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)

The long-term prognosis and prognostic factors were assessed in patients with left ventricular dilatation with impaired function secondary to idiopathic dilated cardiomyopathy (DCM) or to heart diseases of various pathogeneses masquerading as DCM (DCM-like). The echocardiographic criteria for DCM-like disease were 1) left ventricular end-diastolic dimension exceeding 60 mm and 2) fractional shortening less than 15%. Those who showed improvement in either of these 2 parameters within 3 months were excluded from this study. One hundred and fifty-eight of 35,250 serially examined patients fulfilled the definitions. The pathogeneses of diseases were valvular heart disease (VHD) in 30 patients, ischemic heart disease (IHD) in 37, alcoholic cardiomyopathy (AC) in 12, hypertensive heart disease (HHD) in 31 and DCM in 48. All of the survivors were followed for more than 24 months; an average of 40 months. During this period, there were a total of 75 deaths, 18 (27%) of whom were judged as sudden death. Five-year survival rates calculated using the Kaplan-Meier method in AC and HHD were 86% and 77%, respectively, which were significantly higher than those in DCM (48%; p < 0.05); whereas, patients with VHD and IHD had lower values (60% and 46%, respectively) which were nearly equal to those in DCM. Factors that contributed to the increase in total cardiac mortality were advanced age, higher NYHA functional class, larger cardiac size on chest radiograph and history of heavy alcohol intake. Each of these factors were closely related to the specific pathogeneses as follows: age to IHD, cardiac size to VHD, and NYHA functional class to DCM. Long-term prognosis of DCM-like heart diseases, especially those of IHD and VHD, seemed to be as bad as those of DCM.
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PMID:[Long-term prognosis in patients with echocardiographic left ventricular dysfunction masquerading as dilated cardiomyopathy]. 184 21

Two dimensional echocardiographic studies were performed in 70 patients with chronic heart failure. Thirty six had dilated cardiomyopathy and normal coronary arteries and 34 had ischemic cardiomyopathy with severe multivessel coronary disease. All patients had a dilated and hypocontractile left ventricle. Ejection fraction assessed by radionuclide ventriculography was less than 40% in all patients. Regional wall motion abnormalities were detected in 16 (44%) of 36 patients with dilated cardiomyopathy and 22 (65%) of 34 patients with ischemic cardiomyopathy (NS). High echodensity of the regional wall motion abnormality suggesting a myocardial scar were found in 4 (25%) of 16 patients with dilated cardiomyopathy and in 9 (41%) of 22 with ischemic cardiomyopathy (NS). Diffuse wall motion abnormalities were present in 20 (56%) patients with dilated cardiomyopathy and 12 (35%) with ischemic cardiomyopathy (NS). Right ventricular dilatation was found in 21 (58%) and 20 (59%) patients with dilated and ischemic cardiomyopathy, respectively (NS). No differences between groups were found regarding the left ventricular size and function. In conclusion, two dimensional echocardiography cannot be reliably used in patients with chronic heart failure to differentiate dilated cardiomyopathy from ischemic cardiomyopathy.
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PMID:[Differential diagnosis of congestive cardiomyopathy and myocardial ischemia: two-dimensional echocardiography has a limited value]. 184 52

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

Eighteen patients were examined by echocardiography one month before, and one month after orthotopic heart transplantation (OHT). The right-heart echocardiographic parameters were compared with pulmonary haemodynamics. All recipients showed increased mean pulmonary artery pressure (PAP) (42 +/- 8 mmHg) and pulmonary vascular resistance 3.0 +/- 1.3 u.) before OHT. The causes of the pulmonary hypertension, and indications for OHT, were the end stage of dilated cardiomyopathy (n = 8), ischaemic heart disease (n = 9) and aortic valve disease (n = 1). After transplantation, the donor's right ventricle dilates due to the recipient's elevated pulmonary vascular resistance. The right ventricular dimension after OHT was greater than 30 mm in 1/3 of patients. The right ventricular diastolic dimension correlates statistically significantly with mean PAP of the recipient before the procedure. Right ventricular dilatation is accompanied by a mild degree of tricuspid insufficiency (in 89% of cases), as documented by Doppler examination. Neither the degree of right ventricular dilatation, nor the degree of tricuspid insufficiency show a tendency to progression during follow-up.
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PMID:Right ventricle in patients after orthotopic heart transplantation. 220 22

Prognosis in classically described dilated congestive cardiomyopathy has been reported to be related to ventricular size. Mildly dilated congestive cardiomyopathy (MDCM) has been defined as end-stage heart failure of unknown etiology (New York Heart Association class IV, left ventricular ejection fraction less than 30%), occurring with neither typical hemodynamic signs of restrictive myopathy nor significant ventricular dilatation (less than 15% above normal range). The present study includes follow-up in 12 nontransplant patients. In the first 4 months after diagnosis, two patients improved and are living, and two showed cardiac dilation and clinical deterioration and died. Six of the remaining eight with persistent MDCM died (four with intractable heart failure and two, sudden deaths) without change in ventricular size before death, despite medical therapy over 20 +/- 8 months. Eight comparable transplanted patients with persistent MDCM demonstrated improved total survival by life table analysis (p less than 0.05). A family history of congestive cardiomyopathy was found in nine of 16 patients (56%) with persistent MDCM. Nontransplant patients were older (p less than 0.02), but other findings were similar in the two groups. Endomyocardial biopsies available in 14 of 16 cases showed little or no myofibrillar loss in spite of severe hemodynamic impairment. The degree of myofibrillar loss did not correlate with hemodynamic parameters but showed good correlation with left ventricular size, that is, five of six patients with no myofibrillar loss had normal ventricular size, whereas all eight patients with mild myofibrillar loss had mild cardiomegaly (p less than 0.002). Our current experience suggests a somewhat variable but negative prognosis after prospective diagnosis of MDCM, with poor survival in patients with persistence of the original diagnostic features during follow-up. Preservation of heart size in MDCM is probably related to lack of significant myofibrillar loss. Thus, irrespective of heart size or myofibrillar preservation on biopsy, heart transplantation should be strongly considered in MDCM if signs of severe cardiac dysfunction persist despite therapy.
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PMID:Mildly dilated congestive cardiomyopathy. Use of prospective diagnostic criteria and description of the clinical course without heart transplantation. 229 58

