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 dilated cardiomyopathies are characterized by an increase in left ventricular internal dimensions without an appropriate increase in ventricular wall thickness. The myocardial injury often goes unrecognized until the offending cause is no longer apparent. Although specific diagnoses and treatment can sometimes be established, the majority of cases are designated idiopathic but are believed to result from previous viral infections, autoimmune or genetic predisposition, or abnormalities of the coronary microvasculature. Despite impaired contractility and ventricular dilatation, compensated dysfunction may prevail for some time. Excessive fluid retention, neurohumoral activation, systemic vasoconstriction, and atrioventricular valve regurgitation promote progressive hemodynamic deterioration. The meticulous matching of diuretic and vasodilator therapy to specific hemodynamic goals, particularly the normalization of ventricular filling pressure, frequently allows restoration and maintenance of reasonable functional capacity even in patients with severe heart failure. Nevertheless, sudden death due to ventricular arrhythmias and occasionally to systemic emboli remains a major threat. Prophylactic use of antiarrhythmic agents and anticoagulant therapy is not of proven efficacy. Cardiac transplantation results in significant improvement in life expectancy for patients with dilated heart failure but is available only to a relatively small number of patients because of the limited donor supply. Accordingly, programs providing cardiac transplantation should be equally committed to providing optimal medical management that is the only option for the majority of patients with dilated cardiomyopathy.
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PMID:The dilated cardiomyopathies: clinical aspects. 306 82

Cardiac failure caused by high doses of amphetamine-like drugs is rare. We report a case of decompensated congestive cardiomyopathy occurring in a 29 year old woman addicted to clobenzorex (Dinintel). This patient had been taking 5 to 7 capsules per day for 5 years. No other cause of cardiac failure was detected. A rapid improvement was obtained by digitalis and diuretic therapy; no further episodes of cardiac failure were observed after one year. However, the drug could not be completely withdrawn and echocardiography has shown increasing left ventricular dilatation. The possible mechanisms of amphetamine induced myocardial toxicity are discussed and the analogy with the group of adrenergic cardiomyopathies is underlined.
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PMID:[Congestive cardiomyopathy in addiction to clobenzorex, an anorexigenic drug]. 309 Sep 71

Five patients with only mildly dilated ventricles but other features typical of congestive cardiomyopathy underwent cardiac transplantation for class IV NYHA heart failure. The findings of clinical studies, cardiac catheterization, endomyocardial biopsy, and pathologic examination of the removed hearts in this group with mildly dilated congestive cardiomyopathy (MDCM) were compared with similar data in four patients with idiopathic restrictive cardiomyopathy (IRCM) and in 10 patients with typical dilated congestive cardiomyopathy (DCM). In comparison with the other groups, patients with MDCM had a higher incidence of familial cardiomyopathy (p = .02) and a shorter symptomatic period than patients with IRCM (p less than .02). Patients with both MDCM and DCM had globular hearts (with predominant left ventricular dilatation), congestive hemodynamics and poor left ventricular contractility (ejection fraction 12% to 19%), and high incidence of ventricular thrombi. Patients with IRCM showed normal ventricular size, marked atrial dilatation, restrictive hemodynamics, mild-to-moderate decrease in left ventricular contractility (ejection fraction 29% to 55%), and absence of ventricular thrombi. Cardiac index, ventricular wall thickness, and light microscopic findings were similar in the three groups of patients. Electron microscopy showed no myofibrillar loss in patients with IRCM but mild (partial) or moderate-to-severe (almost total) myofibrillar loss in those with MDCM and DCM, respectively. We conclude that end-stage congestive cardiomyopathy may occur without significant ventricular dilatation and patients with MDCM have heart sizes intermediate between those found in IRCM and DCM but their clinical, hemodynamic, and pathologic findings are virtually identical to those of patients with typical DCM.
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PMID:Mildly dilated congestive cardiomyopathy. 315 8

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Hypertrophic cardiomyopathy with left ventricular dilatation]. 324 61

We present a report of cardiac dilatation and symptomatic congestive heart failure in two patients receiving treatment with continuous ambulatory peritoneal dialysis (CAPD). Both patients had previous partial parathyroidectomies and persistent hypocalcemia prior to the development of a congestive cardiomyopathy. The hypocalcemia was unresponsive to treatment with activated vitamin D therapy; however, intravenous replenishment of the ionized serum calcium level was accompanied by improvement in cardiac functional parameters. In one of the two patients, chronic calcium repletion with high dialysate calcium was associated with significant improvement in cardiac symptoms and a decrease in left ventricular dilatation. These observations suggest that partial parathyroidectomy and associated hypocalcemia place patients on CAPD at increased risk of cardiac dysfunction.
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PMID:Congestive cardiomyopathy in patients on continuous ambulatory peritoneal dialysis. 333 2

To investigate the pathogenesis and pathophysiology of dilated cardiomyopathy (DCM), we studied 28 patients with DCM by echocardiography and endomyocardial biopsy, and compared their findings with those of 34 patients including eight with myocarditis, seven with alcoholics, 12 with hypertensives and seven patients with hypertrophic cardiomyopathy. All 12 patients in the hypertensive group had congestive heart failure without accompanying high blood pressure, and prominent dilatation and uniform wall motion abnormality of the left ventricle observed echocardiographically on admission. After medical management, both heart failure and the echocardiographic abnormalities gradually resolved. Those in the alcoholic group had larger left ventricles and uniform wall motion abnormality compared to those in the other groups. The myocarditis and hypertrophic cardiomyopathy groups had smaller left ventricles, non-uniform wall motion and larger % myocardial fibrosis. Both ventricles in the hypertrophic cardiomyopathy group were thicker than those of the other three groups. Each patient with DCM had individual echocardiographic abnormalities, which could be categorized as two subsets depending on the degree of left ventricular dilatation and uniformity of the wall motion. The one was characterized by a prominently dilated left ventricle and uniform wall motion abnormality similar to the alcoholic group, and the other had less marked left ventricular dilatation and heterogeneous wall motion abnormality similar to the myocarditis group. From these findings, it was suggested that there are common factors to specific myocardial disease in the pathogenesis and pathophysiology of DCM, and thus, DCM might include many subsets of different etiologies.
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PMID:[Pathogenesis of dilated cardiomyopathy: a study based on comparison of the clinical features with other related conditions]. 342 22

