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)

Chest roentgenograms in 13 infants and angiocardiograms in 11 infants with persistent transitional circulation (PCT) syndrome were reviewed. Chest radiographs typically revealed congestive heart failure with pulmonary venous congestion, cardiomegaly, hepatomegaly, and pleural effusions. Angiocardiography demonstrated a right-to-left shunt through the ductus arteriosus, ventricular dilatation, poor myocardial function, and ventricular emptying. Cardiopulmonary abnormalities resolved over a period of 2-6 days in survivors. PTC syndrome as seen at the authors' institution has been an important and relatively common cause of congestive heart failure and cyanosis in the newborn. The incidence of congestive failure was higher than in other reported series.
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PMID:Persistent transitional circulation. Roentgenographic findings in thirteen infants. 13 73

Diastolic wall stress and compliance were determined in 74 patients with essential hypertension during diagnostic cardiac catheterization. Ventricular compliance was normal in compensated essential hypertension without coronary artery disease even at severe left ventricular hypertrophy. In contrast, additional coronary stenosis and ventricular dilatation due to cardiac decompensation was asscociated with considerable decrease in ventricular compliance. Thus, left ventricular hypertrophy in essential hypertension does not imply per se a change in ventricular compliance. A decrease in ventricular compliance was followed by a decrease of forward pump function of the left ventricle. whereas ventricular work index (as estimated as the product out of systolic wall stress and the stroke volume) increased. This disproportion between external and internal ventricular work increased with increasing ventricular dilatation and was greatest in decompensated essential hypertension. Accordingly, decompensated essential hypertension had largest ventricular work load and lowest forward pump function in comparison to all other patient groups with essential hypertension. The mass to volume ratio may be considered an important determinant of the degree of left ventricular hypertrophy in essential hypertension. The relationship between the mass to volume ratio and the systolic wall stress may provide a diagnostic and prognostic evaluation of the left ventricle in essential hypertension on the basis of dynamic ventricular geometry.
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PMID:[The heart in hypertension. III. Determinants of left ventricular hypertrophy and diastolic left ventricular compliance (author's transl)]. 15 7

Congestive heart failure with dilated left ventricle developed in two patients with symptomatic hypertrophic obstructive cardiomyopathy. Both patients previously underwent cardiac surgery for relief of their outflow obstruction. Alterations in structure and function of the left ventricle during their episode of cardiac failure and thereafter were documented by echocardiography. The findings suggest that progression to left ventricular dilatation is a potential complication in patients with hypertrophic obstructive cardiomyopathy.
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PMID:Progression to left ventricular dilatation in patients with hypertrophic obstructive cardiomyopathy. 57 Dec

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
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PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

Becker muscular dystrophy is associated with abnormal cardiac features in about 75% of cases; up to one-third will develop ventricular dilatation leading to congestive cardiac failure. As this form of muscular dystrophy is relatively benign, failure to respond to medical treatment warrants assessment for cardiac transplantation.
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PMID:Cardiac transplantation in Becker muscular dystrophy. 148 41

Aortic valve replacement (AVR) for aortic regurgitation (AR) results in the reduction of left ventricular dimensions. But postoperative death or congestive heart failure may occur in patients with left ventricular dysfunction. Pre- and postoperative stress (ESS)-volume (ESVI) relationship by M-mode echocardiography was examined in 30 patients undergoing AVR. Postoperatively, 23 patients (Group A) achieved a normal left ventricular dimension (LVDd less than 55 mm, LVDs less than 45 mm) and 7 patients (Group B) had persistent left ventricular dilation (LVDd greater than or equal to 55 mm, LVDs greater than or equal to 45 mm). Correlation between preoperative ESS and ESVI was significant (r = 0.92, p less than 0.001), and the ESS/ESVI was greater in Group A of 1.62 +/- 0.29 kdy/cm2/ml/m2 than in Group B of 1.18 +/- 0.19 kdy/cm2/ml/m2 (p less than 0.001). Three patients with ESVI greater than 180 ml/m2 and ESS/ESVI less than 1.2 kdyn/cm2/ml/m2 died after operation. Echocardiographic variables correlated with ESS/ESVI were ESVI (r = -0.57), FS (r = -0.53) and CSA (r = -0.47). The changes in LVDs (delta Ds) after AVR correlated with ESS/ESVI in 12 patients with severe left ventricular dilatation. Postoperative left ventricular function could be predicted by ESS-ESVI relationship by preoperative DBcAMP infusion test. ESS/ESVI is sensitive to changes in the left ventricular contractility. The patients with ESVI greater than 180 ml/m2 and ESS/ESVI less than 1.2 kdyn/cm2/ml/m2 may result in poor prognostic outcome.
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PMID:[Assessment of left ventricular function with ESS-ESVI relationship in patients undergoing aortic valve replacement for aortic regurgitation]. 161 78

