Hypertension — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr David Nguyen, 52 years old. ^[1]

Presenting complaint: Referred by his GP for uncontrolled blood pressure. He has been hypertensive for 10 years. Despite treatment his BP readings remain in the 160s/90s. He feels well — no headaches, chest pain, palpitations, visual symptoms, or exertional dyspnoea. He has noticed waking unrefreshed and his wife reports he snores loudly. ^[1]

Past history:

• Hypertension diagnosed age 42
• Type 2 diabetes (HbA1c 58 mmol/mol), on metformin
• Dyslipidaemia
• No prior cardiovascular events ^[1]

Current medications:

• Perindopril 10 mg daily
• Amlodipine 10 mg daily
• Indapamide modified-release 1.5 mg daily
• Metformin 1 g BD
• Atorvastatin 40 mg nocte ^[1]

Examination findings (trainee elicits):

• BMI 32, large neck circumference (44 cm)
• BP 164/94 seated (right arm), 168/96 left arm; standing 158/92
• Pulse 72 regular, normal character
• Apex beat: thrusting, 5th ICS mid-clavicular line (LVH)
• S4 gallop audible at apex
• No murmurs, no parasternal heave, JVP not elevated, chest clear
• No abdominal or flank bruits, no radio-femoral delay, all pulses present
• Fundoscopy: arteriolar narrowing and AV nipping (grade 2 retinopathy) ^[1]

Investigations:

• eGFR 58, potassium 3.4 mmol/L (on indapamide)
• Urine ACR 8 mg/mmol (microalbuminuria)
• ECG: sinus rhythm, Sokolow-Lyon criteria positive for LVH (SV1 + RV5 = 38 mm)
• Fasting lipid: LDL 2.4 mmol/L, HDL 1.0 mmol/L, TG 2.1 mmol/L
• HbA1c 58 mmol/mol ^[1]

Candidate's structured presentation (model)

Opening statement: ^[1]

"Mr Nguyen is a 52-year-old man with a 10-year history of hypertension, now resistant to three agents, and with coexisting type 2 diabetes and dyslipidaemia. He presents with objective evidence of target organ damage and features suggesting a secondary cause. ^[1]

His main problems are:

1. Resistant hypertension — BP 164/94 despite perindopril, amlodipine, and indapamide at maximal doses, with confirmed adherence
2. Possible secondary cause — onset at 42, resistance, and hypokalaemia (3.4) on a thiazide raise suspicion for primary aldosteronism; he also has features of obstructive sleep apnoea (loud snoring, unrefreshed sleep, BMI 32, large neck)
3. Target organ damage — left ventricular hypertrophy (thrusting apex, S4, ECG voltage criteria), microalbuminuria, hypertensive retinopathy
4. Type 2 diabetes and dyslipidaemia — elevated cardiovascular risk
5. Obesity (BMI 32) contributing to resistance" ^[1]

Management plan: ^[1]

1. Confirm resistant hypertension and exclude pseudo-resistance:

   • 24-hour ABPM to exclude white-coat effect and assess nocturnal dipping
   • Confirm adherence (non-judgemental discussion; pharmacy refill data)
   • Screen for OSA — STOP-BANG questionnaire and home sleep study (he scores at least 6 of 8: snoring, tiredness, hypertension, age over 50, neck 44 cm, male — high risk, even though his BMI of 32 is below the BMI criterion of 35) ^[1]

2. Screen for primary aldosteronism:

   • Measure aldosterone-to-renin ratio (ARR), correcting hypokalaemia first
   • If elevated, proceed to confirmatory suppression testing per Endocrine Society guideline
   • Localise with adrenal CT then adrenal venous sampling if confirmed ^[1]

3. Pharmacological escalation:

   • Add spironolactone 25 mg daily — the PATHWAY-2 trial (335 patients) demonstrated superiority over placebo, bisoprolol, and doxazosin as the fourth-line agent in resistant hypertension
   • Monitor potassium and renal function at 1 week, then monthly
   • Target BP under 130/80 given diabetes and target organ damage ^[1]

4. Address OSA:

   • CPAP therapy if sleep study confirms OSA — lowers BP by a few mmHg on average and improves daytime symptoms ^[1]

5. Lifestyle and risk factor management:

   • Weight reduction, salt restriction, exercise
   • Optimise diabetes and lipid control ^[1]

Examiner discussion questions

Q: "Why is the ARR the correct screening test, and what interferes with it?" ^[1]

"The ARR detects autonomous aldosterone production by combining an elevated aldosterone with suppressed renin. It is the recommended first-line screen because it is more sensitive than aldosterone alone and detects primary aldosteronism even when potassium is normal — which it is in most patients. Several factors interfere with the ratio. Hypokalaemia suppresses aldosterone secretion, so I correct it first. The ACE inhibitor he takes suppresses aldosterone (via reduced angiotensin II) and raises renin, which can lower the ratio and cause a false negative — so a clearly elevated ARR despite the ACE inhibitor is highly significant, while a borderline result may require withdrawing the ACE inhibitor for two weeks and retesting. Diuretics raise renin. Spironolactone and eplerenone must be withdrawn for at least four weeks. Beta-blockers suppress renin and can give a false positive." ^[1]

Q: "What is the role of renal artery stenosis, and would you stent it?" ^[1]

"Renal artery stenosis, usually atherosclerotic, can cause or worsen hypertension. Clues include abrupt onset, abdominal bruit, flash pulmonary oedema, and a creatinine rise on starting an ACE inhibitor. Mr Nguyen has none of these. If I suspected it, I would image with renal artery Doppler or CT angiography. However, the CORAL trial (PMID 24245566) showed that routine stenting added to medical therapy did not significantly reduce the composite cardiovascular/renal endpoint (35.1% vs 35.8%, HR 0.94). ^[4] I would reserve stenting for resistant hypertension despite optimal medical therapy, refractory flash pulmonary oedema, or rapidly progressive renal dysfunction." ^[1]

Q: "How would his diabetes and CKD change your drug choice?" ^[1]

"The ACE inhibitor he is already on is exactly right — it is first-line in diabetes with albuminuria for renoprotection, reducing intraglomerular pressure. His target BP is under 130/80 given the combination of diabetes, CKD, and target organ damage. I would ensure the ACE inhibitor is not stopped for his modest CKD — a creatinine rise up to 30% on initiation is acceptable. I would avoid thiazide-induced hyperglycaemia worsening his diabetes (indapamide has a weaker glycaemic effect than hydrochlorothiazide, so his current choice is reasonable). I would also add an SGLT2 inhibitor for dual BP and renal protection in diabetic kidney disease." ^[1]