Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During myocardial ischaemia, either in chronic coronary insufficiency or the acute phase of myocardial infarction, the renin-angiotensin system is activated which, by its deleterious cardiac effects, aggravates the ischaemia. Angiotensin Converting Enzyme (ACE) inhibitors, by their indirect effects (improved conditions of left ventricular load, negative inotropism, attenuation of catecholaminergic stimulation), reduce myocardial oxygen consumption, and by their direct coronary vasodilator effect reduce myocardial ischaemia. In addition, by attenuating the formation of oxygen-free radicals, by participating in the inactivation of some of them and protecting the lysosomal membranes, they combat reperfusion injury. In the animal model of acute myocardial infarction, they reduce myocardial infarct size and the prevalence of reperfusion arrhythmias. In the clinical situation, their effects on the ischemic response to effort in anginal patients remain controversial, appear to be more marked in abnormalities of the coronary micro-circulation especially in syndrome X and in hypertensive heart disease. In ischemic heart disease, long-term treatment may be beneficial by their trophic coronary and myocardial effects and two large scale trials report a decrease in the recurrence of myocardial infarction with ACE inhibitors. In the acute phase of myocardial infarction if their possible actions on reducing the infarct size and reperfusion arrhythmias require further confirmation, they do limit expansion of the infarct and decrease early left ventricular dilatation. However, the appreciation of tolerance is variable and the timing of their introduction remains controversial.
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PMID:[Action of converting enzyme inhibitors on myocardial ischemia and reperfusion injuries]. 830 19

Obesity has been identified as an independent risk factor for coronary heart disease and congestive heart failure. Although congestive heart failure can be secondary to coronary heart disease, in morbid obesity these conditions can be independent. Cardiac structure and function can be altered even in the absence of systemic hypertension and underlying organic heart disease. In obese patients total blood volume increases and creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The frequent coexistence of systemic hypertension in obese individuals facilitates development of left ventricular dilatation and hypertrophy. Congestive heart failure may occur and may be attributable to left ventricular diastolic dysfunction or to combined diastolic and systolic dysfunction. The risk of coronary heart disease seems to be more strictly correlated to central obesity than to increased body mass index. Insulin resistance seems to be the key factor that links obesity and ischaemic heart disease. In such a condition the so called Syndrome X appears. It is characterized by: obesity, systemic hypertension, diabetes mellitus, hypertriglyceridaemia and reduced HDL cholesterol levels. Considering that left ventricular hypertrophy is often present, many risk factors coexist in obese patients. Weight loss is very useful in obese patients. It may reduce mortality and morbidity for coronary heart disease and delay or avoid the appearance of congestive heart failure. It is proved that after weight loss, blood pressure, glucose, cholesterol, triglycerides and left ventricular mass decrease.
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PMID:[Obesity and the heart]. 1649 82