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)

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

Myocardial dysfunction and silent myocardial ischemia have been identified as important prognostic factors following acute myocardial infarction, also in low risk patients. In postinfarction patients, impaired left ventricular function is the result of fixed scar and reversible contractile dysfunction of viable stunning or hibernating myocardium. Post-extrasystolic potentiation (PESP) during 2-dimensional echocardiographic monitoring may be used to detect the presence of viable myocardium in asynergic myocardial segments. Incidence of reversible contractile dysfunction is a very common phenomenon at predischarge examination after myocardial infarction in asymptomatic patients, and it is independent on the persistence of silent ischemia. A progressive loss of myocardial viability occurs over the first year following the acute phase despite the maintenance of an asymptomatic clinical status. This phenomenon is associated with significant dilatation of the left ventricle. Moreover, silent ischemia is strongly related with this progressive loss of myocardial viability and left ventricular dilatation. Thus, it becomes evident that the most important role of medical and interventional approaches consists of limiting the acute necrosis by reperfusion and in preventing the loss of viable chronically hypoperfused myocardium that appears to be a major factor of left ventricular remodeling and changes over time of prognostication in individual patients. Finally, the presence of viable myocardium by PESP in the arterial zone at risk is highly predictive of 4-year mortality, particularly in patients with low ejection fraction (< 40%), and identifies patients who are suitable candidates for revascularization after myocardial infarction.
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PMID:Reversible contractile dysfunction of viable myocardium. Implications for decision making process in post-infarction patients. 795 36

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

Central, intracardiac hemodynamics and myocardial contractility were assessed in 97 inpatients with macrofocal myocardial infarction. Of them, 71 received conventional chemotherapy versus 26 patients given additionally intravenous phosphocreatine (neoton). The total dose of neoton 30 g was injected during the course of 6 days following the disease onset. With minimal changes in central hemodynamics, phosphocreatine was found to prevent left-ventricular dilatation and development of congestive heart failure by decreasing preload, to maintain myocardial contractility without reduction.
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PMID:[Exogenous phosphocreatine in the prevention and treatment of cardiac insufficiency in patients with myocardial infarction]. 804 97

Reperfusion reduces left ventricular dilatation in patients with acute myocardial infarction, but it is unclear to what extent this is a primary effect or only a consequence of the limiting effect of reperfusion on infarct size. To address this issue, 56 consecutive patients were examined by means of two-dimensional echocardiography on day 1, on day 3, before discharge, and at 6 months after an acute myocardial infarction. From this population two groups of 12 patients each, perfectly matched for site of myocardial infarction, extent of ventricular asynergy at two-dimensional echocardiography (akinesis + dyskinesis), and clinical characteristics were identified according to the creatine kinase (CK) time to peak, which was regarded as a marker of spontaneous or induced reperfusion: (1) CK time to peak of 12 hours or less (reperfused patients, n = 12), and (2) CK time to peak of more than 12 hours (nonreperfused patients, n = 12). In these two groups of patients end-diastolic and end-systolic left ventricular volumes and endocardial lengths of asynergic and normal ventricular segments, imaged in a cross-sectional view at the level of the papillary muscles, were then computed. At the first examination end-diastolic volume, end-systolic volume, and endocardial segment lengths of normal and asynergic segments were similar in the two groups of patients. Patients with late CK time to peak, however, showed a progressive increase in left ventricular systolic volumes and in asynergic endocardial segment lengths between the first and third (predischarge) examinations (p < 0.05 for both), with no change in systolic length of the normal myocardium. The left ventricular end-systolic volume and the asynergic endocardial segment length of patients with early CK time to peak, however, did not increase during hospitalization. The increment in end-systolic volume and in systolic infarct segment length from the first to the third examinations was higher in nonreperfused patients (p = 0.018 and p = 0.04, respectively). Changes similar to those detected in systole were found for diastolic volume and diastolic infarcted and noninfarcted segment length in both groups, but they did not reach statistical significance. After 6 months, an increases in volume and endocardial length were found in both groups of patients. Relative to the first examination, however, the increase in systolic volume and in asynergic systolic endocardial lengths remained greater for nonreperfused patients (p = 0.077 and p = 0.01, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reperfusion reduces left ventricular dilatation by preventing infarct expansion in the acute and chronic phases of myocardial infarction. 812 95