The mother and three children of a family whose parents were consanguineous, each had cardiomyopathy with various patterns of hypertrophy and dilatation. All members had asymmetrical septal hypertrophy (ASH), and three of them were characterized as hypertrophic cardiomyopathy (HCM). Another one had ventricular dilatation mimicking dilated cardiomyopathy (DCM). Case 1: The 57-year-old mother had a typical ASH pattern; her septal/posterior wall thickness ratio (IVST/LVPWT) was 2.5. Case 2: The 37-year-old daughter had basal septal hypertrophy. Case 3: The 32-year-old elder son had typical concentric hypertrophy. Case 4: The 30-year-old younger son had an episode of congestive heart failure, and showed DCM-like features with considerable dilatation and impaired wall motion of the left ventricle. The hypertrophic pattern in cardiomyopathies is thought to depend partially on the ages of the onset, or its evolution with aging.
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PMID:[Familial cardiomyopathy with different clinical features in individual members]. 350 15

112 consecutive asymptomatic patients who assumed alcohol in excess (1-2 g/kg/die) for 5 years or more were admitted to our hospital for detoxication. They were examined both clinically and with chest x-rays, ecg, phonocardiography, external pulse recording, and M-mode/2-D echocardiography to detect myocardial involvement. Heart disease not related to alcohol abuse was found in 6 cases. In the remaining 106/112 patients electrocardiographic abnormalities (aspecific ST-T changes, left bundle branch block, intraventricular conduction defects, left ventricular strain pattern and atrial fibrillation) were present in 18 per cent of cases. PEP, LVET intervals and PEP/LVET, were calculated only in 39/106 patients and did not differ significantly from the control group. The echocardiographic study showed hypokinesis and left ventricular dilatation in 9/106 patients. In other 5 cases echocardiographic findings were at upper limits of normal for left ventricular dimension and motility. Therefore in 13 per cent of cases a dilated cardiomyopathy was revealed by the echocardiographic study. In 6 of these 13/106 patients ecg was either normal or showed only aspecific ST-T changes. Echocardiography failed to confirm augmented left ventricular thickness and mass as reported in asymptomatic alcoholic patients in the literature. Probably several factors (different interval of time between the interruption of the alcoholic abuse and the time of examination, the quantity of alcohol in excess and the echocardiographic technique) may influence the results of such studies. The present report nevertheless points out to the validity of the echocardiographic study in the detection of subclinical myocardial involvement in alcoholic patients and should be performed in such cases.
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PMID:[Alcoholic cardiomyopathy in the preclinical stage: non-invasive clinico-instrumental research study on 112 chronic alcoholics]. 367 28

Dilated cardiomyopathy is a moderately common syndrome resulting from many causes, many of which are yet to be defined. The syndrome is relatively easy to diagnose in its late congestive stage if valvular abnormality, hypertensive disease, and gross myocardial infarction are absent. However, it should be suspected in patients with undiagnosed chest pain, in patients whose severe arrhythmia has no obvious cause, and in any patient with demonstrable ventricular dilatation or systolic malfunction. It may follow infections, especially viral ones and is found in many deficiency diseases, especially diabetes. Repeated episodes of angina due to epicardial disease may result in myocardial "stunning" with ultimate dilation and failure. Microvascular spasm or occlusion may be etiologically important. Dilated cardiomyopathy may be a manifestation of toxins, with ethanol being the most important. Immune mechanisms may play a major role, either independently or in connection with other factors. Early diagnosis may be made with the help of echocardiography, radionuclide angiography, and even coronary arteriography. Gallium scan may be helpful, and if positive myocardial biopsy is indicated. Therapy includes classic measures for congestive failure if it is present: cardiac glycosides, diuretics, antiarrhythmics, and anticoagulants. There is evidence that vasodilators, calcium channel blockers, and beta-adrenergic blockers may be helpful for both general and specific reasons, but these should be used with care. Prednisone and azathioprine may help if there is an inflammatory component. Cardiac replacement remains an ultimate measure.
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PMID:Dilated cardiomyopathy: current concepts. 372 Feb 70

Five cases of peripartum cardiomyopathy are presented. All patients were aged less than 35 years, and four were multiparous. Two cases followed twin deliveries. Pulmonary embolism was diagnosed in four patients. Electrocardiograms showed left ventricular hypertrophy or left bundle branch block. On echocardiography, left ventricular minor axis dimensions were increased (diastolic, 67 +/- 7 mm; systolic, 59 +/- 7 mm) and mean fractional shortening was reduced (13% +/- 5%). All patients had hypokinesis or akinesis of the left ventricular segments and two had right ventricular dilatation. Gallium scanning performed in three patients was negative. Viral serologic testing was negative in all cases. All patients died within 5 years, three within 5 months. Survival duration was closely correlated with left ventricular fractional shortening. Autopsy in three patients confirmed the diagnosis of a dilated cardiomyopathy.
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PMID:Peripartum cardiomyopathy: echocardiographic features in five cases. 372 77


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