Effects of RAAS Blockers on Atrial Fibrillation Prophylaxis

Chaugai, Sandip; Meng, W.; Sepehry, Amir Ali

doi:10.1177/1074248415619490

Cited by 40 publications

(20 citation statements)

References 66 publications

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“…The atrial fibrosis induced by heart failure leads to slower, heterogeneous conduction promoting wavebreak and re-entry (Li et al, 1999 ; Sanders et al, 2003 ; Akkaya et al, 2013 ). In an effort to prevent the deleterious effects of structural remodeling, anti-fibrotic agents have been explored and shown to reduce atrial fibrosis and vulnerability to AF in models of heart failure (Lee et al, 2006 ; Le Grand et al, 2014 ) and appear to reduce the incidence of AF in clinical trials (Chaugai et al, 2016 ).…”

Section: The Interplay Between Heart Failure and Atrial Fibrillationmentioning

confidence: 99%

Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure

et al. 2018

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Atrial fibrillation (AF) is commonly associated with heart failure. A bidirectional relationship exists between the two—AF exacerbates heart failure causing a significant increase in heart failure symptoms, admissions to hospital and cardiovascular death, while pathological remodeling of the atria as a result of heart failure increases the risk of AF. A comprehensive understanding of the pathophysiology of AF is essential if we are to break this vicious circle. In this review, the latest evidence will be presented showing a fundamental role for calcium in both the induction and maintenance of AF. After outlining atrial electrophysiology and calcium handling, the role of calcium-dependent afterdepolarizations and atrial repolarization alternans in triggering AF will be considered. The atrial response to rapid stimulation will be discussed, including the short-term protection from calcium overload in the form of calcium signaling silencing and the eventual progression to diastolic calcium leak causing afterdepolarizations and the development of an electrical substrate that perpetuates AF. The role of calcium in the bidirectional relationship between heart failure and AF will then be covered. The effects of heart failure on atrial calcium handling that promote AF will be reviewed, including effects on both atrial myocytes and the pulmonary veins, before the aspects of AF which exacerbate heart failure are discussed. Finally, the limitations of human and animal studies will be explored allowing contextualization of what are sometimes discordant results.

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Section: The Interplay Between Heart Failure and Atrial Fibrillationmentioning

confidence: 99%

Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure

et al. 2018

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“…Treatment with an angiotensin receptor blocker or an angiotensin-converting enzyme inhibitor was reported to inhibit cardiac remodeling in dogs [26,27,28]. Results of clinical trials appear to indicate that inhibition of the rennin-angiotensin system may prevent the new-onset or recurrence of atrial fibrillation [29,30,31,32,33]. Angiotensin II also has acute hypertensive and antidiuretic effects through induction of vascular contraction and aldosterone release.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II Induces Automatic Activity of the Isolated Guinea Pig Pulmonary Vein Myocardium through Activation of the IP3 Receptor and the Na+-Ca2+ Exchanger

Tanaka

Obata

Ohmori

et al. 2019

IJMS

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The automaticity of the pulmonary vein myocardium is known to be the major cause of atrial fibrillation. We examined the involvement of angiotensin II in the automatic activity of isolated guinea pig pulmonary vein preparations. In tissue preparations, application of angiotensin II induced an automatic contractile activity; this effect was mimicked by angiotensin I and blocked by losartan, but not by PD123,319 or carvedilol. In cardiomyocytes, application of angiotensin II induced an increase in the frequency of spontaneous Ca2+ sparks and the generation of Ca2+ transients; these effects were inhibited by losartan or xestospongin C. In tissue preparations, angiotensin II caused membrane potential oscillations, which lead to repetitive generation of action potentials. Angiotensin II increased the diastolic depolarization slope of the spontaneous or evoked action potentials. These effects of angiotensin II were inhibited by SEA0400. In tissue preparations showing spontaneous firing of action potentials, losartan, xestospongin C or SEA0400 decreased the slope of the diastolic depolarization and inhibited the firing of action potentials. In conclusion, in the guinea pig pulmonary vein myocardium, angiotensin II induces the generation of automatic activity through activation of the IP3 receptor and the Na+-Ca2+ exchanger.

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“…Clinical targeting of modifiable AF risk factors such as diabetes, hypertension, obesity, and obstructive sleep apnea should be early and aggressive. Statins, and anti-inflammatory drugs targeting cytokines (IL-1β, IL-6, and TNF-α) and the reninangiotensin-aldosterone system (RAAS) have been tried as potential therapies to forestall the progression of inflammation and fibrosis (Savelieva et al, 2011a;Savelieva et al, 2011b;Chaugai et al, 2016). Unfortunately, clinical success is still lacking, consistent with the irreversibility of structural remodeling.…”

Section: Targeting Structural Remodelingmentioning

confidence: 99%

“…For example, following T 5 spinal cord transection, parasympathetic hyperinnervation causes dilation of left ventricular chamber, thinning of myocardial wall, and increased collagen content ( Lujan et al, 2014 ). Therefore, it comes as no surprise that suppression of vagal stimulation by anticholinergic drugs or vagal denervation may improve the efficacy of pulmonary vein isolation to prevent AF recurrence ( Chen and Tan, 2007 ) and reduces AF inducibility ( Elvan et al, 1995 ). Likewise, suppression of vagal stimulation by ablation of pulmonary vein ganglionated plexi may increase the success of pulmonary vein isolation by mitigating vagally-induced shortening of atrial ERP ( Lemola et al, 2008 ).…”

Section: Redefining Therapeutic Goalsmentioning

confidence: 99%