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Titlebook: Angiogenesis and Direct Myocardial Revascularization; Roger J. Laham,Donald S. Baim Book 2005 Humana Press 2005 Chemokine.angiogenesis.car

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https://doi.org/10.1007/3-540-28297-1 may be limited to incomplete percutaneous coronary intervention (PCI) or surgical procedures (.,.–.). These so-called no-option patients often progress to end-stage ischemic cardiomyopathy with an annual mortality in excess of 30% (.). Treatment options for this group remain limited to multidrug me
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https://doi.org/10.1007/978-3-658-10723-9isease (CAD) in the last few decades. As a result of these improvements in cardiovascular care and the aging of the population, anincreasing number of patients have incomplete revascularization or recurrent myocardial ischemia and are suboptimal candidates for surgical (coronary artery bypass grafti
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Schirmdämpfung eines Drahtgeflechtesent of atherosclerosis. The respective roles of the endothelium, inflammatory mediators, and thrombosis in the pathogenesis of vascular disease are beginning to be better understood. As more is learned about the initiation of atherosclerotic cardiovascular disease, new targets for systemic therapies
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Metallgehäuse mit Magnetmaterialienalities in angiogenesis are associated with a number of pathological states. Strategies designed to promote angiogenesis to treat disorders of inadequate tissue perfusion, such as occurs in peripheral arterial disease, have led to the area of therapeutic angiogenesis. Angiogenic growth factors of va
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Metallgehäuse mit Magnetmaterialien myocardial infarction, angina pectoris, or both (.). Although recent advances in medical treatment and interventional procedures have reduced the mortality in patients with coronary artery disease (.), the number of patients with refractory myocardial ischemia and congestive heart failure is rapidl
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Schirmdämpfung an Schichten für Leitungenlion Americans suffer a myocardial infarction (MI) annually. Of those who survive, 22% of men and 46% of women are disabled with heart failure (.). Although cardiomyocytes of infarcted or failing human hearts have been shown to undergo mitoses (.,.), this regenerative capacity is by far too limited
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