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

Five patients with hypertrophic cardiomyopathy developed left-ventricular dilatation and congestive heart failure during an observation period of 16-29 years. In one patient cardiac transplantation had to be performed. The initial predominant symptoms of outflow-tract obstruction and diastolic dysfunction developed into progressive left-ventricular systolic failure. The question of whether this is a well-defined subgroup of patients with hypertrophic cardiomyopathy, or whether hypertrophic cardiomyopathy turns into a phase of left-ventricular dilatation and failure after some years remains to be elucidated by long-term studies.
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PMID:[Course of dilatative hypertrophic cardiomyopathy]. 187 8

The clinical literature on the subject of inotropic therapy of heart failure, particularly use of digitalis glycosides, is full of contradictions. Most of this disparity can be accounted for if not reconciled by taking the methodology of the clinical trials into consideration. Because drug interventions may produce subtle effects requiring a subjective determination, the questions being asked in these studies cannot be answered without removing as many sources of bias as possible from the patient management and data analysis. If a study has not been adequately randomized, double-blinded, and placebo-controlled, the clinical findings will be inconclusive at best. Systolic myocardial dysfunction plays a pivotal role in the pathogenesis of CHF in many patients and is a prerequisite for the use of cardiotonic drugs. Although the clinical signs of heart failure may be relieved initially by diuretics and vasodilators, compensation may require the addition of a positive inotrope, particularly in advanced cases. In veterinary medicine, the choice of positive inotrope is limited to digoxin, digitoxin, dobutamine, or amrinone. Digoxin possesses superior pharmacokinetics and is the cardiac glycoside of choice for use in the dog. Dobutamine and amrinone are more potent inotropes, but since they must be administered by continuous intravenous infusion, their use is limited to critical care therapy. At the present time, only digoxin can be administered orally for sustained long-term maintenance therapy. Milrinone, a more potent derivative of amrinone, also offers this option, but it has not been available since its brief trial debut as an investigational drug. None of the nonglycoside alternatives couples the benefits of positive inotropic and negative chronotropic effects. Consequently, digoxin remains the mainstay for chronic inotropic support of the heart. Atrial fibrillation with a rapid ventricular response rate is the prime indication for digoxin. In the last few years, evidence from methodologically sound clinical trials on humans has also restored faith in the efficacy of digoxin for treating heart failure in patients with normal sinus rhythm. From these studies, the profile of a digitalis responsive heart failure patient has emerged. Digoxin is most likely to be efficacious when heart failure is associated with chronic, severe ventricular systolic dysfunction, which has resulted in ventricular dilatation. The most reliable clinical marker is the presence of a third heart sound (gallop rhythm). Although the patients in the worst heart failure generally have the shortest survival time, they may also have the most dramatic short-term clinical benefit. However, once cardiac reserve is exhausted in the terminal stages of failure, cardiotonic stimulation ceases to be effective.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Efficacy of inotropic support of the failing heart. 194 98

A 22-year-old man presented with congestive heart failure following flulike symptoms. The diagnosis of acute myocarditis was confirmed by endomyocardial biopsy, which revealed mild infiltration of inflammatory cells. A favorable response to beta-adrenergic receptor blockade was seen, and the patient was discharged without symptoms. Five months later, however, congestive heart failure recurred, and intracardiac thrombi were demonstrated. The patient died after two months. Postmortem examination revealed left ventricular dilatation with slight interstitial fibrosis; the diagnosis was dilated cardiomyopathy. Thus, progression of biopsy-proven myocarditis to dilated cardiomyopathy 10 months after the onset of disease was documented.
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PMID:A case of biopsy-proven myocarditis progressing to autopsy-proven dilated cardiomyopathy. 197 28


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