Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also being antifibrillatory and of raising the threshold for ventricular fibrillation. Lidocaine and bretylium are available only in i.v. form. Procainamide is available in i.v. as well as oral form. Other oral antiarrhythmic agents include quinidine, disopyramide, beta-blockers such as propranolol and verapamil. The latter may be useful in ventricular arrhythmias induced by ischemia; of these, only beta-blockers appear to significantly raise the threshold for ventricular fibrillation. Control of ventricular ectopy does not always preclude ventricular tachycardia and ventricular fibrillation. In treating ventricular tachycardia, bretylium tosylate is generally given 5 to 10 mg/kg i.v. over 10 to 20 minutes. Given too rapidly, it may cause nausea and vomiting. Orthostatic hypotension, a common side effect, generally abates with continued use and may be ameliorated with tricyclic antidepressants such as protriptyline. Significant supine hypotension may be encountered in patients with acute myocardial infarction and may be managed with pressor agents or fluids, or both. The antiarrhythmic efficacy of bretylium was analyzed in 40 patients. Five etiologic groups were defined by cardiac catheterization: 19 patients had atherosclerotic heart disease, 6 had primary myocardial disease, 4 had mitral valve prolapse, 4 had rheumatic heart disease and 7 had miscellaneous or no heart disease. All patients had recurrent ventricular tachycardia (VT); 23 had ventricular fibrillation (VF) as well. Other antiarrhythmic agents had failed in 38 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapy of ventricular tachycardia. 646 97

Electrophysiologic evaluation before and after the serial administration of verapamil, lidocaine, propranolol, and procainamide was undertaken in 4 young, asymptomatic patients with recurrent, sustained ventricular tachycardia (VT). No patient had obvious organic heart disease. The electrocardiogram during sinus rhythm showed S-T depression and T-wave inversion over the inferior and lateral precordial leads in 3 patients. QRS morphologic characteristics during episodes of VT showed a pattern of right bundle branch block and left axis deviation. In all 4 patients, VT could be both induced and terminated with electrical stimulation. Verapamil terminated VT and prevented the induction of sustained VT in 3 patients, and markedly slowed the rate of VT in 1 patient. Procainamide effectively prevented the induction of sustained VT in 2 patients, and although ineffective in preventing induction in 2 patients, it slowed the rate of tachycardia in both. Lidocaine and propranolol did not prevent the induction of VT in any patient. These findings suggest that slow-response tissues may be involved in the genesis of VT in these patients, and that VT in these patients may represent a unique clinical entity with distinct electrocardiographic, electrophysiologic, and electropharmacologic properties.
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PMID:Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties. 685 37

In a 4 1/2 year period fetal, echocardiographic studies were performed on 1600 fetuses. In 55 with arrhythmia, 44 had supraventricular ectopic beats, resolved in all, and none had heart disease. Sustained arrhythmias occurred in 11 fetuses. Atrial flutter was present in 3 all with heart disease (Ebstein disease, right atrial tumour and WPW diagnosed after birth). Another 3 fetuses had supraventricular tachycardia (SVT), all with a normal heart. In the bradycardia group, 2 had complete heart block (CHB) associated with AVSD; 2 sinus bradycardia and one had non conducted atrial ectopic beats. Digoxin was the first choice drug for tachyarrhythmia therapy; association with Verapamil, Flecainide, Quinidine and Procainamide was used in 4 of the 6. One fetus with CHB received Orciprenaline with no results. Atrial flutter resolved or improved; in SVT 2 fetuses converted to sinus rhythm and one died in utero. All fetuses with CHB died in cardiac failure. Mortality was 27% (3 cases) in utero and global 36%. In our experience most fetal arrhythmias (90%) were transitory ectopic beats or non lasting bradycardia in normal heart and did not trigger other kinds of arrhythmias. In sustained arrhythmias, heart failure and heart disease had a negative effect on prognosis.
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PMID:[Fetal arrhythmia. A case load of 4 years and a half]. 777 Dec 7

Safe and effective control of rapid ventricular rates in acute-onset atrial fibrillation (AF) can be accomplished with intravenous calcium antagonists, beta-blockers or amiodarone; digoxin is less effective. If pharmacologic cardioversion of AF is desired, single oral doses of propafenone or flecainide are safe and effective in patients without structural heart disease. Intravenous ibulitide is moderately effective in the conversion of persistent AF or atrial flutter, with a small risk of proarrhythmia. In wide QRS complex tachycardia of uncertain origin, adenosine and lidocaine are no longer recommended. Procainamide or amiodarone are the treatment options, but attempts should be made to define the origin of tachycardia. In the treatment of monomorphic ventricular tachycardia, lidocaine is no longer recommended; procainamide or amiodarone are the recommended therapies. In polymorphic ventricular tachycardia with a normal QT interval, beta-blockers are recommended. In shock-refractory ventricular fibrillation, lidocaine, and magnesium are ineffective; intravenous amiodarone should be the treatment of choice.
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PMID:Advances in the acute pharmacologic management of cardiac arrhythmias. 1291 54