can be particularly challenging for patients with hypertension because they are generally asymptomatic, yet acquire a sick label and start lifelong medication and lifestyle adjustments to prevent complications. Through adopting a concordant approach in practice, the outcome of adherence can be increased. This case study demonstrates how concordant strategies were implemented throughout the consultation to create a therapeutic patient–professional relationship. This optimised the creation of an individualised treatment plan which the patient engaged with and adhered to.

Hypertension is a growing worldwide problem
Appropriate clinical assessment, diagnosis and management is key to prevent misdiagnosis
Long-term conditions are associated with high levels of non-adherence to treatments
Adopting a concordance approach to practice optimises adherence and promotes positive patient outcomes

CPD reflective questions

How has this article developed your assessment, diagnosis or management of patients presenting with a high blood pressure?
What measures can you implement in your practice to enhance a concordant approach?

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v.173(4); 2000 Oct

Evidence-Based Case Review

Treating hypertension, rosemary morgan.

1 Department of Medicine for the Elderly Arrowe Park Hospital Upton Wirral L49 5PE, UK

CASE HISTORY

The patient, a 66-year-old retired bar owner, Mr C, was admitted to the hospital with a sudden onset of weakness affecting his right arm and right leg. His wife had been unable to get him out of bed earlier that morning. She had noted that his speech was slurred and initially had thought that he was very confused. The day before, he had knocked his head against a car door but had seemed all right at the time. He had no history of transient ischemic attacks. A diagnosis of essential hypertension had been made 4 years previously, and angina pectoris had been diagnosed 2 years previously. Although his general practitioner had prescribed antihypertensive treatment, Mr C did not like the side effects of the drug and stopped taking it 3½ years ago. His only other medication was sublingual glyceryl trinitrate (nitroglycerin) as required. He smoked 20 cigarettes a day, having started at age 20, and consumed 40 units of alcohol per week. Mr C's father had died of a myocardial infarction at age 69, and his mother had died of a stroke at age 70. He had no siblings.

Physical examination revealed his power to be reduced at 3/5 in his right arm and right leg, and he had an expressive dysphasia. Tone was increased on the right, with a right extensor plantar response, and he had hyperreflexia on the right compared with the left. He was continent and had fair sitting balance.

A 12-lead electrocardiogram confirmed that Mr C was in sinus rhythm with left ventricular hypertrophy and an old inferior myocardial infarction. His full blood cell count, erythrocyte sedimentation rate, random blood glucose concentration, and levels of troponin T, urea, creatinine, and electrolytes were all within the normal range. A fasting lipid profile revealed a cholesterol concentration of 7.2 mmol/L (278 mg/dL). A computed tomographic scan of the brain showed a cerebral infarct in the internal capsule. Doppler studies showed no significant stenosis of the carotid arteries. Echocardiography showed good left ventricular function with an ejection fraction of 59% and mild mitral regurgitation. After rehabilitation, Mr C was discharged home, independently mobile with a walker.

When the patient was seen in the outpatient clinic 8 weeks later, his primary care physician had sent a letter expressing concern at Mr C's continued raised blood pressure, which in the clinic was 182/102 mm Hg sitting. On further inquiry, the patient indicated that although he had been discharged home with the medications aspirin, pravastatin, and atenolol, he had taken only aspirin after discharge. He had not had any adverse effects from the drugs but was reluctant to take any medication and wanted to know exactly what evidence existed that he would benefit from taking regular antihypertensive medication, especially because he was totally free of symptoms.

WHAT IS THE EVIDENCE FOR TREATING ONGOING HYPERTENSION IN PATIENTS WHO HAVE HAD A STROKE?

Searching for the evidence.

With increasing access to the Internet and articles on health in popular media, patients are becoming more knowledgeable about their illnesses, and some want to discuss with their physician the information they obtain from these sources. For physicians to keep abreast of every new development in every field of medicine is impossible, but it is important that they develop skills in seeking new information that they can assess and use to make informed decisions.

Mr C wants to know what evidence exists that would support his taking antihypertensive and lipid-lowering drugs. Although most of the standard medical textbooks clearly state that hypertension is a risk factor for stroke (see box) and should be treated, few quote the exact evidence on which this conclusion is based.

The ideal evidence to convince Mr C to take antihypertensive drugs would be large randomized controlled trials showing a substantial benefit in patients who received treatment. One of the easiest and most readily available sources to start with is MEDLINE. First, I need to decide which words to use in my search and how far back to extend the search. Although initially I was going to use “hypertension” and “stroke,” by consulting MEDLINE's thesaurus, I learn that “cerebrovascular disorders” is a better term to use than “stroke.” I decide to go back as far as 1990 for the search.

Appraising the evidence

When I use the terms “hypertension” and “cerebrovascular disorders,” MEDLINE provides 970 records, but when I limit the search to randomized controlled trials and only those in the English language, it gives 43 references. Although it might be possible to restrict the search further, I prefer to print out the references and look at the title of the study and the journal in which the study was published. By doing this, I was able to select 3 references that may answer Mr C's question. 1 , 2 , 3

Summarizing the evidence

Fortunately, someone has already done an overview of 14 randomized controlled trials of blood pressure, stroke, and coronary heart disease. 1 These trials involve a total of 37,000 people randomly allocated to antihypertensive treatment (mainly diuretics or β blockers), with a mean treatment duration of 5 years. For most of these trials, a cutoff blood pressure of 140/90 mm Hg was used to determine hypertension. The results indicate that a decrease in the diastolic blood pressure of 5 to 6 mm Hg reduces the risk of stroke by 42% and coronary heart disease by 14%. The Systolic Hypertension in the Elderly Program, 2 in which 4,736 people from 447,921 screened participants aged 60 years and older were randomly allocated to either active or placebo treatment, showed that the treatment of isolated systolic hypertension in elderly people decreases their risk of stroke by 36%.

In another study, 4,396 patients aged 65 to 74 years with mild to moderate hypertension were randomly assigned to receive diuretic, β blocker, or placebo. 3 Patients in the treatment group had a 25% reduction in stroke and a 19% reduction in coronary artery events. In this study, supported by others, 4 diuretics seem to be superior to β blockers in reducing the risk of stroke in older people with hypertension. None of the trials included very elderly patients, as a consequence of which the question of whether they will benefit is somewhat uncertain (a trial is under way to answer this). 5

Firm evidence exists that treating hypertension in persons at risk is beneficial and substantially reduces the risk of both stroke and, to a lesser extent, coronary heart disease. I relayed the information back to Mr C, who is now agreeable to taking his antihypertensive drugs. Given the findings on the electrocardiogram of an old myocardial infarction and his history of angina, I have decided to prescribe a β blocker. If these were absent, however, the available evidence would support the use of a thiazide diuretic as first-line treatment. If on subsequent review his blood pressure is not adequately controlled with a β blocker, I will add a thiazide diuretic.

Summary points

Reduction of diastolic blood pressure by 5 to 6 mm Hg reduces the risk of stroke by 42% in hypertensive patients
The same reduction in diastolic blood pressure reduces the risk of coronary heart disease by 14%
Most of the randomized controlled trials have used either β blockers or diuretics as the antihypertensive agent
Diuretics (thiazides) seem to be superior to β blockers in reducing the risk of stroke

This article was published in Student BMJ 2000;6:228-229

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Clinical pearls, case study: treating hypertension in patients with diabetes.

