1,721,142 research outputs found

    Epidemiology and the physiopathological link between depression and cardiovascular disease

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    AbstractIn the future, cardiovascular disease, together with depression, will be one of the leading causes of global disease in the Western World. It is well known that depression is independently associated with a poor prognosis in patients with ischemic heart disease.Epidemiological studies suggest that in patients with coronary artery disease, depression symptoms identify patients with higher risk of adverse cardiovascular outcomes, other studies maintain that depression symptoms might influence the progression of coronary and peripheral atherosclerosis.The defined pathophysiological pathways which link depression and cardiovascular outcomes are not well recognized although various mechanisms have been proposed to explain this association. Beyond traditional cardiovascular risk factors, autonomic nervous system, low grade of inflammation, platelet function, abnormal function of the hypothalamic–pituitary–adrenal axis and genetic factors can adversely impact the endothelium and arterial walls. Consequently, these mechanisms might be crucial factors in promoting and accelerating atherosclerosis and its complications due to plaque rupture and thrombosis. For these reasons, depression symptoms should be considered as a new cardiac risk factor in the general population and in patients with coronary artery disease

    Targeting subclinical ventricular dysfunction in atrial fibrillation: What can myocardial work add?

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    : Atrial fibrillation (AF) could impact on left ventricular function leading to a sublinical myocardial dysfunction, as identified by myocardial work parameters in a population-based cohort of AF patients compared with healthy individuals; factors associated with these parameters are also shown. SBP: systolic blood pressure; LAVI: left atrial volume index

    Angiotensin-converting enzyme inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A reductase in cardiac syndrome X: role of superoxide dismutase activity.

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    Background - Morbidity of patients with Syndrome X (SX; chest pain and normal coronary angiograms) is high and is associated with continuing episodes of chest pain and hospitalization. Impairment of microvascular endothelial function caused by increased oxidative stress has been suggested to be a mechanism of the disease. Superoxide dismutase ( SOD) is the major antioxidant enzyme system of the vascular wall. This study sought to establish whether combination treatment with ACE inhibitors and statins reduces oxidative stress and improves quality of life of patients with cardiac SX. Methods and Results - Forty-five patients with SX were randomly assigned to receive either a combination of ramipril (10 mg/d) and atorvastatin ( 40 mg/d) or placebo for 6 months. We determined the activity of extracellular SOD and its relation to flow-dependent endothelium-mediated dilation (FMD) and quality of life ( exercise capacity and score with Seattle Angina Questionnaire [SAQ]) before and after treatment. After 6 months, patients with SX who received atorvastatin and ramipril had significantly reduced ( P = 0.001) SOD levels (188.1 +/- 29.6 U/mL). No significant changes were seen on placebo (262.9 +/- 48.8 U/mL). Reduction of SOD after therapy was negatively correlated with FMD (r = 0.38; P = 0.01) and positively with total cholesterol (r = - 0.56; P < 0.001). At follow-up, patients taking atorvastatin and ramipril improved their quality of life both in terms of exercise duration (by 23.46%) and SAQ (by 64.1%). Conclusions - Six months of therapy with atorvastatin and ramipril improves endothelial function and quality of life of patients with SX. Reduced SOD activity may reflect low superoxide anion production. Benefits of these drugs may be related to reduction of oxidative stress

    Hallmarks of Left Ventricular Apical Cardiac Mass in a Young Patient

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    We present the case of a young patient with an apical cardiac mass exhibiting an anterior pseudonecrosis pattern on the electrocardiogram. Cardiac ultrasound revealed a hyperechoic mass infiltrating the apical wall. However, cardiac magnetic resonance ruled out signs of infiltration and demonstrated significant contrast uptake. Vascularization was confirmed through cardiac computed tomography, and 18-fluorodeoxyglucose positron emission tomography showed mild radiotracer uptake. These findings suggested a benign mass despite the presence of significant vascularization. This thorough evaluation enabled the Heart Team to plan and perform a successful surgical excision. The subsequent histologic report demonstrated a cardiac hamartoma

    Effect of Pravastatin on myocardial perfusion after percutaneous transluminal coronary angioplasty

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    We studied the effect of pravastatin on coronary perfusion after percutaneous, transluminal coronary angioplasty. An exercise test performed within 2 weeks after percutaneous transluminal coronary angioplasty induced reversible perfusion defects in 66% of patients taking pravastatin and 64% of those taking placebo. At follow-up, the exercise test still induced reversible perfusion defects in 3% of patients taking pravastatin and 29% of those taking placebo
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