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)

Early in the acute phase of myocardial infarction the phenomenon of expansion may occur, with regional thinning and dilatation of necrotic region. This complication may be detected by echocardiography since the first hours of infarction. During the two subsequent weeks, an additional increase of left ventricular volume may occur, due to an increase of length of the infarcted segments and, as well, of the contractile segments which suffer a "volume overload hypertrophy". This is the phenomenon of remodeling. Finally during the first year post infarction, a progressive left ventricular dilatation may develop. This late dilatation seems to be due to an increase of perimeter of the contractile regions only. By the time this topographic changes have occurred, the left ventricle assumes a more spheric configuration. Left ventricular dilatation affects adversely cardiac function, with higher incidences of heart failure and death. Experimental and clinical studies show that, in selected patients, remodeling and ventricular dilatation may be attenuated by the administration of angiotensin-converting-enzyme inhibitors, with better indices of left ventricular function. Final results of several on-going multicenter studies are awaited for; they will allow a better definition of the role of ACE inhibitors on prevention and treatment of left ventricular dysfunction after myocardial infarction.
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PMID:[Expansion of infarction, dilatation and ventricular remodelling. Therapeutic potential of angiotensin-converting enzyme inhibitors]. 161 Jun 13

Left ventricular modeling after myocardial infarction may be modified in three ways: firstly, by limiting the infarct size; secondly, by administering ACE inhibitors: these drugs limit infarct expansion and ventricular dilatation. They reduce the prevalence of secondary left ventricular failure and, in the animal, improve the prognosis. Glyceryl trinitrate also appears to be effective. The third therapeutic option is maintaining the patency of the artery responsible for the infarction, which has a beneficial effect on ventricular remodeling. The respective therapeutic indications of these three options are still a matter of discussion.
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PMID:[Left ventricular remodeling and ischemic heart diseases. Therapeutic possibilities]. 168 44

Early treatment of patients with myocardial infarction and left ventricular dysfunction was performed in 90 patients aiming at influencing left ventricular remodelling. After twelve months of treatment with 25 mg captopril t.i.d. left ventricular ejection fraction was improved by 10% in comparison to a treatment with 40 mg of frusemide or placebo (p = 0.001). Late treatment of the patients not treated with captopril resulted in partial reversal of left ventricular dilatation, while withdrawal of captopril therapy in stable patients with ejection fractions over 30% and without clinical signs of congestive heart failure did not result in deterioration of left ventricular function. These results give a sound rationale for the earlier use of ACE-inhibitors in the treatment of congestive heart failure and left ventricular dysfunction.
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PMID:Studies of left ventricular dysfunction following myocardial infarction. 182 Feb 93

It has been shown that converting enzyme inhibitors (CEI) attenuate ventricular dilatation and hypertrophy after myocardial infarction. In most studies, CEI treatment was started when ventricular dilatation and hypertrophy were already well under way. Therefore, we studied the effects on ventricular dilatation and hypertrophy, when CEI treatment was started in the acute phase of myocardial infarction. Immediately after a sham-operation or myocardial infarction in rats (sham: n = 8; MI: n = 17), treatment with zofenopril, a novel ACE-inhibitor, was started and continued during 42 days (long-term treatment). In a second group of rats, zofenopril was administered only during the first 5 days after myocardial infarction (short-term treatment); these rats were not treated with zofenopril during the remaining period of 37 days (sham: n = 5; MI: n = 13). Untreated rats served as controls (sham: n = 9; MI: n = 24). The results from this study showed that long-term treatment with zofenopril caused a significant reduction of left ventricular cavity volume in rats with moderate-to-large infarctions, which was accompanied by a significant reduction in the ratio of total heart weight to body weight. However, short-term treatment with zofenopril did not significantly reduce ventricular volume or total heart weight. Finally, both long- and short-term treatment resulted in a small, but statistically significant, reduction of septal wall thickness in sham-operated and infarcted rats. We conclude that CEI therapy decreases ventricular dilatation and hypertrophy after myocardial infarction, only when treatment is continued during the chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of short- and long-term treatment with an ACE-inhibitor in rats with myocardial infarction. 182 83

Before efficacy of therapy has been proven in large populations years or decades may pass. Meanwhile the medical profession has to rely on probabilities. This holds true regarding improvement of prognosis of CHF by ACE inhibition. While symptomatic improvement of CHF by addition of ACE-inhibition. While symptomatic improvement of CHF by addition of ACE-inhibitors has been demonstrated in numerous studies, improvement of prognosis has not yet been demonstrated entirely sufficiently. Only one trial has been published so far in a severely ill but not very exactly defined population (66). Animal studies and several small or interim published trials, however, show that the positive influence of ACE-inhibitors on CHF pathophysiology and symptomatology might favourable affect the prognosis as well. The SAVE trial and the SOLVD trial - both have randomized several thousand patients - will give answers concerning the influence of Captopril and Enalapril on prognosis of symptomatic as well as asymptomatic left ventricular dysfunction and on progression of left ventricular dilatation. The VHEFT II trial will compare the effect of ACE-inhibitors with the combination of ISDN and Hydralazine. Results will be available within the first few years of this decade.
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PMID:[Heart insufficiency and life expectancy--the role of ACE inhibitors]. 240 50

