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)

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.
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PMID:[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension]. 174 69

A 38-year-old female had felt exertional dyspnea for six months. Physical examination and laboratory data including angiotensin-converting enzyme, failed to diagnose sarcoidosis. Her chest X-ray showed cardiomegaly but no hilar lymph node enlargement. Holter ECG showed nonsustained and sustained ventricular tachycardias, monomorphic or polymorphic tachycardia. Echocardiography and contrast left ventriculography showed left ventricular dilatation and generalized hypo- and akinesis. Endomyocardial biopsy revealed myocardial sarcoidosis. Administration of corticosteroids, metoprolol of 20 mg/day and cibenzoline of 300 mg/day was markedly effective for the treatment of ventricular tachycardia. This patient is alive for one year after treatment and the combination therapy seems to contribute to good prognosis.
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PMID:Polymorphic ventricular tachycardia with cardiac sarcoidosis: treatment with low-dose metoprolol and cibenzoline. 794 33

We report an extremely rare case of dilated cardiomyopathy manifested by exercise-induced left bundle branch block. A 63-year-old female came to our hospital because supraventricular arrhythmia had been detected at a check-up. A treadmill exercise test induced left bundle branch block. However, chest X-ray and echocardiography revealed no abnormal finding. Two years later, the patient experienced exertional dyspnea. A chest X-ray examination showed cardiomegaly, and echocardiography showed a moderate impairment of left ventricular function with left ventricular dilatation. The diagnosis of dilated cardiomyopathy was made by left ventricular myocardial biopsy. No previous cases have initially shown exercise-induced left bundle branch block which was followed by left ventricular dysfunction due to dilated cardiomyopathy. Careful long-term observation of the clinical course is necessary in patients with exercise-induced left bundle branch block which shows no significant underlying disease.
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PMID:A case of dilated cardiomyopathy manifested by exercise-induced left bundle branch block. 834 Oct 5

It has been reported that a variety of cardiovascular side effects are induced by drugs, including psychotropic drugs. Among them, myocarditis/cardiomyopathy and long QT syndrome are addressed in this article. Myocarditis is due to inflammation of the myocardium, and the pericardium is also often involved. In that case, it is called myopericarditis. Myocarditis is caused by a variety of etiologies, including viruses, bacteria, inflammatory diseases, and drugs. Psychotropic drugs such as clozapine have been reported to induce myocarditis. In critical cases, the hemodynamics deteriorate due to cardiac insufficiency, which can be fatal. The principal of treatment of drug-induced myocarditis is, of course, cessation of the causative drug. Cardio-circulatory support including inotropes and, in severe cases, mechanical support, are also necessary. Cardiomyopathy can also be induced by drugs. Drug-induced cardiomyopathy usually presents as dilated cardiomyopathy, characterized by left ventricular dilatation and reduced contraction. Anthracyclin is well-known as a cause of drug-induced cardiomyopathy. The treatment of drug-induced cardiomyopathy is in accordance with chronic heart failure. Long QT syndrome (LQTS) is also a relatively common manifestation of the cardiovascular side effects of drugs. Especially, many psychotropic drugs can induce LQTS. LQTS does not simply mean prolongation of the QT interval in electrocardiography, but it includes life-threatening ventricular arrhythmia derived from QT prolongation. Torsade de Pointes is a common ventricular arrhythmia accompanying LQTS. To avoid or detect the occurrence of these serious cardiovascular side effects in time, careful monitoring based on ECG, symptoms, and blood tests is recommended when a drug reported to induce such side effects must be used. ECG must be routinely taken before the drug is initiated. In 2 to 4 weeks after initiation, ECG may be taken regardless of the cardiovascular symptoms. If any ECG changes are noted, such as QT prolongation or ST change, consultation with a cardiologist and further evaluation are required. After the initial check-up for cardiovascular side effects, ECG should be taken regularly every 3 to 6 months. If new changes in ECG or any symptoms suggesting cardiovascular disease, such as palpitation, chest pain, and exertional dyspnea, cardiology consultation is again needed. To detect early myocardial damage due to myocarditis or cardiomyopathy, the measurement of serum troponin T or I is also useful.
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PMID:[Cardiovascular monitoring of psychotropic drugs]. 2471 72