To clarify the mechanism of initiation and progression of right ventricular myocardial infarction, 35 cases were examined among 236 cases of consecutively autopsied hearts. Twenty-six (52%) of 50 cases with posterior left ventricular infarction showed right ventricular infarction, and no statistical differences were observed in the age, gender, and number of impaired vessels among patients with and without right ventricular infarction. However, more proximal occlusion or more extensive thrombi in the right coronary artery did play a very important role in the genesis of the infarction and its progression. Right ventricular dilatation was frequently associated, probably resulted from the functional disorder of contraction and relaxation of the myocardium. Unusual asynchronous ischemia was observed in the right ventricle concomitantly with posterior left ventricular infarction, suggesting the presence of a protective mechanism against ischemia by the abundant collateral circulation of the right ventricle. In conclusion, right ventricular infarction occurs only with the cease of collateral circulation due to proximal occlusion and the presence of long thrombi in the right coronary artery.
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PMID:[Clinico-pathological study of the mechanism of initiation and progression of right ventricular infarction]. 816 34

Eighty patients (43 M, 37 F), aged 23-89 years who were referred for emergency echocardiography over a 12-month period were prospectively studied in order to determine the reasons for emergency echocardiography and the influence of its results on patient management. The most frequent emergency request was to clarify whether the basis for cardiomegaly in a haemodynamically unstable patient was pericardial effusion or left ventricular dilatation. Other reasons for requests were for assessment for source of systemic emboli, acute complications of myocardial infarction, endocarditis, valve dysfunction and cardiac trauma. As a consequence of the emergency echocardiography, management was immediately influenced in 19 patients. This study has provided information on the specific settings in which emergency echocardiography can be justified.
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PMID:An audit of emergency echocardiography in a district general hospital. 822 74

To investigate the contribution of the cardiac renin-angiotensin system to ventricular dilatation after myocardial infarction, we examined the effects of 3-week treatments with an angiotensin converting enzyme inhibitor, delapril, and a selective angiotensin II type 1 (AT1) receptor antagonist, TCV-116, on haemodynamics and ventricular angiotensin II contents in myocardial-infarcted rats. TCV-116 reduced mean aortic pressure, and prevented the increase of right and left ventricular weight, left ventricular end-diastolic pressure and volume of myocardial-infarcted rats, to a similar extent to delapril. Thus, AT1 receptor-mediated action of angiotensin II plays a central role in the development of ventricular dilatation. Angiotensin II contents in the right and non-infarcted left ventricles (6.0 +/- 1.0 and 5.9 +/- 0.7 pg/g tissue, respectively, mean +/- S.E.M.) of myocardial-infarcted rats were not different from those of sham-operated rats. However, angiotensin II contents in the infarcted scar (21.7 +/- 3.5 pg/g) of myocardial-infarcted rats were 4.2-fold higher than those in the left ventricle of sham-operated rats. Delapril reduced angiotensin II contents in the right and non-infarcted left ventricles, and the scar by 48, 81 and 60%, respectively, but did not reduce plasma angiotensin II in myocardial-infarcted rats. TCV-116 also decreased angiotensin II in the right and non-infarcted left ventricles by 57 and 56%, respectively, while increased plasma angiotensin II by 4.3-fold. Thus, the prevention of ventricular dilatation by these two agents was associated with the decrease in ventricular angiotensin II contents. These observations suggest that the cardiac renin-angiotensin system rather than the circulating system may play an important role in ventricular dilatation after myocardial infarction.
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PMID:Contribution of cardiac renin-angiotensin system to ventricular remodelling in myocardial-infarcted rats. 830 70

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

The aim of this prospective study was to investigate if left ventricular dilatation is confined to the early months following myocardial infarction, or if it is a progressive process over several years. One hundred patients (pts) who suffered from stable angina or had undergone myocardial infarction, could be examined twice by coronary arteriography including ventriculography in an interval of 52 +/- 14 months. The patients were retrospectively divided into three groups: 41 pts (group A) had coronary heart disease without prior myocardial infarction, in 29 pts (group B) the first examination was performed within (mean 2 +/- 1 mo.) and in 30 pts (group C) beyond 6 months after myocardial infarction (mean 32 +/- 24 mo). The three groups were comparable concerning clinical data, but more pts with former myocardial infarction had multi-vessel disease (34 of 59 vs 16 of 41 pts) and depressed left ventricular function. Left ventricular angiography was performed in RAO view 30 degrees after enddiastolic pressure (LVEDP) was registered. Left ventricular enddiastolic and endsystolic volumes (EDVI and ESVI) were calculated by use of a modified Simpson's rule equation. In group A, EDVI and LVEDP remained constant, whereas ESVI increased slightly but significantly. Pts of group B and C had significantly higher volumes, which increased significantly in both groups over a mean of 52 months. About half the pts suffered from ventricular dilatation independent of progression of underlying coronary sclerosis. Consecutively, left ventricular ejection fraction decreased and LVEDP rose significantly in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Left ventricular dilatation after myocardial infarct]. 832 77


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