Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation

Kumagai, Koji; Nakashima, Hideko; Urata, Hidenori; Gondo, Naoki; Arakawa, Kikuo; Saku, Keijiro

doi:10.1016/s0735-1097(03)00464-9

Cited by 426 publications

(309 citation statements)

References 35 publications

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“…29,31 Other mechanisms by which ARBs could reduce the incidence of new or recurrent stroke include the beneficial effects of some ARBs on blood glucose control by increasing insulin sensitivity, 49,50 their platelet antiaggregating effects, [51][52][53][54] their hypouricemic effects 66,67 and their atrial antifibrillatory effects. [69][70][71] All these actions of ARBs could add to their AII-mediated stroke protective effects. However, these positive effects of ARBs on stroke protection should not by any means exclude the critical role of blood pressure control on stroke prevention, since the blood pressure levels (systolic and diastolic) have a continuous and direct effect on stroke incidence for all age groups.…”

Section: Discussionmentioning

confidence: 99%

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Possible pathophysiologic mechanisms supporting the superior stroke protection of angiotensin receptor blockers compared to angiotensin-converting enzyme inhibitors: clinical and experimental evidence

Chrysant

2005

J Hum Hypertens

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Stroke is a major cause of death and disability and its incidence increases linearly with age and the level of systolic and diastolic blood pressure. Stroke, besides being a cause of long-term disability for the affected person, also imposes a significant burden on society and healthcare costs. Although good blood pressure control is very critical for stroke prevention, angiotensin receptor blockers (ARBs) may be superior to angiotensin-converting enzyme inhibitors (ACEIs) for the same degree of blood pressure control. This hypothesis has clinical and experimental support. ARBs prevent stroke incidence by blocking the angiotensin II (AII), AT 1 receptors preventing brain ischaemia and allowing AII to stimulate the unoccupied AT 2 receptors, which improve brain ischaemia. ACEIs, by reducing AII generation, are less effective in preventing stroke. This hypothesis provides evidence that AII plays an important role in the prevention of stroke. Certain ARBs like losartan, and telmisartan, irbesartan and candesartan possess additional properties which may play a role in stroke prevention, which is independent of AII. These include antiplatelet aggregating, hypouricemic, antidiabetic and atrial antifibrillatory effects. However, the most critical factor in stroke prevention is good blood pressure control irrespective of drug used.

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Section: Discussionmentioning

confidence: 99%

“…These positive effects of candesartan were attributed to its suppression of structural atrial remodelling. 70 These beneficial effects of ARBs on AF could add to their stroke protective effects.…”

Section: Aii-mediated Effects Of Arbsmentioning

confidence: 99%

Possible pathophysiologic mechanisms supporting the superior stroke protection of angiotensin receptor blockers compared to angiotensin-converting enzyme inhibitors: clinical and experimental evidence

Chrysant

2005

J Hum Hypertens

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“…The irregular beats of frequent VPCs lead to an LV mechanical dyssynchrony, which can contribute to the increase of the LV filling pressures and atrial overload 26, 27. As a result, those hemodynamic changes activate the renin‐angiotensin‐aldosterone system in ventricle and atria through stretch of the heart and inflammatory cytokines, which might be associated with the progression of cardiac remodeling and finally lead to heart failure 4, 28, 29, 30. We speculate that ventricular chamber dilatation and myocardial fibrosis are the consequence from those pathological influences.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effect of Renal Denervation on Ventricular Premature Complex Induced Cardiomyopathy

