PS-BPR02-6: NOT FOR THE FAINT OF HEART: A CASE REPORT OF BRADYCARDIA INDUCED HYPERTENSION

Abstract

Background: Bradycardia is an underreported and often overlooked contributor to resistant hypertension. We present a case of refractory hypertension and bradycardia with atrial fibrillation and marked improvement in BP control following pacemaker implantation. Case Presentation: A 66-year-old asymptomatic Chinese male with a past history of hypertension with unilateral adrenalectomy (no hyperaldosteronism), remote myocardial infarction, treated obstructive sleep apnea, and type 2 diabetes presented with gradually increasing blood pressure (BP) and decreasing heart rate (HR). From 2019 to 2020, his 24-hour ambulatory BP average increased from 140/49 mmHg to 188/66 mmHg with a decrease in HR from 55 to 43 bpm; there was no significant nocturnal dipping. Home and office BPs were similar. Daily medications included candesartan 64 mg, amlodipine 20 mg, chlorthalidone 50 mg, spironolactone 50 mg, doxazosin 8 mg, hydralazine 300 mg, nitropatch 0.8 mg/hour, and kayexalate for persistent hyperkalemia. Medication adherence was confirmed by a pharmacy database review. Secondary hypertension workup was negative for Cushing's Disease, pheochromocytoma, and renal artery stenosis. Plasma aldosterone was undetectable and plasma renin activity was 1.95 (normal 0.10–1.10ng/L/s) while taking the above medications. Serial 24-hour Holter monitors captured sinus bradycardia without pauses. Echocardiogram revealed concentric left ventricular (LV) hypertrophy, left atrial enlargement, and LV ejection fraction of 55%. Subsequent 2-week Holter monitoring revealed atrial fibrillation with average HR of 44 bpm and multiple prolonged ventricular pauses (longest 5.1 seconds). Following pacemaker insertion, BP normalized to an average of 130/80 mmHg with only 3 agents. Conclusion: There is a paucity of literature on severe bradycardia resulting in resistant hypertension; the English language PubMed database documents 3 reported cases. Severe bradycardia may impair cerebral and renal blood flow, increase LV filling pressures through prolonged diastole causing greater ventricular stretch and increased force of contraction, and may alter arterial stiffness. This case demonstrates a rare but important phenomenon of refractory hypertension and bradycardia with marked improvement in BP control following pacemaker insertion. It is important that physicians are aware of this potential phenomenon when evaluating patients with resistant hypertension and bradycardia.