The aim of this study of 20 young subjects (28 +/- 10.6 years) with no apparent cardiac disease on clinical examination and chest X-ray was to determine the origin of complex ventricular arrhythmias: monomorphic or polymorphic ventricular extrasystoles, isolated or in valves (average 18 158 +/- 12 388 per 24 hours) and/or ventricular tachycardia (5 cases, sustained in 3). These arrhythmias were aggravated (N = 6), disappeared (N = 8) or remained unchanged (N = 5) during exercise. The inter-critical ECG showed ST changes in 5 cases. The extrasystoles had a left bundle branch block configuration in 14 cases and a right bundle branch block configuration in 9 cases. Nine patients were Grade 2 (45%) and 11 patients Grade 4B of Lown's classification. Complementary investigations (echocardiography), radionuclide investigations, right and left heart catheterisation, selective right and left ventriculography and coronary angiography) showed a high incidence of arrhythmogenic right ventricular dysplasia (N - 14) associated with left ventricular abnormalities in 13 cases: hypofixation of Thallium (N = 14) associated with left ventricular abnormalities in 13 cases: hypofixation of Thallium (N = 11), abnormal global left ventricular function (N = 13) with decreased ejection fractions in half the cases, left ventricular dilatation in a third of cases (average and diastolic volume: 109.8 ml/m2), mean velocity of circumferential fibre shortening decreased in 86% of cases (average 0.88 cir/sec), angiographic abnormalities of segmental left ventricular wall motion in 36% of cases; 2 clinically silent cases of mitral valve prolapse were associated with these left ventricular changes; these cases represent forms of arrhythmogenic cardiac disease localised to the right ventricle or involving both ventricles which should be searched for routinely in young patients with apparently normal hearts but with idiopathic and severe ventricular arrhythmias. The diagnosis can only be established by angiography. In other cases, isolated left ventricular abnormalities are detected: two cases of hypertrophic non obstructive cardiomyopathy including one apical form, a condition which may be suspected from analysis of the surface ECG and careful 2D echocardiographic study; phonomechanography may be normal; one idiopathic left ventricular aneurysm which was only diagnosed at ventriculography; one dilated cardiomyopathy affecting the left ventricle. In our series, none of the patients had coronary artery disease and two patients even had no abnormality of any of these investigations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Complex ventricular arrhythmia in apparently healthy young subjects]. 241 70

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

Arrhythmogenic right ventricular dysplasia is characterized by fibrous and adipose replacement of the right ventricular myocardium and recurrent ventricular arrhythmias of left bundle branch block morphologic pattern. Sometimes the diagnosis is difficult because not all the clinical and instrumental findings are present and the separation between arrhythmogenic right ventricular dysplasia and other right ventricular cardiopathies is uncertain. In such cases the angiographic appearance of the right ventricle has been considered the "gold standard". To assess the diagnostic value of right ventricular morphology in identifying arrhythmogenic right ventricular dysplasia, we compared the angiographic findings of 8 patients with arrhythmogenic right ventricular dysplasia, 10 with biventricular dilated cardiomyopathy and 10 with Ebstein's anomaly. The following aspects were considered: deep fissuring of the anterior or inferior wall, outflow tract enlargement, contrast persistence in the right ventricle during the levophase, regional wall motion abnormalities including aneurysmal formations and tricuspid regurgitation. Aneurysmal formations of the right ventricle were found only in arrhythmogenic right ventricular dysplasia whereas the other angiographic findings were common to all the above mentioned diseases. Right ventricular angiography is an important adjunct to the clinical and instrumental diagnosis of arrhythmogenic right ventricular dysplasia, but most of its angiographic features are common to other diseases which cause right ventricular dilatation.
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PMID:[Angiographic findings in arrhythmogenic dysplasia of the right ventricle]. 280 89

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

The purpose of this study was to assess the frequency of inflammatory lesions in the myocardium of subjects with dilated cardiomyopathy and to determine if there was any correlation between the results of two methods of evaluation, one (endomyocardial biopsy) invasive and the other (gallium-67 scintigraphy) noninvasive. Of 115 subjects recruited in seven centres, 91 met the inclusion criteria (left ventricular dilatation greater than or equal to 100 ml m-2 and ejection fraction less than 55% with normal coronary arteriography) and had endomyocardial biopsy (mean five specimens) and Ga-67 myocardial scintigraphy after several days. Scanning was considered doubtful 19 times and positive 13 times. The histologic count of mononuclear cells in the myocardial interstitium in 20 fields was greater than 5 cells field-1 in only four cases. No correlation was found between the two methods. Subjectivity in the choice of the criterion of positivity of Ga-67 scintigraphy and difficulties in identifying lymphocytes upon pathological examination were the major problems encountered. Despite limitations, both techniques suggest that cellular infiltrates are minimal and quite infrequent in dilated cardiomyopathy.
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PMID:Detection of myocarditis during the first year after discovery of a dilated cardiomyopathy by endomyocardial biopsy and gallium-67 myocardial scintigraphy: prospective multicentre French study of 91 patients. 304 99


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