Yamada

Chou

et al. 2017

JAHA

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BackgroundFrequent ventricular premature complexes (VPCs) can lead to the development of dilated cardiomyopathy and sudden cardiac death. Renal artery sympathetic denervation (RDN) may protect the heart from remodeling. This study aimed to investigate the effect of frequent VPCs on structural and electrical properties and whether RDN can protect the heart from remodeling.Methods and ResultsEighteen rabbits were randomized to control (n=6), VPC (n=6), and VPC‐RDN (n=6) groups. Surgical and chemical RDNs were approached through bilateral retroperitoneal flank incisions in the VPC‐RDN group. Pacemakers were implanted to the left ventricular apex to produce 50% VPC burden for 5 weeks in the VPC and VPC‐RDN groups. In addition, ventricular myocardium was harvested for western blot and trichrome stain. Echocardiographic results showed left ventricular enlargement after 5‐week pacing in the VPC group, but not in the VPC‐RDN group, when compared to baseline. In biventricles, ion channel protein expressions of Nav1.5, Cav1.2, Kir2.1, and SERCA2 were similar among 3 groups. However, the degree of biventricular fibrosis was extensive in the VPC group, compared to the control and VPC‐RDN groups. Importantly, ventricular fibrillation inducibility was higher in the VPC group (41%) when comparing to the control (13%; P<0.05) and VPC‐RDN groups (13%; P<0.05), respectively.ConclusionsFrequent VPCs are associated with the development of cardiac structural remodeling and high ventricular fibrillation inducibility. RDN prevents cardiac remodeling and the occurrence of ventricular arrhythmia through antifibrosis.

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“…There is strong experimental evidence that angiotensin receptor blockers (ARBs) and angiotensin converting enzyme (ACE) inhibitors can prevent electrical remodeling and reduce interstitial fibrosis in heart failure or rapid atrial pacing models of AF independently of the reduction in intra-atrial pressures. 22,23 These observations open the possibility of exploitation of these agents to prevent or delay atrial remodeling in patients with AF even in the absence of routine indications for such therapy.…”

Section: Angiotensin Ii-mediated Remodelingmentioning

confidence: 99%

Update on Atrial Fibrillation: Part I

Savelieva

Camm

2008

Clinical Cardiology

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SummaryAtrial fibrillation (AF) is an epidemic, affecting 1% to 1.5% of the population in the developed world. Projected data from the population-based studies suggest that the prevalence of AF will grow at least 3-fold by 2050. The health and economic burden imposed by AF and AFrelated morbidity is enormous.Atrial fibrillation has a multiplicity of causes ranging from genetic to degenerative, but hypertension and heart failure are the commonest and epidemiologically most prevalent conditions associated with AF as both have been shown to create an arrhythmogenic substrate. Several theories emerged regarding the mechanism of AF, which can be combined into two groups: the single focus hypothesis and the multiple sources hypothesis. Several lines of evidence point to the relevance of both hypotheses to the mechanism of AF, probably with a different degree of involvement depending on the variety of AF (paroxysmal or persistent). Sustained AF alters electrophysiological and structural properties of the atrial myocardium such that the atria become more susceptible to the initiation and maintenance of the arrhythmia, a process known as atrial remodeling. Angiotensin II has been recognized as a key element in atrial remodeling in association with AF opening the possibility of exploitation of "upstream" therapies to prevent or delay atrial remodeling. The clinical significance of AF lies predominantly in a 5-fold increased risk of stroke. The limitations of warfarin prompted the development of new antithrombotic drugs, which include anticoagulants, such as direct oral thrombin inhibitors (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban). Novel mechanical approaches for the prevention of cardioembolic stroke have recently been evaluated: percutaneous left atrial appendage occluders, minimally invasive surgical isolation of the left atrial appendage, and implantation of carotid filtering devices.

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Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation

Abstract: Candesartan can prevent the promotion of AF by suppressing the development of structural remodeling.

Cited by 426 publications

References 35 publications

Possible pathophysiologic mechanisms supporting the superior stroke protection of angiotensin receptor blockers compared to angiotensin-converting enzyme inhibitors: clinical and experimental evidence

Possible pathophysiologic mechanisms supporting the superior stroke protection of angiotensin receptor blockers compared to angiotensin-converting enzyme inhibitors: clinical and experimental evidence

Beneficial Effect of Renal Denervation on Ventricular Premature Complex Induced Cardiomyopathy

Update on Atrial Fibrillation: Part I

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