[Significance of circulatory changes, left-ventricular form and calcium metabolism in ventricular hypertrophy in patients with ischemic heart disease].
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We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated ...
Collateral circulation
Coronary circulation
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Myocardial hypertrophy
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Cardiac myocyte
Cardiac Fibrosis
Myocardial fibrosis
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Coronary circulation
Coronary vasodilator
Coronary arteries
Coronary flow reserve
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Left ventricular hypertrophy is a serious condition, strongly associated with the development of coronary artery disease, cerebrovascular disease, cardiac failure, sudden cardiac death, and overall mortality. 1‐4 In addition, regression of left ventricular hypertrophy is associated with reduction in all cause and cardiovascular mortality. The existence, therefore, of left ventricular hypertrophy in apparently healthy people has generated considerable interest ever since its initial description. 5 Debate has centred on two major issues. The first concerns the nature of left ventricular hypertrophy of athleticism: is it simply a physiological response to periodic myocardial loading or does it have a pathological component and therefore carry implications for long term prognosis? The second concerns the diagnosis of left ventricular hypertrophy of athleticism: is it possible to diVerentiate with confidence physiological left ventricular hypertrophy from pathological conditions?
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Detection of right ventricular hypertrophy during life has often been exceedingly difficult. In a group of 40 patients with pulmonary artery hypertension either at rest or during exercise, in whom right ventricular hypertrophy of varying degree could therefore be anticipated, an attempt is made to correlate the pulmonary hypertension and the electrocardiographic evidence of right ventricular hypertrophy.
Right ventricular hypertrophy
Ventricular hypertrophy
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The interactions between pressure and volume overload that occur in hypertension lead to different patterns of cardiac hypertrophy and to increase in natriuretic peptides (NPs). The profiles of ANP and BNP synthesis and secretion have been investigated in models of hypertension; however, the different evolution of these profiles during the acute and chronic periods of pressure overload-induced cardiac hypertrophy is still unknown. For this reason, we studied DOCA-salt treated Sprague-Dawley rats at weeks 2, 4, 6 and 12 and correlated the evolution of these profiles with cardiac hypertrophy and hypertension. Cardiac hypertrophy had a positive correlation with ANP expression in the left ventricle and with ANP plasma levels. BNP expression increased after 4 weeks of treatment while ANP increased significantly after 6 weeks. In addition, BNP plasma levels increased only in the group treated for 12 weeks, while ANP plasma levels increased from week 2. NP secretion has a differential response in the early stages of the development of cardiac hypertrophy induced by the DOCA-salt model, with an early increase in ANP. As ANP levels were exceeded to those of BNP in all the DOCA-salt groups, ANP might be considered a more specific marker of volume overload.
Atrial natriuretic peptide
Volume overload
Pressure overload
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Exertion
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Mass index
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