1,721,062 research outputs found

    Role of RAAS inhibition in preventing left ventricular remodeling in patients post myocardial infarction

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    Left ventricular remodeling after myocardial infarction has been identified as a predictor of adverse outcome and as a relevant therapeutic target. It has been shown that upregulation of the renin-angiotensin-aldosterone system (RAAS)* has an important role in the pathogenesis of cardiac remodeling. In this paper we summarize evidence on the role of the RAAS in the development of left ventricular remodeling and review major trials based on the addition of an RAAS inhibitor to standard therapy in the post myocardial infarction setting to prevent remodeling and improve outcome

    Myocardial ischemia as a multifactorial: Disease: What is new?

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    Strategies for ischemic heart disease (IHD) focus almost exclusively on coronary atherosclerosis because access to interventional procedures is easy and gives gratifying angiographic results. This assumes that coronary artery disease and IHD are functionally identical. Recent reports, however, challenge the "plaque-centric" hypothesis of IHD. Alternative mechanisms, including coronary microvascular dysfunction, endothelial dysfunction, platelet dysfunction, coronary vasospasm, and inflammation, can precipitate myocardial ischemia (MI) in man. So, to assume that stenosis removal is a consistent cure for IHD is unwise, as is discounting MI because an angiogram appears "normal" after percutaneous coronary intervention or assuming MI is present because an atherosclerotic plaque is visible on angiography. © 2011 LLS SAS. All rights reserved

    Persistent angina

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    We are witnessing an exponential increase in the use of percutaneous transluminal coronary angioplasty (PTCA) for the treatment of coronary heart disease. Given that available evidence does not support a significant reduction of morbidity or mortality after PTCA, the widespread use of revascularization procedures is based on the assumption of a superior symptomatic relief of angina and on improved exercise tolerance. Unfortunately, randomized controlled trials suggest that symptomatic relief after PTCA may be partial, and limited in time. Several studies have shown that patients may remain symptomatic for angina even after removal of coronary obstructions. This observation challenges the assumption that coronary stenosis is the only cause of angina and calls for innovative therapeutic approaches, independent of the classic agents developed to counteract the adverse effects of flow-limiting coronary obstructions
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