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Evan M. Benjamin; Case Study: Treating Hypertension in Patients With Diabetes. Clin Diabetes 1 July 2004; 22 (3): 137–138. https://doi.org/10.2337/diaclin.22.3.137

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L.N. is a 49-year-old white woman with a history of type 2 diabetes,obesity, hypertension, and migraine headaches. The patient was diagnosed with type 2 diabetes 9 years ago when she presented with mild polyuria and polydipsia. L.N. is 5′4″ and has always been on the large side,with her weight fluctuating between 165 and 185 lb.

Initial treatment for her diabetes consisted of an oral sulfonylurea with the rapid addition of metformin. Her diabetes has been under fair control with a most recent hemoglobin A 1c of 7.4%.

Hypertension was diagnosed 5 years ago when blood pressure (BP) measured in the office was noted to be consistently elevated in the range of 160/90 mmHg on three occasions. L.N. was initially treated with lisinopril, starting at 10 mg daily and increasing to 20 mg daily, yet her BP control has fluctuated.

One year ago, microalbuminuria was detected on an annual urine screen, with 1,943 mg/dl of microalbumin identified on a spot urine sample. L.N. comes into the office today for her usual follow-up visit for diabetes. Physical examination reveals an obese woman with a BP of 154/86 mmHg and a pulse of 78 bpm.

What are the effects of controlling BP in people with diabetes?

What is the target BP for patients with diabetes and hypertension?

Which antihypertensive agents are recommended for patients with diabetes?

Diabetes mellitus is a major risk factor for cardiovascular disease (CVD). Approximately two-thirds of people with diabetes die from complications of CVD. Nearly half of middle-aged people with diabetes have evidence of coronary artery disease (CAD), compared with only one-fourth of people without diabetes in similar populations.

Patients with diabetes are prone to a number of cardiovascular risk factors beyond hyperglycemia. These risk factors, including hypertension,dyslipidemia, and a sedentary lifestyle, are particularly prevalent among patients with diabetes. To reduce the mortality and morbidity from CVD among patients with diabetes, aggressive treatment of glycemic control as well as other cardiovascular risk factors must be initiated.

Studies that have compared antihypertensive treatment in patients with diabetes versus placebo have shown reduced cardiovascular events. The United Kingdom Prospective Diabetes Study (UKPDS), which followed patients with diabetes for an average of 8.5 years, found that patients with tight BP control (< 150/< 85 mmHg) versus less tight control (< 180/< 105 mmHg) had lower rates of myocardial infarction (MI), stroke, and peripheral vascular events. In the UKPDS, each 10-mmHg decrease in mean systolic BP was associated with a 12% reduction in risk for any complication related to diabetes, a 15% reduction for death related to diabetes, and an 11% reduction for MI. Another trial followed patients for 2 years and compared calcium-channel blockers and angiotensin-converting enzyme (ACE) inhibitors,with or without hydrochlorothiazide against placebo and found a significant reduction in acute MI, congestive heart failure, and sudden cardiac death in the intervention group compared to placebo.

The Hypertension Optimal Treatment (HOT) trial has shown that patients assigned to lower BP targets have improved outcomes. In the HOT trial,patients who achieved a diastolic BP of < 80 mmHg benefited the most in terms of reduction of cardiovascular events. Other epidemiological studies have shown that BPs > 120/70 mmHg are associated with increased cardiovascular morbidity and mortality in people with diabetes. The American Diabetes Association has recommended a target BP goal of < 130/80 mmHg. Studies have shown that there is no lower threshold value for BP and that the risk of morbidity and mortality will continue to decrease well into the normal range.

Many classes of drugs have been used in numerous trials to treat patients with hypertension. All classes of drugs have been shown to be superior to placebo in terms of reducing morbidity and mortality. Often, numerous agents(three or more) are needed to achieve specific target levels of BP. Use of almost any drug therapy to reduce hypertension in patients with diabetes has been shown to be effective in decreasing cardiovascular risk. Keeping in mind that numerous agents are often required to achieve the target level of BP control, recommending specific agents becomes a not-so-simple task. The literature continues to evolve, and individual patient conditions and preferences also must come into play.

While lowering BP by any means will help to reduce cardiovascular morbidity, there is evidence that may help guide the selection of an antihypertensive regimen. The UKPDS showed no significant differences in outcomes for treatment for hypertension using an ACE inhibitor or aβ-blocker. In addition, both ACE inhibitors and angiotensin II receptor blockers (ARBs) have been shown to slow the development and progression of diabetic nephropathy. In the Heart Outcomes Prevention Evaluation (HOPE)trial, ACE inhibitors were found to have a favorable effect in reducing cardiovascular morbidity and mortality, whereas recent trials have shown a renal protective benefit from both ACE inhibitors and ARBs. ACE inhibitors andβ-blockers seem to be better than dihydropyridine calcium-channel blockers to reduce MI and heart failure. However, trials using dihydropyridine calcium-channel blockers in combination with ACE inhibitors andβ-blockers do not appear to show any increased morbidity or mortality in CVD, as has been implicated in the past for dihydropyridine calcium-channel blockers alone. Recently, the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) in high-risk hypertensive patients,including those with diabetes, demonstrated that chlorthalidone, a thiazide-type diuretic, was superior to an ACE inhibitor, lisinopril, in preventing one or more forms of CVD.

L.N. is a typical patient with obesity, diabetes, and hypertension. Her BP control can be improved. To achieve the target BP goal of < 130/80 mmHg, it may be necessary to maximize the dose of the ACE inhibitor and to add a second and perhaps even a third agent.

Diuretics have been shown to have synergistic effects with ACE inhibitors,and one could be added. Because L.N. has migraine headaches as well as diabetic nephropathy, it may be necessary to individualize her treatment. Adding a β-blocker to the ACE inhibitor will certainly help lower her BP and is associated with good evidence to reduce cardiovascular morbidity. Theβ-blocker may also help to reduce the burden caused by her migraine headaches. Because of the presence of microalbuminuria, the combination of ARBs and ACE inhibitors could also be considered to help reduce BP as well as retard the progression of diabetic nephropathy. Overall, more aggressive treatment to control L.N.'s hypertension will be necessary. Information obtained from recent trials and emerging new pharmacological agents now make it easier to achieve BP control targets.

Hypertension is a risk factor for cardiovascular complications of diabetes.

Clinical trials demonstrate that drug therapy versus placebo will reduce cardiovascular events when treating patients with hypertension and diabetes.

A target BP goal of < 130/80 mmHg is recommended.

Pharmacological therapy needs to be individualized to fit patients'needs.

ACE inhibitors, ARBs, diuretics, and β-blockers have all been documented to be effective pharmacological treatment.

Combinations of drugs are often necessary to achieve target levels of BP control.

ACE inhibitors and ARBs are agents best suited to retard progression of nephropathy.

Evan M. Benjamin, MD, FACP, is an assistant professor of medicine and Vice President of Healthcare Quality at Baystate Medical Center in Springfield, Mass.

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© Copyright American Diabetes Association

A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria

Andrea Luk,

* To whom correspondence should be addressed. E-mail: [email protected]

Ching Wan Lam,
Wing Hung Tam,
Anthony W. I Lo,
Enders K. W Ng,
Alice P. S Kong,
Wing Yee So,
Chun Chung Chow
Andrea Luk,
Ronald C. W Ma,
Ching Wan Lam,
Wing Hung Tam,
Anthony W. I Lo,
Enders K. W Ng,
Alice P. S Kong,
Wing Yee So,

Published: February 24, 2009

https://doi.org/10.1371/journal.pmed.1000037
Reader Comments

Citation: Luk A, Ma RCW, Lam CW, Tam WH, Lo AWI, Ng EKW, et al. (2009) A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria. PLoS Med 6(2): e1000037. https://doi.org/10.1371/journal.pmed.1000037

Copyright: © 2009 Luk et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The authors received no specific funding for this article.

