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)

To examine the effects of theophylline toxicity on cardiac rhythm, patients underwent continuous ambulatory ECG recording during acute theophylline toxicity and recovery. The patients, who were recruited form inpatient wards, intensive care units, and emergency departments of a University Medical Center and a Veterans Administration Medical Center, had serum theophylline concentrations (STC) greater than 30 mg/L. There were 14 men and two women with a mean age of 66 years. Fourteen patients had COPD and developed toxicity following long-term theophylline overmedication. Two patients had asthma and ingested an intentional overdose. The STC at the onset of ECG recording ranged from 23 to 67 mg/L. The principal rhythm was sinus in 15 patients; one patient had atrial fibrillation. Sinus tachycardia (heart rate greater than 100/min) was common, and heart rate fell in proportion to STC as toxicity resolved. Supraventricular ectopic beats (SVEs) were noted in seven patients with multiple runs of SVE being present in four. One patient developed multifocal atrial tachycardia (MAT) during toxicity that resolved spontaneously. During the 11 +/- 8 hours of recording during toxicity (STC greater than 20 mg/L), 80 percent of patients had ventricular premature beats (VPBs), 44 percent had paired VPBs, and 25 percent had ventricular runs. One elderly patient with heart disease developed sustained ventricular tachycardia (VT) when STC = 66 mg/L. No other patient had ventricular ectopy that required intervention. During the 10 +/- 6 hours of recording during the "recovery phase" (STC less than 20 mg/L), all patients with VPBs continued to have ectopy; however, the number of VPBs declined significantly. A follow-up 24-hour ECG recording obtained one week after recovery from toxicity in the patient with sustained VT demonstrated marked reduction in the frequency and complexity of VPBs. Patients with frequent (greater than 10/h) or repetitive VPBs were older (p less than 0.05) than those without complex ectopy. There was a trend (p = 0.07) suggesting patients with underlying heart disease were at risk for having complex ventricular ectopy. We conclude that sinus tachycardia, SVE, and VPBs are common among patients with theophylline toxicity; however, sustained ventricular or supraventricular tachyarrhythmias that require antiarrhythmic therapy are uncommon.
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PMID:Cardiac arrhythmias during theophylline toxicity. A prospective continuous electrocardiographic study. 188 98

Calcium antagonists have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, these agents are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle, most readily demonstrated in isolated tissue preparations. In vivo, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the noncompetitive adrenergic-blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil and bepridil; the dihydropyridines are devoid of electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the atrioventricular node but exert little or no effect on atrial, ventricular, His-Purkinje or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of the reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the long-term control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias caused by coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of ventricular premature complexes. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young patients who develop tachycardia with a right bundle branch block and left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity.
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PMID:Use of calcium antagonists for cardiac arrhythmias. 243 30

Fifty patients with supraventricular tachycardia (SVT) underwent clinical electrophysiological studies (EPS), endomyocardial biopsies and cardiac catheterizations. EPS revealed AV nodal reentrant tachycardia (AVNRT) in seven patients, AV reentrant tachycardia utilizing concealed AV bypass tracts (AVR-CBT) in nine patients, AV reentrant tachycardia utilizing AV bypass tracts with ventricular preexcitation (manifest WPW) in 13 patients, sinus nodal or intra-atrial reentrant tachycardia (SNRT or IART) in three patients, atrial flutter (AF) in nine patients, automatic atrial tachycardia (AAT) in five patients, and multifocal atrial tachycardia (MAT) in four patients. According to the clinical observations, three patients with AVNRT (43%), six with AVR-CBT (67%), six with manifest WPW (46%), two with SNRT or IART (67%), eight with AF (89%), two with AAT (40%), and two with MAT (50%) showed other accompanying clinical abnormalities. In all patients who were studied histologically, changes in the myocardium were seen; myocarditic changes, postmyocarditic changes and nonspecific abnormalities were present in six (12%), 15 (30%), and nine (18%) respectively. Myocardial changes were observed in four out of seven cases with AVNRT (57%), in six out of nine with AVR-CBT (67%), in five out of 13 with manifest WPW (38%), in two out of three with SNRT or IART (67%), in six out of nine with AF (67%), in all five cases of AAT (100%), and in two out of four with MAT (50%). Nineteen out of 32 without clinical abnormalities except for arrhythmias (59%) had myocardial changes (six had myocarditic changes, ten had postmyocarditic changes, and three had nonspecific abnormalities). On the other hand, nine out of 21 with myocarditic or postmyocarditic changes were accompanied with various arrhythmias other than SVT (two had SSS, five had AV block or rBBB, and two had VT). Elevated LVEDP was present in 36% of the group with normal myocardium and in 53% of the group with myocardial changes. However, the low EF was shown in no patients with normal myocardium but in 21% of the group with myocardial changes. The low CI was also shown in only 9% of the group with normal myocardium but in 28% of the group with myocardial changes. These results suggest that patients with SVT may exhibit several histopathological changes in the myocardium, even in the absence of any clinical organic heart disease.
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PMID:Clinical, electrophysiological, and histopathological observations in supraventricular tachycardia. 245 68

