Renovascular hypertension (RVH) is an under-recognized but potentially reversible cause of secondary hypertension with significant cardiovascular consequences. Excess aldosterone resulting from renin–angiotensin–aldosterone system activation leads to potassium loss, QT-interval prolongation, and increased susceptibility to malignant ventricular arrhythmias. Hypokalemia combined with hypertension-mediated left-ventricular hypertrophy further increases myocardial electrical instability, predisposing to polymorphic ventricular tachycardia (PVT). We report a woman in her fifties who presented with recurrent syncope secondary to PVT associated with severe hypokalemia. Biochemical evaluation revealed elevated plasma renin activity and aldosterone with a low aldosterone-to-renin ratio. Further evaluation with CT angiography demonstrated critical unilateral atherosclerotic renal artery stenosis. Following percutaneous angioplasty and stent placement, blood pressure and serum potassium normalized, and there were no further arrhythmic episodes. This case highlights a rare but clinically important cardiovascular manifestation of unilateral renal artery stenosis presenting as polymorphic ventricular tachycardia. Recognition of hypokalemia-mediated electrophysiological instability as a reversible cause of life-threatening arrhythmia is essential, as timely revascularization can achieve complete clinical resolution.
Secondary hypertension accounts for a small but clinically significant proportion of hypertensive disease, with renovascular hypertension (RVH) representing one of the few potentially reversible causes. In adults, atherosclerotic renal artery stenosis (ARAS) is the predominant aetiology and is often under-recognized until advanced cardiovascular complications occur. Chronic renal hypoperfusion activates the renin–angiotensin–aldosterone system (RAAS), producing persistent hypertension, volume expansion, and metabolic abnormalities such as hypokalemia and metabolic alkalosis. Although these effects contribute to increased cardiovascular risk, their direct arrhythmic manifestations are rarely documented. Hypokalemia-induced QT-interval prolongation can lead to ventricular electrical instability and, in extreme cases, malignant polymorphic ventricular tachycardia (PVT). Only isolated reports have described PVT as the presenting feature of unilateral renal artery stenosis. Early recognition of this association is crucial because revascularization may completely reverse both the biochemical disturbance and the arrhythmic risk. We report a case of unilateral ARAS presenting initially with recurrent syncope and PVT, illustrating the interplay between renal vascular disease, neurohormonal activation, and ventricular arrhythmogenesis.
Case Presentation
A woman in her mid-fifties with no significant past medical history was referred to our center with recurrent syncopal episodes over 24 hours. On examination, her blood pressure was 200/110 mm Hg, jugular venous pressure was normal, and a fourth heart sound was audible. She was started on antihypertensive therapy with oral nifedipine 20 mg (sustained release, stat), followed by amlodipine 5 mg twice daily.
The initial 12-lead electrocardiogram (ECG) showed sinus rhythm with 1:1 atrioventricular conduction, heart rate 71 beats/min, PR interval 160 ms, QRS duration 60 ms, and a markedly prolonged QT interval of 600 ms (QTc = 720 ms by Bazett’s formula) ( Figure 1 ). During an episode of presyncope, ECG monitoring demonstrated short-coupled premature ventricular complexes (PVCs) occurring in bigeminy, falling on the T wave and producing an R-on-T phenomenon, followed by brief runs of polymorphic ventricular tachycardia (PVT) ( Figure 2 ).
The presenting electrocardiogram (ECG) demonstrated sinus rhythm with 1:1 atrioventricular conduction, heart rate of 71 beats per minute, PR interval of 160 ms, QRS duration of 60 ms, and a markedly prolonged QT interval of 600 ms. The corrected QT interval (QTc), calculated using Bazett’s formula, was 720 ms.
Short-coupled premature ventricular complexes occurring in bigeminy, falling on the T wave (R-on-T phenomenon), resulting in runs of polymorphic ventricular tachycardia.
Laboratory investigations including cardiac biomarkers, thyroid profile, and liver function tests were unremarkable except for serum potassium 2.68 mEq/L. Arterial blood gas analysis revealed metabolic alkalosis (pH 7.55, PaCO₂ 39 mm Hg, HCO₃⁻ 34 mEq/L). The arrhythmia responded acutely to intravenous potassium and magnesium replacement. Emergency overdrive pacing was instituted via a temporary pacemaker introduced through the right internal jugular vein. Intravenous nitroglycerin and a calcium channel blocker were initiated for blood-pressure control.
Transthoracic echocardiography showed concentric left-ventricular hypertrophy with preserved systolic function and no valvular abnormality. Evaluation for the cause of concurrent hypertension and hypokalemia was undertaken. Early-morning cortisol was normal, and an overnight 1 mg dexamethasone suppression test yielded a post-test cortisol of 1.60 µg/dl, excluding Cushing’s syndrome. Despite continuous intravenous potassium supplementation, hypokalemia persisted. Antihypertensive therapy was escalated to amlodipine 10 mg twice daily, spironolactone 25 mg twice daily, and clonidine 100 µg three times daily.
Subsequent biochemical evaluation demonstrated elevated plasma aldosterone (97.3 ng/dl) and plasma renin activity (7.91 ng/mL/h) with a low aldosterone-to-renin ratio of 12.3, consistent with secondary hyperaldosteronism. Further imaging with contrast-enhanced CT angiography revealed approximately 90% stenosis of the ostioproximal segment of the left renal artery, a normal right renal artery, and >2.5 cm difference in kidney size. No adrenal mass was seen ( Table 1 ).
Table 1
List of investigations done and their results consolidated
| Normal | Altered |
|---|---|
|
• Complete blood picture
• Serum magnesium (2.1 mg/dl) • Liver function tests • Thyroid profile (TSH-3.3Miu/L) • Cardiac biomarkers • Overnight dexamethasone suppression test • Early morning serum cortisol |
• ECG-Polymorphic VT
• Serum potassium-decreased • ABG-metabolic alkalosis • Plasma renin-elevated • Aldosterone-elevated • Aldosterone/renin-low • CECT abdomen-unilateral renal artery stenosis |
Question 1:
In patients with renal artery stenosis, which physiological mechanism primarily contributes to severe hypertension?
A. Increased sympathetic discharge from renal nerves
B. Activation of the renin–angiotensin–aldosterone system (RAAS) due to renal hypoperfusion
C. Impaired prostaglandin synthesis in the macula densa
D. Reduced sodium delivery to the distal nephron
E. Increased endothelin release from damaged endothelium
Answer: B. Activation of the RAAS due to renal hypoperfusion.
Reduced perfusion pressure in the affected kidney stimulates renin release from juxtaglomerular cells, causing systemic vasoconstriction and sodium retention mediated by angiotensin II and aldosterone.
Based on clinical, biochemical, and imaging findings, a diagnosis of unilateral atherosclerotic renal artery stenosis (ARAS) causing secondary hyperaldosteronism was made ( Table 2 ). The patient underwent percutaneous transluminal angioplasty with deployment of a 7.0 × 18 mm Herculink Elite renal stent (Abbott Vascular, Santa Clara) ( Figures 3 and 4 ).
Table 2
Differential diagnosis for refractory hypertension and their expected renin and aldosterone levels
| Differentials-refractory hypokalemia & hypertension | Plasma renin activity (PRA) | Plasma aldosterone levels (PAL) | PAL/PRA |
|---|---|---|---|
| Primary hyperaldosteronism | Low | High | >30 |
| Renal artery stenosis | High | High | <30 |
| Cushing’s disease | High | High | <30 |
| Phaeochromocytoma (presents with episodic hypertension) | Low | Low | <30 |
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