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)

Infarct expansion remains an important sequela of myocardial infarction. Both angiotensin converting enzyme inhibitors and intravenous nitrates reduce early infarct expansion in humans. This is believed to be caused by the reduction in left ventricular systolic wall stress that results from the arteriolar vasodilatation they produce. Patients are frequently already receiving calcium channel blockers at the time of infarction or these drugs are sometimes administered in the perimyocardial infarction period. The calcium blockers of the dihydropyridine class might be expected to modify infarct expansion. However, their effect on this process has not been studied. We therefore evaluated the effect of early treatment with the calcium blocker amlodipine, a potent arteriolar vasodilator with minimal negative inotropic properties, on chronic myocardial infarction in the rat. Permanent left coronary occlusion was created after pretreatment with amlodipine, 0.25 mg/kg (low dose) or 1.0 mg/kg (high dose), or placebo, intravenously twice a day, and continued for 7 days after infarction. Hearts (n = 50) were perfusion fixed 21 days after infarction and analyzed for infarct extent, scar thickness, left ventricular shape and size, and expansion index. Both doses decreased mean blood pressure (119 +/- 3 to 99 +/- 5 mm Hg low dose, p = 0.004; 110 +/- 5 to 84 +/- 4 mm Hg high dose, p = 0.0003), with reflex tachycardia only after the high dose (heart rate 395 +/- 9 to 434 +/- 11, p = 0.001). Infarct extent was equal in the three groups (39 +/- 2%, 41 +/- 2%, and 41 +/- 3% of left ventricular circumference for control, low, and high doses, respectively). The three groups did not differ significantly with regard to left ventricular cavity cross-sectional area (80 +/- 4, 77 +/- 3, and 87 +/- 3 mm2, control, low, and high doses, respectively; p = 0.07 high dose vs control), mean scar thickness (0.74 +/- 0.06, 0.73 +/- 0.05, and 0.65 +/- 0.06 mm, control, low, and high doses, respectively; p = NS), and expansion index (1.52 +/- 0.10, 1.58 +/- 0.12, and 1.95 +/- 0.19, control, low, and high doses, respectively; p = 0.08 high dose vs control). In the subgroup with larger infarcts (infarct extent greater than 0.39 of left ventricle), the expansion index was higher in the high-dose group (2.37 +/- 0.23 vs 1.64 +/- 0.17 control; p = 0.04). In this model, treatment with amlodipine does not limit infarct extent or reduce early infarct expansion and left ventricular dilatation, even when initiated before infarction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of amlodipine on myocardial infarction, infarct expansion, and ventricular geometry in the rat. 138 6

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

An acute myocardial infarction, particularly one that is large and transmural, can produce expansion and alterations in the topography of both the infarcted and non-infarcted regions or the ventricle. This remodelling can importantly affect the function of the ventricle and the prognosis. Side-to-side slippage of myocytes in the myocardium occurring in association with ventricular dilatation is responsible for wall thinning. The increased internal load that is sustained through the cardiac cycle is thought to promote further stress, dilatation and hypertrophy of the non-infarcted area. The collagen network has been showed to be high responsible for the remodelling of the interstitium and therefore for the scar formation involved in the expansion. The process for ventricular enlargement can be influenced by infarct size, healing end ventricular wall stresses. The process of scarification can be interfered with during the acute infarct period by the administration of glucorticosteroids and non-steroidal anti-inflammatory agents, which results in thinner infarct and further expansion. A most effective way to prevent or minimize the increase in ventricular size is to limit the initial insult. Acute thrombolytic reperfusion therapy may work in this way. Finally early and long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions of the left ventricle, reducing progressive enlargement with a prolongation in survival.
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PMID:[Left ventricular remodelling]. 184

Chronic cor pulmonale is defined as right heart hypertrophy or right ventricular dilatation and/or chronic right heart failure. There are many etiologies which largely determine mortality and drug therapy, but the common cause is increased right ventricular work from primary or secondary pulmonary hypertension assuming two prototypes, the asphyxial and the vascular obliterative type. The main focus of this review concentrates on the various drugs to reduce pulmonary vascular pressure and resistance. The value to correct hypoxaemia is mentioned with regard to its demonstrated important effect of asthmatic patients with cor pulmonale. Continuous oxygen therapy and a potential therapy by almitrine, a respiratory stimulant, have been suggested. Phosphodiesterase inhibitors and dopaminergic drugs have been used successfully to improve right cardiac function in a small number of patients. The use of prostacyclin has a large potential to effectively correct pulmonary vascular haemodynamics but its use is fairly limited by the need of continuous intravenous application. New oral drugs under investigation which stimulate endogenous prostacyclin as well as thromboxane synthetase inhibitors still need further evaluation but might be of potential benefit. The comparison of the side-effects due to vasodilators and calcium antagonists argues for the use of calcium channel blockade for patients with pulmonary hypertension. To define the role of angiotensin converting enzyme inhibitors or the more recently introduced potassium channel openers for treatment of chronic cor pulmonale still await detailed, controlled studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The drug therapy of chronic cor pulmonale]. 186 13

Cardiac failure is the principal medium-term complication of myocardial infarction. Changes in left ventricular geometry are observed after infarction, called ventricular remodeling, which, though compensatory initially, cause ventricular failure in the long-term. Experimental and clinical studies suggest that early treatment by coronary recanalisation, trinitrin and angiotensin converting enzyme inhibitors may prevent or limit the expansion and left ventricular dilatation after infarction, so improving ventricular function, and, at least in the animal, reduce mortality. Large scale trials with converting enzyme inhibitors are currently under way to determine the effects of this new therapeutic option. It would seem possible at present, independently of any reduction in the size of the infarction, to reduce or delay left ventricular dysfunction by interfering with the natural process of dilatation and ventricular modeling after infarction.
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PMID:[Ventricular "remodeling" after myocardial infarction]. 191 Mar 27

An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and uninfarcted regions of the myocardium are equally involved in the process. The remodeling process comprises left ventricular wall thinning (mainly due to cell slippage), chamber dilatation, and compensatory hypertrophy of the uninfarcted segment of the myocardium. The hypertrophy may initially be physiologic but may ultimately become a pathologic process, and thereby contribute to pump dysfunction. The possible reasons why the ventricular hypertrophy may ultimately be dysfunctional include alterations in local architecture and their sequelae alone or in concert with local changes in the beta-adrenergic, alpha-adrenergic, or renin angiotensin systems. At the present time, there are encouraging data to suggest that nitroglycerin, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process.
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PMID:Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. 214 59

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


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