Competing interests: RCWM is Section Editor of the Learning Forum. The remaining authors have declared that no competing interests exist.

Abbreviations: CT, computer tomography; I, iodine; MIBG, metaiodobenzylguanidine; MRI, magnetic resonance imaging; SDH, succinate dehydrogenase; SDHD, succinate dehydrogenase subunit D

Provenance: Commissioned; externally peer reviewed

Description of Case

A 21-year-old pregnant woman, gravida 2 para 1, presented with hypertension and proteinuria at 20 weeks of gestation. She had a history of pre-eclampsia in her first pregnancy one year ago. During that pregnancy, at 39 weeks of gestation, she developed high blood pressure, proteinuria, and deranged liver function. She eventually delivered by emergency caesarean section following failed induction of labour. Blood pressure returned to normal post-partum and she received no further medical follow-up. Family history was remarkable for her mother's diagnosis of hypertension in her fourth decade. Her father and five siblings, including a twin sister, were healthy. She did not smoke nor drink any alcohol. She was not taking any regular medications, health products, or herbs.

At 20 weeks of gestation, blood pressure was found to be elevated at 145/100 mmHg during a routine antenatal clinic visit. Aside from a mild headache, she reported no other symptoms. On physical examination, she was tachycardic with heart rate 100 beats per minute. Body mass index was 16.9 kg/m 2 and she had no cushingoid features. Heart sounds were normal, and there were no signs suggestive of congestive heart failure. Radial-femoral pulses were congruent, and there were no audible renal bruits.

Baseline laboratory investigations showed normal renal and liver function with normal serum urate concentration. Random glucose was 3.8 mmol/l. Complete blood count revealed microcytic anaemia with haemoglobin level 8.3 g/dl (normal range 11.5–14.3 g/dl) and a slightly raised platelet count of 446 × 10 9 /l (normal range 140–380 × 10 9 /l). Iron-deficient state was subsequently confirmed. Quantitation of urine protein indicated mild proteinuria with protein:creatinine ratio of 40.6 mg/mmol (normal range <30 mg/mmol in pregnancy).

What Were Our Differential Diagnoses?

An important cause of hypertension that occurs during pregnancy is pre-eclampsia. It is a condition unique to the gravid state and is characterised by the onset of raised blood pressure and proteinuria in late pregnancy, at or after 20 weeks of gestation [ 1 ]. Pre-eclampsia may be associated with hyperuricaemia, deranged liver function, and signs of neurologic irritability such as headaches, hyper-reflexia, and seizures. In our patient, hypertension developed at a relatively early stage of pregnancy than is customarily observed in pre-eclampsia. Although she had proteinuria, it should be remembered that this could also reflect underlying renal damage due to chronic untreated hypertension. Additionally, her electrocardiogram showed left ventricular hypertrophy, which was another indicator of chronicity.

While pre-eclampsia might still be a potential cause of hypertension in our case, the possibility of pre-existing hypertension needed to be considered. Box 1 shows the differential diagnoses of chronic hypertension, including essential hypertension, primary hyperaldosteronism related to Conn's adenoma or bilateral adrenal hyperplasia, Cushing's syndrome, phaeochromocytoma, renal artery stenosis, glomerulopathy, and coarctation of the aorta.

Box 1: Causes of Hypertension in Pregnancy

Pre-eclampsia
Essential hypertension
Renal artery stenosis
Glomerulopathy
Renal parenchyma disease
Primary hyperaldosteronism (Conn's adenoma or bilateral adrenal hyperplasia)
Cushing's syndrome
Phaeochromocytoma
Coarctation of aorta
Obstructive sleep apnoea

Renal causes of hypertension were excluded based on normal serum creatinine and a bland urinalysis. Serology for anti-nuclear antibodies was negative. Doppler ultrasonography of renal arteries showed normal flow and no evidence of stenosis. Cushing's syndrome was unlikely as she had no clinical features indicative of hypercortisolism, such as moon face, buffalo hump, violaceous striae, thin skin, proximal muscle weakness, or hyperglycaemia. Plasma potassium concentration was normal, although normokalaemia does not rule out primary hyperaldosteronism. Progesterone has anti-mineralocorticoid effects, and increased placental production of progesterone may mask hypokalaemia. Besides, measurements of renin activity and aldosterone concentration are difficult to interpret as the renin-angiotensin-aldosterone axis is typically stimulated in pregnancy. Phaeochromocytoma is a rare cause of hypertension in pregnancy that, if unrecognised, is associated with significant maternal and foetal morbidity and mortality. The diagnosis can be established by measuring levels of catecholamines (noradrenaline and adrenaline) and/or their metabolites (normetanephrine and metanephrine) in plasma or urine.

What Was the Diagnosis?

Catecholamine levels in 24-hour urine collections were found to be markedly raised. Urinary noradrenaline excretion was markedly elevated at 5,659 nmol, 8,225 nmol, and 9,601 nmol/day in repeated collections at 21 weeks of gestation (normal range 63–416 nmol/day). Urinary adrenaline excretion was normal. Pregnancy may induce mild elevation of catecholamine levels, but the marked elevation of urinary catecholamine observed was diagnostic of phaeochromocytoma. Conditions that are associated with false positive results, such as acute myocardial infarction, congestive heart failure, acute cerebrovascular event, withdrawal from alcohol, withdrawal from clonidine, and cocaine abuse, were not present in our patient.

The working diagnosis was therefore phaeochromocytoma complicating pregnancy. Magnetic resonance imaging (MRI) of neck to pelvis, without gadolinium enhancement, was performed at 24 weeks of gestation. It showed a 4.2 cm solid lesion in the mid-abdominal aorto-caval region, while both adrenals were unremarkable. There were no ectopic lesions seen in the rest of the examined areas. Based on existing investigation findings, it was concluded that she had extra-adrenal paraganglioma resulting in hypertension.

What Was the Next Step in Management?

At 22 weeks of gestation, the patient was started on phenoxybenzamine titrated to a dose of 30 mg in the morning and 10 mg in the evening. Propranolol was added several days after the commencement of phenoxybenzamine. Apart from mild postural dizziness, the medical therapy was well tolerated during the remainder of the pregnancy. In the third trimester, systolic and diastolic blood pressures were maintained to below 90 mmHg and 60 mmHg, respectively. During this period, she developed mild elevation of alkaline phosphatase ranging from 91 to 188 IU/l (reference 35–85 IU/l). However, liver transaminases were normal and the patient had no seizures. Repeated urinalysis showed resolution of proteinuria. At 38 weeks of gestation, the patient proceeded to elective caesarean section because of previous caesarean section, and a live female baby weighing 3.14 kg was delivered. The delivery was uncomplicated and blood pressure remained stable.

Following the delivery, computer tomography (CT) scan of neck, abdomen, and pelvis was performed as part of pre-operative planning to better delineate the relationship of the tumour to neighbouring structures. In addition to the previously identified extra-adrenal paraganglioma in the abdomen ( Figure 1 ), the CT revealed a 9 mm hypervascular nodule at the left carotid bifurcation, suggestive of a carotid body tumour ( Figure 2 ). The patient subsequently underwent an iodine (I) 131 metaiodobenzylguanidine (MIBG) scan, which demonstrated marked MIBG-avidity of the paraganglioma in the mid-abdomen. The reported left carotid body tumour, however, did not demonstrate any significant uptake. This could indicate either that the MIBG scan had poor sensitivity in detecting a small tumour, or that the carotid body tumour was not functional.

