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)

1. The circulating and tissue renin-angiotensin systems (RAS) contribute importantly to cardiovascular homeostasis. Systemic and/or local activation of the RAS is seen in many pathological conditions of the cardiovascular system (e.g. hypertension and congestive heart failure). Increased angiotensin production participates in the pathophysiology of these and other disease states. Accordingly, inhibitors of the renin angiotensin system have a broad spectrum of therapeutic efficacy. 2. Angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents that do not adversely affect serum lipid levels. In addition, they reduce left ventricular hypertrophy. 3. ACE inhibitors cause coronary vasodilation and reduce ventricular work and wall stress. They have been shown to reduce experimental infarct size and to increase anginal threshold in humans. 4. After experimental or human myocardial infarction that results in significant left ventricular dysfunction, ACE inhibitors prevent ventricular dilatation and development of congestive heart failure, and may improve survival. 5. ACE inhibitors can prevent ventricular fibrillation and contractile impairment (stunned myocardium) associated with reperfusion injury after experimental myocardial ischaemia. 6. ACE inhibitors reduce preload and afterload, improve exercise capacity, reduce ventricular arrhythmias, and improve patient survival in clinical cardiac failure. 7. Taken together, inhibition of the RAS may potentially result in primary as well as secondary protective effects on the cardiovascular system.
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PMID:Clinical implications for therapy: possible cardioprotective effects of ACE inhibition. 269 Sep 9

The incidence of hypertrophic cardiomyopathy progressing to dilated cardiomyopathy is rare. A patient diagnosed at age 22 and followed for 24 years who progressed to a dilated cardiomyopathy with severe congestive heart failure is reported. Left ventricular dilatation in hypertrophic cardiomyopathy may be due to a complication of surgery, beta-blocker therapy, or myocardial infarction. It may also represent the natural history in a subset of patients with hypertrophic cardiomyopathy.
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PMID:Progression from hypertrophic cardiomyopathy to dilated cardiomyopathy. 239 73

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts. 288 58

Echocardiography was performed for 246 patients with hypertension. Among the 246 patients, echocardiographic features simulating dilated cardiomyopathy (DCM) were observed in 12. These patients had past history of hypertension and prominent left ventricular dilatation with reduced left ventricular contractility, but no left ventricular wall thickening. To elucidate the mechanism producing DCM-like features in patients with hypertension, the clinical and echocardiographic findings of the 12 hypertensive patients (HT-DCM) were compared with those of 50 hypertensive patients without dilated left ventricles and of 31 patients with DCM. On admission, all patients with HT-DCM had congestive heart failure (CHF) without high blood pressure and their echocardiograms revealed the abnormal findings described above. There were no differences of the clinical and echocardiographic findings on admission between HT-DCM and DCM. Following medical treatment, relatively early improvement of CHF was noted in all patients with HT-DCM; the LV dimension decreased and diffuse wall motion abnormality improved steadily with gradual elevation of blood pressure during the follow-up periods. The LV function of most patients with HT-DCM improved markedly but never reached normal levels. There were no significant differences the right ventricular endomyocardial biopsy findings of between DCM and HT-DCM. It was suggested the DCM-like features in these cases are caused, not only by hypertension, but by other factors, as well.
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PMID:[Hypertensive heart disease simulating dilated cardiomyopathy]. 294 71

A case study is presented of a premature infant delivered at 32 weeks' gestation by cesarean section. At birth the infant had massive cardiomegaly with extreme left ventricular dilatation as well as severe congestive heart failure and respiratory distress. The findings at autopsy suggest that the cardiac dysfunction was secondary to a myocardial infarct occurring in utero.
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PMID:Dilatation of the left ventricle in a newborn: probable in utero myocardial infarction. 294 55

We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months. No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [+/- SEM] of 21 +/- 8 ml (P less than 0.02) in the placebo group, but by only 10 +/- 6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P less than 0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P less than 0.05). Patients given captopril also had increased exercise capacity (P less than 0.05). This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance.
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PMID:Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. 296 17

