MPO levels are modulated by renin-angiotensin system antagonists (RAS-A), commonly used to treat AF comorbidities, and are associated with reduced AF incidence, implicating a potential link.
Hypertensive patients carrying the control genotype of rs2074192 (CC, OR = 2.37, 95% CI: 1.28-4.39) were associated with CAS ≥50%, while those carrying a high-EH-risk genotype of rs4240157 (OR = 2.62, 95% CI: 1.24-5.54), rs4646155 (OR = 2.44, 95% CI: 1.16-5.10), or rs4830542 (CC+CT, OR = 2.20, 95% CI: 1.03-4.69) were associated with atrial fibrillation (AF), larger left atrial diameter, and higher levels of renin-angiotensin-aldosterone system (RAAS) activation (renin and angiotensin I/II).
The present study hypothesizes that apelin/APJ axis exert its anti-thrombus effect in normal left atrial tissue and is disrupted by up-regulated renin-angiotensin-aldosterone system (RAAS) signaling during AF.
Factors associated with AF in multivariate analyses included CHA2DS2-VASc score (odds ratio, OR: 1.48; 95% confidence interval, CI: 1.25-1.75; P < 0.001), peak creatine kinase-myocardial binding (OR: 1.002; 95% CI: 1.00-1.003; P = 0.0024), duration of the coronary intensive care unit stay (OR: 1.69; 95% CI: 1.24-12.30; P = 0.001) and no use of renin-angiotensin system blockers (OR: 2.16; 95% CI: 1.14-4.10; P = 0.0017).
It is uncertain whether an intensive control of BP or the use of specific antihypertensive drugs, such as those inhibiting the renin-angiotensin-aldosterone system, reduces the risk of subsequent AF in hypertensive patients in sinus rhythm.
While the initiation of pathogenic pathways leading to AF varies with disease (including increased glycosylation in diabetes, increased renin angiotensin aldosterone system activation in hypertension, atrial ischemia in coronary artery disease, and sleep apnea) the pathogenesis of AF is united by shared mediators of altered conduction in the atria.
We examined whether the use of a renin-angiotensin-aldosterone system (RAS) inhibitor plays a role in protecting against left atrial appendage thrombus (LAAT) in patients with hypertension complicated by atrial fibrillation (AF).
Renin-angiotensin system inhibition is associated with reduced risk of left atrial appendage thrombosis formation in patients with atrial fibrillation.
Blockade of the renin-angiotensin-aldosterone system (RAAS) with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARB) has been shown to decrease incident atrial fibrillation (AF).
When compared with patients with essential hypertension, patients with PA treated with MR antagonists such that renin remained suppressed (as a proxy for insufficient MR blockade) had a significantly higher risk for incident AF; however, treatment of PA with MR antagonists to substantially increase renin (suggesting sufficient MR blockade), or with surgical adrenalectomy (to remove the source of aldosteronism), was associated with no significant difference in risk for developing AF.
Although atrial fibrillation (AF) guidelines indicate that pharmacological blockade of the renin-angiotensin system may be considered for primary AF prevention in hypertensive patients, previous studies have yielded conflicting results.
Patients with persistent/permanent AF more frequently had elevated renin than patients with paroxysmal AF (34.1% vs 15.8%; P = .007).This prospective study of consecutive cardiac disease patients referred for cardiac catheterization has revealed distinct cardiac disease condition-associated differences in the frequencies of elevations in plasma renin, PAC, and the aldosterone-renin ratio.
Accumulating evidences point to a major role of the renin-angiotensin-aldosterone system in inducing cardiac inflammation and fibrosis, and therefore electric and structural atrial and ventricular remodelling, with changes in ions and cell junctions leading to AF development.
The purpose of this study was to investigate the effect of polymorphisms of renin-angiotensin system genes on the incidence of stroke in a prospective cohort of patients with AF.