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https://doi.org/10.1371/journal.pmed.1000037.g001

https://doi.org/10.1371/journal.pmed.1000037.g002

In June 2008, four months after the delivery, the patient had a laparotomy with removal of the abdominal paraganglioma. The operation was uncomplicated. There was no wide fluctuation of blood pressures intra- and postoperatively. Phenoxybenzamine and propranolol were stopped after the operation. Histology of the excised tumour was consistent with paraganglioma with cells staining positive for chromogranin ( Figures 3 and 4 ) and synaptophysin. Adrenal tissues were notably absent.

The tumour is a well-circumscribed fleshy yellowish mass with maximal dimension of 5.5 cm.

https://doi.org/10.1371/journal.pmed.1000037.g003

The tumour cells are polygonal with bland nuclei. The cells are arranged in nests and are immunoreactive to chromogranin (shown here) and synaptophysin.

https://doi.org/10.1371/journal.pmed.1000037.g004

The patient was counselled for genetic testing for hereditary phaeochromocytoma/paraganglioma. She was found to be heterozygous for c.449_453dup mutation of the succinate dehydrogenase subunit D (SDHD) gene ( Figure 5 ). This mutation is a novel frameshift mutation, and leads to SDHD deficiency (GenBank accession number: 1162563). At the latest clinic visit in August 2008, she was asymptomatic and normotensive. Measurements of catecholamine in 24-hour urine collections had normalised. Resection of the left carotid body tumour was planned for a later date. She was to be followed up indefinitely to monitor for recurrences. She was also advised to contact family members for genetic testing. Our patient gave written consent for this case to be published.

https://doi.org/10.1371/journal.pmed.1000037.g005

Phaeochromocytoma in Pregnancy

Hypertension during pregnancy is a frequently encountered obstetric complication that occurs in 6%–8% of pregnancies [ 2 ]. Phaeochromocytoma presenting for the first time in pregnancy is rare, and only several hundred cases have been reported in the English literature. In a recent review of 41 cases that presented during 1988 to 1997, maternal mortality was 4% while the rate of foetal loss was 11% [ 3 ]. Antenatal diagnosis was associated with substantial reduction in maternal mortality but had little impact on foetal mortality. Further, chronic hypertension, regardless of aetiology, increases the risk of pre-eclampsia by 10-fold [ 1 ].

Classically, patients with phaeochromocytoma present with spells of palpitation, headaches, and diaphoresis [ 4 ]. Hypertension may be sustained or sporadic, and is associated with orthostatic blood pressure drop because of hypovolaemia and impaired vasoconstricting response to posture change. During pregnancy, catecholamine surge may be triggered by pressure from the enlarging uterus and foetal movements. In the majority of cases, catecholamine-secreting tumours develop in the adrenal medulla and are termed phaeochromocytoma. Ten percent of tumours arise from extra-adrenal chromaffin tissues located in the abdomen, pelvis, or thorax to form paraganglioma that may or may not be biochemically active. The malignant potential of phaeochromocytoma or paraganglioma cannot be determined from histology and is inferred by finding tumours in areas of the body not known to contain chromaffin tissues. The risk of malignancy is higher in extra-adrenal tumours and in tumours that secrete dopamine.

Making the Correct Diagnosis

The diagnosis of phaeochromocytoma requires a combination of biochemical and anatomical confirmation. Catecholamines and their metabolites, metanephrines, can be easily measured in urine or plasma samples. Day collection of urinary fractionated metanephrine is considered the most sensitive in detecting phaeochromocytoma [ 5 ]. In contrast to sporadic release of catecholamine, secretion of metanephrine is continuous and is less subjective to momentary stress. Localisation of tumour can be accomplished by either CT or MRI of the abdomen [ 6 ]. Sensitivities are comparable, although MRI is preferable in pregnancy because of minimal radiation exposure. Once a tumour is identified, nuclear medicine imaging should be performed to determine its activity, as well as to search for extra-adrenal diseases. I 131 or I 123 MIBG scan is the imaging modality of choice. Metaiodobenzylguanidine structurally resembles noradrenaline and is concentrated in chromaffin cells of phaeochromocytoma or paraganglioma that express noradrenaline transporters. Radionucleotide imaging is contraindicated in pregnancy and should be deferred until after the delivery.

Treatment Approach

Upon confirming the diagnosis, medical therapy should be initiated promptly to block the cardiovascular effects of catecholamine release. Phenoxybenzamine is a long-acting non-selective alpha-blocker commonly used in phaeochromocytoma to control blood pressure and prevent cardiovascular complications [ 7 ]. The main side-effects of phenoxybenzamine are postural hypotension and reflex tachycardia. The latter can be circumvented by the addition of a beta-blocker. It is important to note that beta-blockers should not be used in isolation, since blockade of ß2-adrenoceptors, which have a vasodilatory effect, can cause unopposed vasoconstriction by a1-adrenoceptor stimulation and precipitate severe hypertension. There is little data on the safety of use of phenoxybenzamine in pregnancy, although its use is deemed necessary and probably life-saving in this precarious situation.

The definitive treatment of phaeochromocytoma or paraganglioma is surgical excision. The timing of surgery is critical, and the decision must take into consideration risks to the foetus, technical difficulty regarding access to the tumour in the presence of a gravid uterus, and whether the patient's symptoms can be satisfactorily controlled with medical therapy [ 8 , 9 ]. It has been suggested that surgical resection is reasonable if the diagnosis is confirmed and the tumour identified before 24 weeks of gestation. Otherwise, it may be preferable to allow the pregnancy to progress under adequate alpha- and beta-blockade until foetal maturity is reached. Unprepared delivery is associated with a high risk of phaeochromocytoma crisis, characterised by labile blood pressure, tachycardia, fever, myocardial ischaemia, congestive heart failure, and intracerebral bleeding.

Patients with phaeochromocytoma or paraganglioma should be followed up for life. The rate of recurrence is estimated to be 2%–4% at five years [ 10 ]. Assessment for recurrent disease can be accomplished by periodic blood pressure monitoring and 24-hour urine catecholamine and/or metanephrine measurements.

Genetics of Phaeochromocytoma

Approximately one quarter of patients presenting with phaeochromocytoma may carry germline mutations, even in the absence of apparent family history [ 11 ]. The common syndromes of hereditary phaeochromocytoma/paraganglioma are listed in Box 2 . These include Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, neurofibromatosis type 1, and succinate dehydrogenase (SDH) gene mutations. Our patient has a novel frameshift mutation in the SDHD gene located at Chromosome 11q. SDH is a mitochondrial enzyme that is involved in oxidative phosphorylation. Characteristically, SDHD mutation is associated with head or neck non-functional paraganglioma, and infrequently, sympathetic paraganglioma or phaeochromocytoma [ 12 ]. Tumours associated with SDHD mutation are rarely malignant, in contrast to those arisen from mutation of the SDHB gene. Like all other syndromes of hereditary phaeochromocytoma, SDHD mutation is transmitted in an autosomal dominant fashion. However, not all carriers of the SDHD mutation develop tumours, and inheritance is further complicated by maternal imprinting in gene expression. While it may not be practical to screen for genetic alterations in all cases of phaeochromocytoma, most authorities advocate genetic screening for patients with positive family history, young age of tumour onset, co-existence with other neoplasms, bilateral phaeochromocytoma, and extra-adrenal paraganglioma. The confirmation of genetic mutation should prompt evaluation of other family members.

