The renin-angiotensin-aldosterone system in atrial fibrillation: a new therapeutic target?

Freestone, Bethan; Beevers, D. G.; Lip, Gregory Y.H.

doi:10.1038/sj.jhh.1001694

Cited by 21 publications

(16 citation statements)

References 29 publications

(25 reference statements)

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“…Activation of RAS plays a central role in the development of cardiovascular diseases [39,40]. Studies have shown that RAS is involved in cardiac structural remodeling and the development of myocardial fibrosis in several disease states, including CHF [41,42], myocardial infarction (MI) [43,44], cardiomyopathy [45] and AF [29,46]. In the RAS system, angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II (Ang-II), which acts via the counter-regulatory Ang-II receptors, type I (AT-1) and type II (AT-2) receptors, that induce opposing responses [42,47].…”

Section: Rasmentioning

confidence: 99%

Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation

Lin

Pan

2008

Cell. Mol. Life Sci.

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Electrical, contractile and structural remodeling have been characterized in atrial fibrillation (AF), and the latter is considered to be the major contributor to AF persistence. Recent data show that interstitial fibrosis can predispose to atrial conduction impairment and AF induction. The interplay between cardiac matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of MMPs (TIMPs), is thought to be critical in atrial extracellular matrix (ECM) metabolism. At the molecular level, angiotensin II, transforming growth factor-beta1, inflammation and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodeling in AF. Therefore, we review recent advances in the understanding of the atrial fibrotic process, the major downstream components in this remodeling process, and the expression and regulation of MMPs and TIMPs. We also describe the activation of bioactive molecules in both clinical studies and animal models to modulate MMPs and TIMPs and their effects on atrial fibrosis in AF.

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Section: Rasmentioning

confidence: 99%

Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation

Lin

Pan

2008

Cell. Mol. Life Sci.

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“…9 Equally, interruption of the RAAS by either angiotensin converting enzyme (ACE) inhibitors (ACE inhibitors) and/or angiotensin II receptor blockers (ARBs) are highly effective in reducing the known cardiovascular outcomes of these diseases. 10 The likelihood that RAAS is also involved in the pathophysiology of AF, and that RAAS blockade improves outcomes in AF merits plausibility.…”

mentioning

confidence: 99%

“…In addition, there are now mounting data to suggest that modulation of the RAAS might have an important role in the prevention of AF and its consequences. 9,10 The development and maintenance of AF is highly complex, and the RAAS may have a key role here. For example, AF leads to well-recognised changes within the atrium known as electrical and structural remodelling that perpetuates the arrhythmia (AF begets AF).…”

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confidence: 99%

Targeting the renin–angiotensin–aldosterone system in atrial fibrillation: from pathophysiology to clinical trials

Boos

Lip

2005

J Hum Hypertens

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“…As the relationship between the RAAS and diabetic macrovascular or microvascular disease is well established, 25 there is also sufficient reason to target the RAAS in patients with AF. 26,27 In addition to the circulating hormone system, local tissue bound RAAS has also been recognised and well described to modulate cardiac hypertrophy and remodelling. 28 Hyperglycaemia, by causing glycosylation of p53, can also affect the transcription of angiotensinogen and subsequent production of angiotensin II from local RAAS.…”

mentioning

confidence: 99%

Antihypertensive therapy in diabetes mellitus: insights from ALLHAT and the Blood Pressure-Lowering Treatment Trialists’ Collaboration meta-analysis

Varughese

Lip

2005

J Hum Hypertens

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Type 2 diabetes mellitus (DM) is closely associated with hypertension, and the presence of both the conditions results in a high risk for the development of cardiovascular disease (CVD), renal impairment and diabetic retinopathy. Thus, most blood pressure (BP) management guidelines emphasise the importance of concomitant DM as part of overall cardiovascular risk assessment, and the need for more aggressive treatment targets. 1 This approach is all the more important given the huge burden of hypertension on stroke and CVD, and the missed opportunities for prevention. 2 How large is the problem of hypertension in the setting of DM? A recent large cross-sectional survey of over 250 000 patients from general practices across the United Kingdom recently reported that 56.2% of pharmacologically treated and 47.2% of diet-treated patients with DM had hypertension, as compared to 10.3% in those without DM. 3 This was consistent with earlier reports, where the association between DM and hypertension has been demonstrated in up to 65% of patients with DM, having major implications for CVD risk. 4,5 However, what is clear is the greater benefits of appropriate BP treatment on CVD, compared to glycaemic control. For example, in the United Kingdom Prospective Study, a systolic and diastolic BP reduction by 10 mmHg and 5 mmHg respectively has greater CVD risk reduction than lowering glycated haemoglobin by a mean of 0.9%. 6 This was further substantiated by the Hypertension Optimal Treatment Study, suggesting that there should perhaps be no lower threshold beyond which BP lowering is not considered to be beneficial in the setting of DM. 7

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The renin-angiotensin-aldosterone system in atrial fibrillation: a new therapeutic target?

Cited by 21 publications

References 29 publications

Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation

Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation

Targeting the renin–angiotensin–aldosterone system in atrial fibrillation: from pathophysiology to clinical trials

Antihypertensive therapy in diabetes mellitus: insights from ALLHAT and the Blood Pressure-Lowering Treatment Trialists’ Collaboration meta-analysis

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