Hypertension and Arrhythmias: A Clinical Overview of the Pathophysiology-Driven Management of Cardiac Arrhythmias in Hypertensive Patients

Abstract

Because of demographic aging, the prevalence of arterial hypertension (HTN) and cardiac arrhythmias, namely atrial fibrillation (AF), is progressively increasing. Not only are these clinical entities strongly connected, but, acting with a synergistic effect, their association may cause a worse clinical outcome in patients already at risk of ischemic and/or haemorrhagic stroke and, consequently, disability and death. Despite the well-known association between HTN and AF, several pathogenetic mechanisms underlying the higher risk of AF in hypertensive patients are still incompletely known. Although several trials reported the overall clinical benefit of renin-angiotensin-aldosterone inhibitors in reducing incident AF in HTN, the role of this class of drugs is greatly reduced when AF diagnosis is already established, thus hinting at the urgent need for primary prevention measures to reduce AF occurrence in these patients. Through a thorough review of the available literature in the field, we investigated the basic mechanisms through which HTN is believed to promote AF, summarising the evidence supporting a pathophysiology-driven approach to prevent this arrhythmia in hypertensive patients, including those suffering from primary aldosteronism, a non-negligible and under-recognised cause of secondary HTN. Finally, in the hazy scenario of AF screening in hypertensive patients, we reviewed which patients should be screened, by which modality, and who should be offered oral anticoagulation for stroke prevention.

Keywords: anticoagulants; antihypertensive agents; artificial pacemakers; atrial fibrillation; hypertension; primary hyperaldosteronism.

Figure 1

Electro-pathological and clinical changes occurring in hypertensive hearts. ARP, atrial refractory period; SNS, sympathetic nervous system; CV, conduction velocity; CX43, connexin 43; DADs, delayed afterdepolarizations; EADs, early afterdepolarizations; ECM, extracellular matrix; LA, left atrial; LA Vol, left atrial volume; LV, left ventricular; RAAS, renin–angiotensin–aldosterone system. See text for further details.

Figure 2

Screening and diagnostic approach for primary aldosteronism. A positive screen for primary aldosteronism should suggest high aldosterone levels and a suppressed renin activity. Confirmatory testing can be used in this setting. Solid arrows indicate recommended decision pathways; dashed arrows indicate other possible diagnostic alternatives in appropriate clinical contexts. * Confirmatory testing suggesting aldosterone hypersecretion: (1) oral sodium suppression (positive if 24 h urinary aldosterone excretion rate is greater than 12–14 mg/die); (2) supine intravenous saline suppression (positive if aldosterone levels are greater than 10 ng/dL after 2 L of saline infusion); (3) fludrocortisone suppression (positive if seated aldosterone greater than 6 ng/dL with plasma renin activity lower than 1.0 ng/mL/h); and, finally, (4) captopril challenge (positive if less than 30% suppression of aldosterone from baseline while plasma renin activity remains suppressed post 25 mg of oral captopril). AF, atrial fibrillation; BP, blood pressure; HTN, hypertension; MRA, mineralcorticoid-receptor antagonists; OSAS, obstructive sleep apnea syndrome; PA, primary aldosteronism. (Modified and adapted from document of The Endocrine Society [101]).

Figure 3

(A–D). Computed tomography of the abdomen in a patient with suspected primary aldosteronism. A 78-year-old patient referred to medical attention for dysregulated hypertension, irregular heartbeat, and remarkable peripheral oedema. Upon admission, 12-lead ECG showed atrial fibrillation with high ventricular rate. Transthoracic echocardiogram displayed signs of moderate left ventricular hypertrophy only. Laboratory tests showed remarkably low potassium levels together with high levels of serum aldosterone and suppressed renin activity. Therefore, computed tomography scan of the abdomen with iodine contrast administration was then carried out to identify any adrenal mass (A–D). A 10 cm, bulky adrenal tumor is well evident from cross-sectional imaging acquired during the arterial phase (A). The mass (white arrows) shows hypodense foci and colliquative areas with signs of compression of the neighboring anatomical structures. From a caudal to a more cranial perspective, the inferior vena cava and renal veins are progressively compressed and anteriorly dislodged by the adrenal mass (dashed arrows, B–D), thus explaining the remarkable peripheral oedema clinically observed in this patient. The patient is currently scheduled for abdominal video laparoscopy for adrenal mass excision and the ensuing histopathologic characterization.

Figure 4

Proposed algorithm for early detection and management of silent and subclinical atrial fibrillation episodes. AF = atrial fibrillation; CIED = cardiac implantable electronic devices; ICM = internal cardiac monitor; ILR = internal loop recorder; HTN = hypertension.