Box 2: Hereditary Phaeochromocytoma/Paraganglioma Syndromes

Von Hippel-Lindau syndrome
Multiple endocrine neoplasia type 2A and type 2B
Neurofibromatosis type 1
Mutation of SDHB , SDHC , SDHD
Ataxia-telangiectasia
Tuberous sclerosis
Sturge-Weber syndrome

Key Learning Points

Hypertension complicating pregnancy is a commonly encountered medical condition.
Pre-existing chronic hypertension must be considered in patients with hypertension presenting in pregnancy, particularly if elevation of blood pressure is detected early during pregnancy or if persists post-partum.
Secondary causes of chronic hypertension include renal artery stenosis, renal parenchyma disease, primary hyperaldosteronism, phaeochromocytoma, Cushing's syndrome, coarctation of the aorta, and obstructive sleep apnoea.
Phaeochromocytoma presenting during pregnancy is rare but carries high rates of maternal and foetal morbidity and mortality if unrecognised.
Successful outcomes depend on early disease identification, prompt initiation of alpha- and beta-blockers, carefully planned delivery, and timely resection of the tumour.

Phaeochromocytoma complicating pregnancy is uncommon. Nonetheless, in view of the potential for catastrophic consequences if unrecognised, a high index of suspicion and careful evaluation for secondary causes of hypertension is of utmost importance. Blood pressure should be monitored in the post-partum period and persistence of hypertension must be thoroughly investigated.

Author Contributions

All authors participated in the management of the patient or writing of the article. AL and RCWM wrote the article, with contributions from all the authors.

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Article Contents

Introduction, supplementary data, declarations, data availability, ethical approval, pre-registered clinical trial number, nocturnal heat exposure and stroke risk.

Michael Ertl and Alexandra Schneider contributed equally to the study.

Article contents
Figures & tables
Supplementary Data

Cheng He, Susanne Breitner, Siqi Zhang, Veronika Huber, Markus Naumann, Claudia Traidl-Hoffmann, Gertrud Hammel, Annette Peters, Michael Ertl, Alexandra Schneider, Nocturnal heat exposure and stroke risk, European Heart Journal , 2024;, ehae277, https://doi.org/10.1093/eurheartj/ehae277

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In recent decades, nighttime temperatures have increased faster than daytime temperatures. The increasing prevalence of nocturnal heat exposure may pose a significant risk to cardiovascular health. This study investigated the association between nighttime heat exposure and stroke risk in the region of Augsburg, Germany, and examined its temporal variations over 15 years.

Hourly meteorological parameters, including mean temperature, relative humidity, and barometric pressure, were acquired from a local meteorological station. A data set was obtained consisting of 11 037 clinical stroke cases diagnosed during warmer months (May to October) between the years 2006 and 2020. The average age of cases was 71.3 years. Among these cases, 642 were identified as haemorrhagic strokes, 7430 were classified as ischaemic strokes, and 2947 were transient ischaemic attacks. A time-stratified case-crossover analysis with a distributed lag non-linear model was used to estimate the stroke risk associated with extreme nighttime heat, as measured by the hot night excess (HNE) index after controlling for the potential confounding effects of daily maximum temperature and other climatic variables. Subgroup analyses by age group, sex, stroke subtype, and stroke severity were performed to identify variations in susceptibility to nighttime heat.

Results suggested a significant increase in stroke risk on days with extreme nighttime heat (97.5% percentile of HNE) (odds ratio 1.07, 95% confidence interval 1.01–1.15) during the full study period. When comparing the results for 2013–20 with the results for 2006–12, there was a significant increase ( P < .05) in HNE-related risk for all strokes and specifically for ischaemic strokes during the more recent period. Furthermore, older individuals, females, and patients with mild stroke symptoms exhibited a significantly increased vulnerability to nighttime heat.

This study found nocturnal heat exposure to be related to elevated stroke risk after controlling for maximum daytime temperature, with increasing susceptibility between 2006 and 2020. These results underscore the importance of considering nocturnal heat as a critical trigger of stroke events in a warming climate.

This 15-year time-stratified case-crossover study provides robust evidence that nighttime heat exposure is associated with increased stroke risk. Urgent action is needed through targeted prevention and urban planning interventions to mitigate its impact, particularly among vulnerable populations. OR, odds ratio.

Stroke is a common and debilitating cardiovascular disease that has a considerable impact on global health, causing the third highest number of healthy life years lost due to illness, disability, and premature death worldwide among all diseases. 1 Therefore, it is essential to identify the risk factors associated with stroke to develop effective public health interventions. Although individual-level risk factors such as arterial hypertension, hypercholesterolaemia, diabetes, alcohol consumption, and smoking are established risk factors, 2–5 environmental factors, such as non-optimal ambient temperature, may also play a role in the burden of stroke due to widespread exposure across the general population. 6

The potential consequences of climate change on human health have fostered research about the impact of high ambient temperatures on stroke risk. 6 Although the association between heat and increased cardiovascular disease risk has been well documented worldwide, 7 , 8 there is currently limited and inconsistent evidence on the effects of heat on stroke, particularly different subtypes of strokes. Additionally, while most studies have focused on the effects of daily average or maximum temperatures, recent research has suggested that increases in daily minimum temperatures may also affect the risk of stroke. 9 Nighttime heat exposure can interrupt the normal physiology of sleep and circadian thermoregulation, which may increase stroke risk. 10 Despite confirmation of the impact of nighttime heat on daily mortality, 11 little research has explored its effect on morbidity, and to date, no study has investigated the effect of nighttime heat exposure on risk of stroke.

Understanding temporal variations in the relationship between ambient temperature and health outcomes has emerged as a crucial issue within efforts to estimate the health impacts of future climate warming. 12 Numerous studies have indicated a declining trend in heat-related mortality risks over time due to factors such as socioeconomic development, 13 , 14 but there is limited understanding of the temporal variations in the health effects of nighttime heat. There is evidence that the urban heat island effect exacerbates nighttime heat exposure, and many projections suggest that nighttime warming will surpass daytime warming in various regions globally by this century. 9 , 15 This increased risk of nighttime heat exposure may particularly affect certain vulnerable populations, such as the elderly and individuals with pre-existing health conditions, due to their comparatively weaker immune systems. Furthermore, populations residing in regions with lower rates of air conditioning usage may be at heightened risk during nighttime heat events.

Considering the potential health impacts of rising nighttime temperatures, the stronger increase in nocturnal exposure, and its pronounced effects on sensitive groups, we conducted a time-stratified case-crossover study using a validated, complete, and detailed data set of all cases of stroke in Augsburg, Germany, from 2006 to 2020, to assess the association between nocturnal heat exposure and the occurrence of stroke for different periods. Subgroup analyses by stroke subtype, age group, sex, and stroke severity were performed to identify subpopulations with increased susceptibility to nighttime heat.

