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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In view of the paucity of reports describing symptoms of increased degree, and deterioration of left ventricular systolic function in patients with apical hypertrophic cardiomyopathy (apical HCM), two cases with congestive heart failure and progressive thinning of previously hypertrophied apical portions of the left ventricle are reported. These were among 13 patients observed from eight to 10 years. Case 1: A 56-year-old man was diagnosed as having apical HCM at the age of 49 years. Severe left ventricular hypertrophy and prominent ST-T changes were observed on ECG during his first admission. His left ventricular end-diastolic pressure (LVEDP) was 24 mmHg and a left ventriculo-gram revealed a decrease in the left ventricular cavity in the apex and marked hypertrophy of the apical wall. Moderate interstitial fibrosis without hypertrophy or disarray of myocytes was observed in a left ventricular endomyocardial biopsy specimen. In two episodes of cardiac arrest he was successfully resuscitated at the age of 50 years. At the age of 55 years, two-dimensional echocardiography revealed thinning and abnormal motion in the apical wall, and a defect in 201T1 accumulation was observed in the same region by perfusion scintigraphy. This patient was readmitted with a diagnosis of cerebral embolism at the age of 56 years. Cardiac catheterization revealed normal LVEDP (8 mmHg), and a left ventriculogram revealed an aneurysm in the left ventricular apex with normal major epicardial coronary arteries. He has been under treatment with antiarrhythmic medications, calcium antagonists and anticoagulants, and has become relatively asymptomatic. Case 2: A 69-year-old-man was diagnosed as having apical HCM after a complete evaluation, including cardiac catheterization, at the age of 59 years. His LVEDP was elevated (17 mmHg), and a left ventricular angiogram revealed marked hypertrophy localized to the apex. Ejection fraction was 64%. A left ventricular endomyocardial biopsy revealed interstitial fibrosis without hypertrophy of myocytes. Thereafter, he has been followed as a New York Heart Association functional class III to IV with occasional elevation of cardiac enzymes but without chest pain or acute changes in his ECGs. However, atrial fibrillation with complete right bundle branch block developed at the age of 60 years. Apical wall thinning and dyskinesis were diagnosed by 2D echocardiography and a defect in the 201T1 accumulation was observed at about 65 years of age. He was readmitted in severe cardiac failure at the age of 69 years, and he was diagnosed as having cardiac asthma with pulmonary capillary wedge pressure of 35 mmHg.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Advanced sequelae of apical hypertrophic cardiomyopathy: report of two cases with wall motion abnormalities]. 322 16

Five patients with right ventricular dysplasia (RVD) and 28 patients with predominantly left sided dilated cardiomyopathy (DCM) were studied. RVD was characterised by syncope, recurrent sustained ventricular tachycardia, which typically had a left bundle branch block pattern on the surface electrocardiogram, right heart failure, and faint or absence of the right ventricular free wall on the myocardial scintigraphy. Two-dimensional echocardiographic, radionuclide angiographic, and contrast ventriculographic studies were typical of the right ventricular abnormalities in both Uhl's anomaly and arrhythmogenic right ventricular dysplasia. Two of them were died suddenly. Pathologic examinations showed "parchment-like" thinning of portions of the right ventricular free wall and its replacement by adipose tissue, although such degenerations were not found in the septum and the left ventricle. By contrast, DCM was characterised by exertional dyspnea and short run ventricular tachycardia, most of which had a right bundle branch block pattern. Ten of them had left ventricular myocardial defects on the scintigraphy, of whom five died suddenly. Hemodynamic data showed that left ventricular dysfunction was predominant more than right ventricle. Thus we postulate that these two syndromes are manifestations of a congenital, pathophysiologic process - the "involved right or left ventricle" syndrome.
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PMID:[Right ventricular dysplasia: clinical features compared with dilated cardiomyopathy]. 401 15

To analyze the clinical features of cardiac sarcoidosis, we reviewed case reports and clinical investigations from Japan and other countries. Female patients were more frequently affected in this disease in Japan. Cardiac sarcoidosis is characterized by a high incidence of complete atrioventricular block, right bundle branch block, and ventricular arrhythmias on the electrocardiogram. Echocardiography often reveals left ventricular dilatation with systolic dysfunction and wall thickening or thinning. Radionuclide testings, such as, thallium-201, gallium-67 or technetium-99m pyrophosphate, are useful for detecting cardiac involvement and evaluating efficacy of corticosteroid therapy in patients with sarcoidosis. Most of the patients died due to recurrent or refractory heart failure. It is noteworthy that cases of sudden death during stable cardiac function have become infrequent.
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PMID:[Cardiac sarcoidosis]. 804 45

An 8-month-old Labrador retriever bitch was evaluated for sudden-onset, progressive abdominal distension. Physical examination revealed an exaggerated inspiratory effort, severe ascites, bilateral jugular vein distension, and hypokinetic femoral arterial pulses. Thoracic auscultation detected tachycardia with muffled heart sounds, without audible cardiac murmurs. Thoracic radiographs identified severe right ventricular enlargement and pleural effusion. The electrocardiogram was consistent with incomplete right bundle branch block or right ventricular enlargement. Echocardiography demonstrated severe right ventricular and atrial dilation, secondary tricuspid regurgitation, and thinning and hypocontractility of the right ventricular myocardium. Left heart chamber sizes were slightly decreased, with normal left ventricular contractility. A diagnosis of arrhythmogenic right ventricular cardiomyopathy was reached, based on the characteristic clinical, electrocardiographic, radiographic and echocardiographic findings, and the exclusion of other causes of isolated right ventricular failure. Treatment effected good control of clinical signs, until acutely decompensated congestive right heart failure led to euthanasia after 4 months. Arrhythmogenic right ventricular cardiomyopathy is a well-described clinical entity in humans, and has previously been documented in 3 male dogs. The condition is characterised by progressive fibro-adipose replacement of right ventricular myocardium, while the left ventricle usually remains unaffected. It should be considered a differential diagnosis in any young dog presented with isolated right heart failure, syncope, or unexplained ventricular tachyarrhythmias. This article reports the 1st case of arrhythmogenic right ventricular cardiomyopathy in a female dog, and highlights its echocardiographic features.
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PMID:Arrhythmogenic right ventricular cardiomyopathy in a dog. 1103 Mar 67