1,721,327 research outputs found

    The symptoms of heart failure

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    Chronic heart failure (CHF) and acutely decompensated heart failure (ADHF) are the most frequent hospital diagnoses in industrialized countries. The clinical presentation of heart failure is dominated by two symptoms: dyspnea and fatigue. These symptoms dictate patients' physical capacity and quality of life. Popular clinical classifications of CHF are based on exercise tolerance, ie, on dyspnea after effort and includes the most popular one proposed many decades ago by the New York Heart Association (NYHA). Traditionally, the reduced exercise capacity of HF patients is attributed to the malfunctioning cardiac pump. More recently, "peripheral" factors have been identified that may contribute to the limited exercise capacity associated with CHF. Morphological and functional abnormalities found in both skeletal muscle and respiratory muscles, including muscle atrophy, fiber type changes, reduced mitochondrial enzymes, decreased mitochondrial volume density, and alterations at the vascular/skeletal muscle interface (greater sympathetic vasoconstrictor tone, decreased capillarity, and smaller capillary diameter) may all contribute to dyspnea and fatigue, in addition to or independently from "central" derangements

    Recurrent and resistant angina: is the metabolic approach an aprropriate answer?

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    Abstract Chronic stable angina is the first manifestation of ischemic heart disease in one half of patients; in the United States, the annual incidence of angina in 213 of 1000 of the population is over 30 years of age. The morbidity associated with ischemic heart disease is considerable: each years millions of patients have an MI, or are hospitalised for unstable angina. In recent years less attention has been paid to chronic ischemic syndrome; a possible explanation is that most patients with angina, refractory to medical treatment, are referred for myocardial revascularization in order to improve symptoms and to prevent death and myocardial infarction. Unfortunately available data do not support this common belief. The current evidence allows us to conclude that percutaneous transluminal coronary angioplasty (PTCA) in chronic coronary artery disease does not reduce the rate of subsequent MI or mortality and that PTCA results in superior symptomatic relief of angina and improved exercise tolerance compared with medical therapy, but the difference narrows with time. Several mechanisms may be considered to explain the persistence of angina/ischemia after a revascularization procedure, including incomplete revascularization, graft/PTCA failure, and disease progression in native coronary arteries. Microvascular dysfunction may play a prominent role in the unexpected prevalence of angina after the removal of obstructions in the major coronary branches. A better understanding of the metabolism derangements associated with ischemia and reperfusion allowed the development of new pharmacological approaches. In contrast to classic "hemodynamic" agents, metabolic agents have no hemodynamic, inotropic or chronotropic effect and interfere with cardiac energy metabolism

    Heart failure: A cardiac or a systemic disease?

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    Heart failure: A cardiac or a systemic disease

    Cardiovascular events in diabetics: A great challenge and an unsolved problem

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    Cardiovascular events in diabetics: A great challenge and an unsolved proble
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