Study population

The study population consists of residents of the region of Augsburg admitted as patients to the Department of Neurology at the University Hospital Augsburg, a stand-alone comprehensive stroke care facility responsible for more than 750 000 inhabitants in the region. The Department of Neurology at the University Hospital Augsburg is one of the biggest stroke centres in Germany with ∼2000 stroke admissions per year. For this study, we obtained 22 284 recorded stroke cases from 1 January 2006 to 31 August 2020 from the Department. All included cases were classified by using the International Classification of Diseases 10th Revision (ICD-10) system. This classification was based on the final medical registries, which were further verified by the medical controlling unit of the University Hospital Augsburg and have been previously employed in our prior research. 16 Based on this information, all cases can be further stratified into three main subtypes. These subtypes include transient ischaemic attacks (TIA, symptoms lasting for a maximum of 24 h) (G45), ischaemic strokes (I63), and haemorrhagic strokes (I60, I61, and I62). In addition, we further combined TIA with ischaemic strokes considering their similar underlying mechanisms involving reduced blood flow to the brain. In addition, all cases were also categorized using the National Institutes of Health Stroke Scale (NIHSS) during first admission to the hospital. The NIHSS is a standardized assessment tool that consists of a numerical scoring system used to evaluate stroke symptom severity and assess and monitor the neurological status of a patient who has suffered a stroke. The NIHSS has already been used in many related studies to evaluate the severity of stroke and the effectiveness of new treatments for stroke. 17 In addition, some of the cases have available information regarding the Trial of Org 10172 in Acute Stroke Treatment (TOAST). This allows for the classification of these stroke cases into categories as large artery disease, cardioembolism, and small vessel disease.

Exposure data

Hourly meteorological variables (air temperature, relative humidity, and barometric pressure), daily particulate matter with an aerodynamic diameter < 10 mm (PM 10 ), nitrogen dioxide (NO 2 ), and daily maximum 8 h average ozone (O 3 ) concentrations were obtained from the local meteorological station and air quality monitoring stations in Augsburg. Details of these exposure data are explained in the online supplementary material .

Extreme heat during the night

In order to quantify the intensity of nocturnal thermal stress, we adopted the hot night excess (HNE) index. Referring to previous studies, 9 , 11 HNE was calculated by determining the excess sum of high temperature during the night (unit: °C):

where n j is the total night hours of day j , which is from the beginning of the night at day j-1 to the end of the night in the morning of day j , t i j is the nighttime temperature in the hour i at night of the day j , T thr is the temperature threshold of nighttime warming, and I thr ( t i j ) is calculated as:

As suggested in previous research, 9 we determined the threshold based on the daily minimum temperature to quantify the intensity of the heat during the night. Specifically, we defined this threshold as the 95th percentile of daily minimum temperature during the whole study period, which is 14.6°C. The local sunset and sunrise times on different days were derived from the Astral package (version 2.2) in the Python platform (version 3.8.10).

Within the study period, more than 96% of hot night events occurred during the months of May to October (see Supplementary data online , Table S1 ). Temperatures were lower during November to April, averaging 3.31°C, whereas from May to October, the average temperature increases substantially to 14.14°C. To focus our study on the period when most extreme heat events occur, to mitigate potential influences from cold exposures, and to avoid the substantial temperature disparity induced by indoor heating during the cold season, we limited our analysis to stroke cases occurring during the months of May to October.

Statistical analyses

The association between HNE and stroke was estimated by an individual-level, time-stratified, case-crossover approach. 18 , 19 Specifically, we applied conditional logistic regression models to analyse the potential relationship between extreme heat during the night and stroke occurrence. For each case, the exposure on the day of stroke occurrence (‘case’ day) was compared with exposure on days during the same month and on the same day of the week (‘control’ days). This method controls for long-term time trends and seasonality in underlying stroke rates, time-trend bias from the exposure, and time-invariant confounding, 20 such as some personal risk factors, including hypertension, diabetes, smoking, alcohol consumption, hypercholesterolaemia, obesity, and cardiovascular history.

To account for the potential non-linear and lagged effects of nighttime extreme heat in the main model, we incorporated a distributed lag non-linear model (DLNM) for HNE. Specifically, we introduced a cross-basis function of daily HNE, which includes a quadratic B-spline with two internal knots placed at the 50th and 90th centiles of daily HNE distributions, as done in previous studies. 9 , 21 We also explored the lag response curves with a natural cubic B-spline with an intercept and three internal knots placed at equally spaced values in the log scale, with a maximum lag of up to 7 days (Lag 0–6). Previous studies have indicated that the lag effect would become insignificant within 5 days due to temperature-related effects on short-term, 20 , 22 so we extended the lag period to 7 days to account for potential short-term harvesting effect. 23 To avoid any confounding effect of daytime temperature, we controlled for daily maximum temperature using a cross-basis function with the same specification as for HNE. Our main model also included natural cubic B-splines with three degrees of freedom of relative humidity and barometric pressure and a categorical variable of the holidays to control for their potential confounding effects. 24 To better interpret the odds ratios (ORs) associated with extreme heat during the night, we chose reference days with non-hot night days (HNE = 0°C) as a reference in the exposure–response curve and reported the ORs of stroke and their 95% confidence intervals (CI) at the given HNE values.

To assess the time-varying effects of HNE values, we conducted separate estimations of the HNE–stroke associations for two distinct periods (2006–12 and 2013–20). We chose these periods due to their similar time durations and the comparable total number of cases, as shown in Table 1 .

Summary statistics of stroke cases in Augsburg, Germany, from 2006 to 2020

The percentile represents the percentage of subgroup cases relative to the total number of cases in that period.

NIHSS, National Institutes of Health Stroke Scale.

We calculated the lag-cumulative stroke risk at the 97.5th percentile of HNE distribution relative to non-hot night days. According to our previous study, 20 we selected this specific cut-off point in order to avoid problems caused by the small sample sizes at extreme temperature levels. To test the statistically significant difference between the estimated exposure–response curves in these two sub-periods, we adopted the multivariate Wald test; a P -value < .05 was considered statistically significant. 25 For the methodology section regarding the significance testing, please refer to the detailed description provided in the online supplementary material .

We then conducted stratified analyses for HNE effects on all stroke events to examine potential effect modification by sex, age, and the scale of NIHSS score, as well as among cases with available TOAST information, for the two time periods.

Finally, for estimating the number of excess stroke cases related to hot night exposure in two time periods (2006–12 and 2013–20). We used the following equation:

in which C a s e i represents the daily average number of stroke cases during the warm months (May to October), which we obtained from our database for the study area. R R i p is the relative stroke risk due to hot night exposure in the day i during the period p ; considering the low prevalence of stroke among the total population, we assumed that RRs could be represented by satisfactory estimates of ORs , which were calculated based on the HNE value observed in day i and estimated exposure–response function for period p from our main analysis.

All analyses were performed with R software, version 4.2.3 (R Foundation for Statistical Computing Vienna, Austria).

Sensitivity analyses

To test the robustness of our findings, we conducted a series of sensitivity analyses for each step of our analysis, including different thresholds of HNE, the removal of daytime temperature control, an alternative daily mean temperature metric as a confounder, potential modifications in the HNE–stroke associations when additionally adjusting for air pollution, and different settings in the knots for exposure–response in our main analysis model. Please see the detailed information for our sensitivity analyses in the online supplementary material .