The data herein presented provides persuasive evidence that in addition to diuretics, and probably digitalis (since all studies have included subjects taking this drug) patients with congestive heart failure should also be placed on a vasodilator regimen to slow the progression of the syndrome and to reduce its mortality. Firm recommendations for the choice of drug and the selection of patients likely to benefit from this treatment must await the results of further studies. At present, ACE inhibitors are preferred because they are usually better tolerated than conventional vasodilators and are clinically more effective. In regard to the question of when to begin vasodilator it is noteworthy that neurohormonal activation may occur early in the course of the disease, even before symptoms appear. If so, perhaps vasodilators should be initiated even in the asymptomatic stage of left ventricular dysfunction to prevent the progressive dilatation and deterioration that lead to clinical heart failure. The just published study of the efficacy of captopril in preventing the progression of left ventricular dilatation in patients with a recent anterior, transmural myocardial infarction supports this view. Further, ongoing studies, will help place these issues in their proper perspective.
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PMID:The medical treatment of congestive heart failure. 248

Acute myocardial infarction continues to be the number 1 killer in industrialised countries. While the more widespread use of thrombolytic therapy has made a dramatic impact on patient survival, changes in long-term prognosis after discharge from hospital have not improved radically and 5-year mortality remains at over 30%. The single most important determinant of survival in the long term is left ventricular function. The process of ventricular dilatation and remodelling begins early after infarction. While such changes may initially go unrecognised clinically, without intervention progressive functional impairment will ensue and the majority of patients will develop signs and symptoms of heart failure, which carries a worse prognosis than many forms of cancer. ACE inhibitors act on both the haemodynamic and neurohormonal mechanisms in heart failure. Several large-scale clinical trials have clearly demonstrated that early use of these agents in stable patients who are not hypotensive or in cardiogenic shock can reduce significantly the development of heart failure and death. A strategy for the early initiation of ACE inhibitor therapy is proposed to improve survival in AMI patients.
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PMID:Improving outcome after acute myocardial infarction: what is the role of ACE inhibitors? 754 52

Prevention of post-infarction ventricular remodeling is an important therapeutic aim since left ventricular dilatation is one of the most important prognostic post-infarction determinants. Early reperfusion and chronic treatment with ACE-inhibitors are able to limit remodeling by means of two distinct mechanisms. Early reperfusion limits the extent of the infarcted area by salvaging a part of the myocardial area at risk of necrosis. ACE-inhibition, on the other hand, by reducing afterload, facilitates cardiac ejection and therefore tends to reduce left ventricular volume. Remodeling could be limited also by drugs which, like L-carnitine, act, as has been demonstrated by experimental studies, on the use of energy substrates both in the area at risk of necrosis and in the area subjected to a greater wall stress because of remodeling and which will progressively dilate over time. The CEDIM study is a double-blind, randomized, placebo-controlled, multicentre trial which has involved 36 Heart Divisions. The CEDIM study aims at evaluating the effects of L-carnitine on left ventricular function, as assessed by echocardiography, in patients with acute anterior myocardial infarction.
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PMID:[Prevention of post-infarction remodelling with L-carnitine: multicenter study CEDIM (L-Carnitine digital echocardiography myocardial infarction)]. 763 89

Prognosis after acute myocardial infarction is strongly associated with left ventricular dysfunction. However, asynergy does not necessarily imply loss of viability and myocardial necrosis. In fact, two different patterns of contractile dysfunction, possibly coexisting, have been shown after acute myocardial infarction: Stunning and hibernation represent distinct patterns of contractile dysfunction that share the character of reversibility. It is noteworthy, then, to identify the presence of these two conditions at the bedside and to develop medical treatment to effect recovery of myocardial dysfunction. This strategy has the potential to ameliorate the outcome of patients after acute myocardial infarction by improving left ventricular function. Beta-blocker therapy significantly reduces mortality and the incidence of reinfarction after an acute myocardial infarction: These benefits result from the prevention of sudden death, the reduction of the extent of myocardial injury during the acute phase, and a further antiischemic action. Nevertheless, beta-blocker therapy increases left ventricular dilatation. Recent experimental and clinical data show that ACE inhibitors confer positive therapeutic effects after myocardial infarction by reducing the extent of left ventricular dilation, by reducing mortality, and by improving the clinical outcome. Not all patients, however, can be subjected to this therapeutical approach because of the possible detrimental effects produced by hypotension and by block of neurohormonal activation, sometimes truly compensatory in the early phase. Therefore, it would be interesting to suggest a combination therapy of a beta-blocker with a vasodilator agent (ACE inhibitor or calcium-channel blocker.
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PMID:Left ventricular function and prognosis after myocardial infarction: rationale for therapeutic strategies. 794 74

ACE inhibitors improve not only symptoms and signs of heart failure in patients with symptomatic left ventricular dysfunction but also lead to a slower progression of heart failure. In asymptomatic patients with left ventricular dysfunction, the progression to symptomatic heart failure is retarded by ACE inhibitors. As heart failure is preceded in about 80% by myocardial infarctions, trials were designed to influence the development of heart failure after myocardial infarction. It could be shown that therapy with ACE inhibitors ameliorates the progressive left ventricular dilatation and that this effect is translated into a significant increase of life expectancy. Mainly based on the CONSENSUS I study, large doses of ACE inhibitors were used in most subsequent trials. The mean daily doses of enalapril were 18.4 mg in the CONSENSUS I trial and 16.6 and 16.7 mg in both arms of the SOLVD trial. There is a trend towards lower doses of ACE inhibitors, as in the SAVE trial only 79% of the patients taking captopril received the target dose of 150 mg daily. Smaller studies used similar target doses, but a beneficial effect on left ventricular enlargement has been shown with a daily dose of only 75 mg captopril. Based on the hypothesis that the left ventricular enlargement is mainly determined by the activation of the local cardiac renin angiotensin system, even lower, and therefore better tolerated, doses of ACE inhibitors may prove effective. However, studies comparing the effect of different doses of ACE inhibitors on left ventricular remodeling are missing. Consequently, the above-mentioned target doses of ACE inhibitors should be aimed at when treating patients after myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dosing of ACE inhibitors in postinfarct protection. 801 63


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