Hypertension and Atrial Fibrillation: Bridging the Gap Between Mechanisms, Risk, and Therapy

Overview

Journal Medicina (Kaunas)

Publisher MDPI

Specialty General Medicine

Date 2025 Feb 26

PMID 40005478

Authors

Ibrahim Antoun

Georgia R Layton

Ali Nizam

Joseph Barker

Ahmed Abdelrazik

Mahmoud Eldesouky

Abdulmalik Koya

Edward Y M Lau

Mustafa Zakkar

Riyaz Somani

Ghulam Andre Ng

Affiliations

Soon will be listed here.

Abstract

Atrial fibrillation (AF), the most prevalent sustained arrhythmia, poses a significant public health challenge due to its links with stroke, heart failure, and mortality. Hypertension, a primary modifiable cardiovascular risk factor, is a well-established risk factor for AF that facilitates structural and electrical changes in the atria, including dilation, fibrosis, and pressure overload. we conducted a literature search regarding the shared mechanisms, risks and treatments of hypertension and atrial fibrillation. The renin-angiotensin-aldosterone system plays a pivotal role in this remodelling and inflammation, increasing AF susceptibility. Uncontrolled hypertension complicates AF management, diminishing the effectiveness of mainstay treatments, including antiarrhythmic drugs, catheter ablation, and cardioversion. Effective blood pressure management, particularly with therapies targeting the renin-angiotensin-aldosterone system (RAAS), can lower the risk of new-onset AF and reduce the incidence of recurrent AF, enhancing the success of rhythm control strategies. These antihypertensive therapies mitigate myocardial hypertrophy and fibrosis and attenuate both atrial pressure strain and the inflammatory response, mitigating the substrates for AF. This review highlights the urgent need for integrated strategies that combine BP control, AF screening, and lifestyle modifications to minimise the burden of AF and its complications. Future research should investigate the specific mechanisms of cellular-level interactions associated with a hypertensive predisposition to AF, including systematic inflammation and the role of genetics, the impact of blood pressure variations on AF risk, and individualised treatment strategies specifically targeting the shared mechanisms, simultaneously propagating hypertension and AF.

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