Stroke case and nighttime heat exposure

After the exclusion of fatal cases to concentrate on the effects of nighttime heat exposure on stroke incidence, along with other case selections as depicted in Supplementary data online , Figure S1 , our analysis ultimately encompassed 11 037 cases of first hospitalization for each individual that did not result in death during the study period, recorded within the warm periods (May to October) from 2006 to 2020. Across these cases, the mean (standard deviation) age was 71.3 (13.2) years. Among these cases, 2947 were TIA, 7430 were ischaemic strokes, and 642 were haemorrhagic strokes. Most of these stroke cases (52.5%) were categorized as moderate strokes (NIHSS score > 5 and <15) 26 ( Table 1 ). During the two periods, 2006–12 and 2013–20, there are similarities in the total number of stroke cases, with 5343 cases in 2006–12 and 5694 cases in 2013–20. There were also similar numbers of each stroke subtype during the two periods. In the 2006–12 period, there were 301 cases of haemorrhagic stroke and 5024 cases of ischaemic strokes and TIA; in 2013–20, there were 341 cases of haemorrhagic strokes and 5353 cases of ischaemic strokes and TIA. The proportion of moderate strokes increased from 46.2% in 2006–12 to 58.4% in 2013–20 ( Table 1 ). As shown in Supplementary data online , Figure S2 , the daily mean temperature during the warm season experienced a marginal and statistically non-significant rise, from 14.5°C (2006–12) to 14.8°C (2013–20) ( P > .05). The daily maximum temperature also experienced a minor increase from 19.6°C (2006–12) to 20.3°C (2013–20) ( Table 2 ). The frequency of days with extreme nighttime heat increased from 79 days (2006–12) to 82 days (2013–20). Notably, the daily mean HNE showed significant variations ( P < .05) between these two periods, allowing us to investigate whether changes in exposure conditions had any noticeable impact on the risk of stroke.

Summary statistics of daily temperature and extreme nighttime heat during the warm months (May to October) calculated by hourly observation data in Augsburg, Germany, from 2006 to 2020

HNE, hot night excess.

a The significance test was performed through a comparison of the differences between the daily mean temperature, maximum temperature, and HNE series during the periods 2006–12 and 2013–20.

b HNE calculated by the excess sum of high temperature during the night. No. days HNE > 0°C is calculated during the warm periods (May to October) for each study year.

Time-varying association of temperature and stroke occurrences

During the entire study period, we observed a significant increase in stroke risk on days with extreme nighttime heat (97.5% percentile of HNE) for all pooled stroke cases and specifically for ischaemic strokes and TIA but not for the haemorrhagic stroke subtype alone (see Supplementary data online , Figure S3 and Table 3 ). The lag response pattern indicated that the impact of nighttime heat on stroke was immediate, with significant effects appearing within the first 2 days (Lag 0–1) (see Supplementary data online , Figure S4 ).

Cumulative odds ratios estimated for daily stroke cases (95% confidence interval) associated with extreme heat exposure during the night [97.5th percentile of hot night excess (HNE) distribution] for the overall study period and the periods 2006–12 and 2013–20

TIA, transient ischaemic attack.

a Significance test based on the difference between OR estimates in 2006–12 and 2013–20.

We found a significant increase in stroke risk associated with nighttime heat exposure over time when comparing the two time periods. The exposure–response curves for all stroke subtypes displayed notable differences ( Figure 1 ). During the recent period (2013–20), extreme nighttime heat (97.5th percentile of HNE) exerted significant effects on the risk for all stroke cases and all subtypes, including haemorrhagic and ischaemic stroke. In contrast, there was no significant influence of extreme nighttime heat on all stroke risk, including all subtypes, observed during the earlier period (2006–12). When comparing the results from the time periods 2013–20 to 2006–12 ( Table 2 ), the findings highlight a significant increase ( P < .05) over time in nocturnal thermal stress for all stroke cases and the subgroup comprising ischaemic strokes or TIA. However, it is worth noting that no significant change was observed for haemorrhagic strokes, which may be attributed to the limited number of cases in this category.

Cumulative exposure–response relationships between hot night excess (HNE) and stroke risk over Lag 0–6 days for 2006–12 and 2013–20 with corresponding 95% confidence intervals (shaded areas). The vertical dashed line represents the 97.5th percentiles of the HNE distribution. Hot night excess represents the excess sum of high temperatures during the night when hourly temperatures are higher than the 95th percentile of daily minimum temperature during the whole study period. For instance, HNE = 0°C indicates non-hot night days during the warm months. HNE = 40°C represents the cumulative sum of hourly nighttime temperatures exceeding the threshold with values accumulating up to 40°C

In addition, as shown in Supplementary data online , Figure S5 , by using a consistent and same methodology, we also observed an increase in the impact of daytime temperature ( T max ) after controlling the effect of HNE. Additionally, at the same 97.5th percentile, the OR for HNE was slightly higher than for T max , although this difference did not achieve statistical significance.

The estimation results indicate that from 2006 to 2012, hot nights were attributed to an annual excess of two (95% CI −14–12) cases. However, from 2013 to 2020, hot nights were associated with a total of 33 (95% CI 9–60) excess cases annually among the residents in the study area.

Subgroup analyses

Results of the subgroup analyses point to a significant rise in the risk of stroke associated with HNE within specific subpopulations over the study period. Figure 2 highlights a notable increase in stroke risk for female individuals, older adults (>60 years), and patients diagnosed with minor strokes (NIHSS ≤ 4) from 2006–12 to 2013–20. Specifically, the risk of HNE-related stroke increased from 1.02 (95% CI 0.90–1.15) to 1.33 (95% CI 1.09–1.62) in females, 0.99 (95% CI 0.91–1.08) to 1.36 (95% CI 1.19–1.56) in older adults, and 1.04 (95% CI 0.93–1.16) to 1.52 (95% CI 1.26–1.83) in patients with minor strokes.

Cumulative odd ratio estimated for daily stroke cases (95% confidence interval) associated with extreme heat exposure during the night [97.5th percentile of hot night excess (HNE) distribution] predicted for 2006–12 and 2013–20 stratified by three different subgroups. Asterisks and coloured groups indicate statistical significance for differences in odd ratio estimates between 2006–12 and 2013–20 ( P < .05)

During the more recent period, significant HNE-related stroke risks were also found for males and younger age groups. In contrast, there were no significant effects detected for these subgroups from 2006 to 2012.

Furthermore, analysis of cases with available TOAST information revealed that nighttime temperatures significantly increased the risk of strokes due to small vessel disease during 2013–20 compared with the period of 2006–12 (see Supplementary data online , Table S2 ). Additionally, during the 2013–20 phase, we observed a significant impact on strokes caused by cardioembolism (see Supplementary data online , Table S2 ). However, no significant influence was detected for strokes related to large artery disease.

As shown in Supplementary data online , Table S3 and Figure S6 , the results of the sensitivity analyses consistently revealed an increased risk of stroke when comparing the estimations between the periods 2006–12 and 2013–20, particularly when alternative thresholds (specifically, the 97.5th percentile of daily minimum temperature) were utilized for calculating HNE. As illustrated in Supplementary data online , Table S4 and Figures S7–S9 , it is noteworthy that while the influence of HNE on all stroke cases lost significance during the period 2006–12 when adjusting for PM 10 , the impact remained statistically significant during 2013–20, despite small changes in effect size that occurred after controlling for the other three types of pollutants. The observed distinctions between the two periods continued to be statistically significant ( P < .05) after accounting for various pollutants.

As shown in Supplementary data online , Table S5 and Figures S10 and S11 , the main analysis model also showed no significant changes for the evaluated HNE–stroke associations after removing daily maximum temperature as a covariate or controlling for daily mean temperature instead of daily maximum temperature. The adjustments of knots for the exposure–response functions also did not significantly affect our main results (see Supplementary data online , Table S5 ).