We investigated the natural course of 59 patients with hypertrophic cardiomyopathy (HCM) in follow-up periods of one to 13 years and analyzed the clinical, hemodynamic and echocardiographic parameters to determine the factors influencing the prognosis. Among these patients, 44 (75%) remained stable in a compensated condition with or without medications. Five patients died suddenly and two died of congestive heart failure. Heart failure developed in another eight. At the initial evaluation, these 15 patients had high left ventricular end-diastolic pressure (mean: 22 +/- 8 mmHg) significantly higher than that of 44 compensated patients (mean: 13 +/- 6 mmHg, p less than 0.001). There were no differences in age at the initial evaluation between compensated and end stage groups. Atrial fibrillation occurred persistently in three and transiently in two among ten patients with heart failure during follow-up periods. Ventricular dimensions and systolic function did not statistically differ between the two groups. However, six patients with heart failure had cavity dilatation and deteriolated ventricular contractile function at the initial evaluation. Four of them did not show any change in left ventricular hypertrophy, but the regional thinning of the wall was observed in the remaining two. There were no characteristic features to predict sudden death in the clinical, hemodynamic or echocardiographic parameters. Thus, increased left ventricular end-diastolic pressure, atrial fibrillation, left ventricular dilatation and the regional thinning of the left ventricular wall are useful predictive markers for poor prognosis in HCM.
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PMID:[Natural course of hypertrophic cardiomyopathy: clinical, hemodynamic and echocardiographic features in the end stage]. 297 74

This study determines the noninvasive prognostic predictors (using radionuclide angiography) in patients with severe left ventricular dysfunction (resting ejection fraction less than or equal to 35 percent) secondary to coronary artery disease. We retrospectively evaluated 94 such patients using rest and exercise radionuclide ventriculography. At a mean follow-up of 16 months, cardiac events occurred in 22 patients: ten patients died of cardiac causes, five patients sustained nonfatal myocardial infarction, and seven patients developed severe congestive heart failure (class 4). Results indicate that patients with severe left ventricular dysfunction may be stratified into different risk groups according to left ventricular size. Marked left ventricular dilatation identifies a subgroup at high risk.
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PMID:Left ventricular dilatation. Prognostic value in severe left ventricular dysfunction secondary to coronary artery disease. 299 Aug 23

The angiotensin converting enzyme (ACE) inhibitors constitute a major breakthrough in the medical management of congestive heart failure. The incidence of side effects with these agents is surprisingly low when they are used in the appropriate dosage. They produce sustained beneficial hemodynamic and symptomatic improvement in most patients with congestive heart failure and may produce greater symptomatic benefit than digoxin when given as second-line therapy to patients with heart failure on diuretics. Their neurohumoral effects generally are advantageous, resulting in normalization of sodium and potassium balance and a reduction in ventricular arrhythmias. The ACE inhibitors may improve survival in patients with congestive heart failure, and recent data suggest that they may prevent or delay the development of left ventricular dilatation and overt heart failure in patients with asymptomatic left ventricular dysfunction.
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PMID:The multifacetted role of angiotensin converting enzyme inhibitors in congestive heart failure. 305 10

Serial two-dimensional echocardiographic and thallium-201 scintigraphic findings are described in a patient with acute myocarditis diagnosed by endomyocardial biopsy. On the 4th day of illness, just before the onset of congestive heart failure, the echocardiogram showed asymmetric septal hypertrophy (IVS/PW = 16 mm/10 mm = 1.6) and thallium-201 scintigram showed the ventricular septal thickening. On the 8th day of illness, when severe congestive heart failure was seen, asymmetric septal hypertrophy disappeared (IVS/PW = 8 mm/8 mm = 1.0), the left ventricle dilated markedly (LVDd = 63 mm), and the wall motion became poor (EF = 0.24). After one month, when congestive heart failure and clinical inflammatory findings disappeared, the contractility somewhat improved (EF = 0.43), although marked left ventricular dilatation remained. Thallium-201 scintigram showed some scattered persistent perfusion defects, thinning of the ventricular septal thickening, and dilatation of the left ventricle. The right ventricular endomyocardial biopsy revealed the histologic findings of the late stage of acute myocarditis. It is concluded that transient thickening of the ventricular wall may represent early changes in acute myocarditis.
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PMID:Reversible asymmetric septal hypertrophy in acute myocarditis. Serial findings of two-dimensional echocardiogram and thallium-201 scintigram. 316 41


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