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 pharmacologic treatment of atrial fibrillation (AF) is aimed at controlling the ventricular response, restoring sinus rhythm, and preventing or delaying relapses. In the control of ventricular response, digitalis maintains a primary role when the arrhythmia is accompanied by heart failure. In ischemic, hypertensive, and degenerative (whose number is increasing at present) cardiopathies without evident ventricular dilatation, treatments with calcium antagonists (such as verapamil, gallopamil, or diltiazem) or beta-blocking agents must be preferred. In order to control the ventricular response in patients with chronic AF during physical activity, the association of digitalis with beta-blocking agents or calcium antagonists seems to provide satisfactory results. The drugs of the IC class, especially flecainide, represent a certain therapeutical progress in the restoration of sinus rhythm in the treatment of paroxysmal atrial fibrillation affecting subjects without evident alterations of ventricular function, particularly in subjects with Wolff-Parkinson-White syndrome, with forms of vagal origin, or with atrial fibrillation alone. A therapeutic combination of digitalis and quinidine may produce resolution of the arrhythmia in the presence of altered ventricular function or when AF is of an uncertain onset. In patients with hypertensive, ischemic, and/or degenerative cardiopathy without evident ventricular or advanced heart failure, the verapamil-quinidine association may also be effective and even quicker. The combination of drugs of the I and III class for restoration of the sinus rhythm in particularly resistant forms of AF without evident structural heart alterations is promising but must be verified in a greater number of patients. In the prevention of relapses amiodarone appears to have the widest spectrum of advantages from an electrophysiologic point of view; however, because of its many side effects, amiodarone represents a late therapeutical choice. The promising results obtained with flecainide are disputed by the results of the CAST, which limit the possibilities of using this drug to a low number of cases (W.P.W. syndrome, AF of vagal origin, atrial fibrillation alone). In the past, quinidine and disopyramide have been the drugs most widely used in the prophylaxis of AF. These drugs have a similar efficacy, and both of them provided some positive results. However, because of untoward side effects (especially for quinidine) during chronic treatment, the use of these drugs has been questioned. Perhaps in the majority of patients, the less dangerous therapeutic choice after the termination of the fibrillation is a combination of drugs slowly down AV node activity (digitalis or calcium antagonists and beta blockers) with class IA antiarrhythmics.
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PMID:The pharmacologic treatment of atrial fibrillation. 167 64

We examined cardiac changes in 8 patients (4 men and 4 women, age 21-43 years) with congenital myopathy proven by skeletal muscle biopsy. Of 8 patients, 4 showed cardiac changes, including 1 with cytoplasmic body myopathy (patient 1), 2 with minimal change myopathy (patients 2 and 3) and 1 with nemaline myopathy (patient 4). Patients 1 and 2 showed left ventricular dilatation with severe global hypokinesis of left ventricular wall. These clinical features were quite similar to those of dilated cardiomyopathy and the patients were in NYHA class 3 or 4. Patient 3 had severe mitral regurgitation with mitral valve prolapse. This patient also had a persistent left superior vena cava and hypoplasia of the aorta, and her cardiac function was in NYHA class 3. Patient 4 showed moderate global left ventricular hypokinesis but the left ventricle was not dilated. This patient also had sino-atrial block and type A Wolff-Parkinson-White syndrome. His cardiac function was NYHA class 1. In conclusion, various types of congenital myopathy are associated with cardiac changes which can result in severe congestive heart failure.
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PMID:Cardiac involvement in congenital myopathy. 405 49

Familial hypertrophic cardiomyopathy (HCM) with Wolff-Parkinson-White (WPW) syndrome is extremely rare and associated with a high risk of ventricular tachyarrhythmia and sudden death. We report a familial form of hypertrophic cardiomyopathy associated with Wolff-Parkinson-White syndrome in two siblings 7 and 12-year-old. These patients showed progression to left ventricular dilatation. Early recognition and treatment of such forms can improve such evolution and the risk of sudden death.
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PMID:[Familial hypertrophic cardiomyopathy associated with Wolff-Parkinson-White syndrome]. 1272 63