This time-stratified case-crossover study over 15 years showed that nocturnal heat exposure was related to an increased stroke risk after controlling for daytime temperature. We also found that this risk increased during the recent period (2013–20) compared with an earlier period (2006–12). In addition to the effects on all strokes that we observed, we also found effects for ischaemic and haemorrhagic stroke subtypes during the more recent period. Older adults, women, or patients diagnosed with minor strokes (NIHSS < 5), small vessel disease, or cardioembolism experienced a significant increase in nighttime heat-related stroke risk over time ( Structured Graphical Abstract ). These findings suggest that exposure to nighttime heat should be considered a potentially preventable trigger of stroke events under a warming climate, especially given that the intensity of future warming at night is projected to be significantly higher than increases in daytime temperature.

Our results are aligned with existing evidence that nighttime heat can induce an extra health impact in addition to the daily temperature. 9 , 11 Specifically, we found that nighttime heat significantly increases the odds of stroke occurrence, suggesting that it may affect health outcomes other than total mortality. This finding is supported by numerous studies that have shown a significant association between heat exposure and increased stroke-related mortality. 7 , 27 Our study expands on this knowledge by identifying the specific impact of nighttime heat on stroke occurrence and highlights a clear trend of rising risk in more recent years, further emphasizing the urgent need to address this issue through public policy.

The increased risk of morbidity due to ambient heat detected in this study is in line with our previous finding, 20 which suggested that population susceptibility to heat-related myocardial infarction increased in Augsburg between the time periods 1987–2000 and 2001–14. There is substantial evidence of increasing tolerance to ambient heat in many parts of the world which may be due to many aspects of adaptation, such as physiological change and behavioural changes like air conditioning usage. 14 This inconsistency can be explained in a few ways. First, although the average daily mean temperature increases in Augsburg were mild (from 14.5°C during 2003–12 to 14.8°C during 2013–20), the number of days with high temperatures at night and the average HNE was much increased in the recent period. It is also important to note that in Germany, residential air conditioning usage is generally limited and average of usage rates across country lower than 20%. 28 In addition, according to the German Environment Agency, only ∼4.7% of households in Germany used air conditioning in their living space in 2017. Consequently, people may become more vulnerable to increased heat exposure, especially at night. Additionally, changes in population-level socioeconomic status may also modify that population’s HNE-related stroke risk over time. 20 In summary, changes in underlying drivers from climatic factors, stroke risk factors, and socioeconomic conditions may contribute to the increased susceptibility to nighttime heat-related stroke over time.

We also found varying results in risk of the stroke subtypes included in this study. We observed that extreme nighttime heat significantly increased the risk of ischaemic strokes and TIA in the full study period, and the magnitude of this risk was higher in the more recent period (2013–20) as compared with the earlier period (2006–12) ( P < .05). This finding aligns with a recent study indicating a positive association between increased hourly temperature and ischaemic strokes while suggesting that the incidence of haemorrhagic strokes is correlated with low temperatures. 29 The observed increase in the risk of ischaemic strokes during recent periods can be attributed to factors such as dehydration, elevated blood viscosity, and alterations in blood vessel functioning, which may be exacerbated by the occurrence of more frequent extreme nighttime heat. Specifically, dehydration increases the risk of ischaemic stroke because it concentrates the blood and raises the likelihood of blood clot formation, 30 especially under the condition of hot weather and with insufficient hydration during the night. Elevated blood viscosity during a hot night increases the risk of ischaemic strokes by promoting blood clot formation, reducing blood flow efficiency, and contributing to hypertension and atherosclerosis. 31 The potential hypoperfusion in patients with underlying carotid stenosis or intracranial stenosis due to higher nocturnal temperatures may also exacerbate the risk of ischaemic strokes. 32 The influence of enhanced heat exposure on haemorrhagic strokes appears to be less pronounced, possibly due to the relatively low number of cases. 33 However, high temperatures can increase the risk of hypertension, 34 which is one of the risk factors for haemorrhagic stroke. 35

Differences in risk within population subgroups may be due to differences in physiological characteristics. Increased risk among older individuals as compared with younger individuals can be explained by age-related physiological changes and decreased heat tolerance. These factors also make older individuals especially vulnerable during increasingly frequent of hot night events. In comparison with males, females face an increased risk of nighttime heat-related stroke, which may be explained by hormonal influences and physiological differences. Fluctuations in hormone levels during menstruation and menopause can lower women’s heat tolerance. 36 Furthermore, women generally possess a higher body fat percentage than men, which reduces their heat dissipation capacity. 37 Overall, these results suggested that the frequency of hot night events during the recent period may have a more detrimental effect on certain types of patients or sensitive population groups.

The main strength of the present study is the validated, complete, and detailed registration of all stroke cases over 15 years. This large sample size and long coverage enhance the reliability and generalizability of our findings. Second, the case-crossover design strengthens the validity of the findings and helps to rule out alternative cofounders. Third, we found that the impact of nocturnal heat exposure on stroke risk was greater in certain population groups, including older adults, women, and patients treated with minor strokes (NIHSS < 5). This underscores the importance of targeted prevention efforts and interventions to protect those most at risk.

Our findings carry significant public health implications. Firstly, healthcare systems should prioritize implementing heat health action plans that include targeted messaging and resources to mitigate the risks of nocturnal heat exposure. Secondly, community-level interventions such as providing education on heat-related illness prevention and improving urban green spaces can help protect vulnerable populations. Lastly, policymakers should consider integrating climate adaptation measures into urban planning, including implementing heat-resilient infrastructure and urban greening initiatives to reduce the urban heat island effect and mitigate the impact of rising nighttime temperatures.

Our study also has several limitations. First, our exposure data were obtained from one outdoor monitoring station, which may not be able to accurately represent the temperature exposures of cases living in different regions within the study area. However, this measurement error is likely to be random and might result in an underestimation of effect estimates. Second, indoor temperatures experienced by the cases may differ from outdoor temperatures. However, as the study period was limited to the warm season (May to October), the difference between indoor and outdoor temperatures may be less pronounced compared with the colder months. Third, our results are based on a monocentric study in Augsburg, Germany, and may not apply to other regions with different climatic, demographic, and socioeconomic conditions. Future studies using multicentre stroke registries are warranted to confirm our findings in other areas. In addition, our classification of stroke types relied on ICD-10 codes which, despite validation, may still harbour some inaccuracies and potentially introduce biases. Finally, due to the incompleteness of TOAST classification information, our results were unable to provide complete subgroup analysis results. Nevertheless, our current findings still reveal certain significant influencing mechanisms.

In conclusion, our 15-year registry-based time-stratified case-crossover study provides robust evidence that nocturnal heat exposure is associated with an increased risk of stroke. Moreover, we found a significant increase in this risk during the more recent period (2013–20) compared with the earlier period (2006–12), with significant impacts observed for all strokes and the ischaemic stroke subtypes. Certain population groups, including older adults, women, and patients treated with minor strokes, experienced a higher risk of nighttime heat-related stroke. These findings highlight the urgent need for preventive measures to mitigate the potential impact of nocturnal heat stress on stroke events, particularly in the context of future warming at night, which is projected to be significantly higher than daytime warming.

Supplementary data are available at European Heart Journal online.

Disclosure of Interest

All authors declare no disclosure of interest for this contribution.

Data were collected under a data sharing agreement and cannot be made publicly available.

C.H. is supported by the Alexander von Humboldt Foundation. V.H. received funding from the European Union’s Horizon 2020 research and innovation programme (Marie Skłodowska-Curie Grant Agreement No.: 101032087).

Ethical approval was not required.

None supplied.

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Author notes

transient ischemic attack
cerebrovascular accident
ischemic stroke
heat (physical force)
temperature
older adult
heat exposure
stroke risk
hemorrhagic stroke

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