In recent years calcium channel blockers have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, they are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle. In isolated muscle, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the nonocompetitive adrenergic blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil, and bepridil; the dihydropyridines are devoid of significant electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the AV node, but exert little or no effect on atrial, ventricular, His-Purkinje, or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the chronic control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias due to coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of premature ventricular contractions. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young subjects developing tachycardia with a right bundle branch block with left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity. The role of calcium antagonists in reducing the incidence of sudden death in the survivors of acute myocardial infarction remains uncertain.
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PMID:Control of cardiac arrhythmias by calcium antagonism. 328 60

To clarify the clinical and electrophysiological characteristics of atrial standstill (AS) we studied 11 patients (7 males and 4 females), whose average age was 62 years and who were followed over a period of 4-179 months. Underlying heart disease was present in nine patients and two cases were idiopathic. Major clinical symptoms in the 11 cases included Adams-Stokes attacks, and dyspnea on exertion. In the standard 12-lead ECGs obtained on admission, the P wave was absent in six cases. Atrial flutter (AF) was noted in 3, atrial fibrillation (Af) in 1, and multifocal atrial tachycardia in 1. In some cases, the ECG initially showed AF or Af, and was transformed after several years into ectopic atrial tachycardia or an ectopic atrial rhythm with a markedly decreased amplitude of the P wave. Finally, the P wave disappeared over a prolonged period. When intracardiac mapping was performed, the atrial electrograms tended to diminish at the site of high, mid-lateral right atrium (RA). Electrograms were remained present in the vicinity of the tricuspid valve (TV) annulus. A repeated mapping and pacing study conducted in two patients revealed that the "silent" area spread toward the lower site of RA. During the average follow-up period of 64 months, four patients died. The interval until death in one patient with myocarditis was 6 months, and in another with dilated cardiomyopathy (DCM) it was 8 months. It appears that the atrial muscular lesion starts in the high lateral RA and progresses toward the lower RA, then to the vicinity of the TV annulus. A diffuse and progressive disturbance may occur not only in the atrial muscle, but also in the atrioventricular conduction system in patients with AS who had progressive myocarditis or DCM.
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PMID:Clinical and electrophysiological characteristics of atrial standstill. 765 78

Patients with chronic obstructive pulmonary disease (COPD), especially during acute exacerbations of their disease, show a greater incidence of cardiac arrhythmias than healthy subjects of the same age. The type of arrhythmias found may be supraventricular (premature atrial beats, paroxysmal supraventricular tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation) or ventricular (premature ventricular beats, sustained ventricular tachycardia, torsades de pointes, ventricular fibrillation) that may lead to sudden cardiac death. The pathogenesis of arrhythmias is complex and many factors may be involved such as hypoxemia, hypercapnia, respiratory acidosis, metabolic and respiratory alchalosis, hypokalemia, concomitant ischemic heart disease, chronic cor pulmonale, left ventricular diastolic dysfunction. Remarkable attention has been drawn to the possible arrhythmogenic effect of drugs such as theophylline, beta-adrenergic stimulants and digitalis which are commonly used in the therapy of COPD. Both of the main classes of bronchodilators (methylxanthynes and beta-adrenergic agonists), even when used together, apparently do not increase the incidence of dangerous cardiac arrhythmias. However, these drugs should be used with caution in the elderly, in patients with preexisting cardiac arrhythmias, with heart disease or with reduced hepatic function. In these cases Holter monitoring, repeated measurements of plasma drugs concentration and prompt hospitalization of high risk patients in Intensive Care Unit may be needed.
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PMID:[Evaluation of hyperkinetic cardiac arrhythmia in chronic obstructive bronchopneumopathy]. 944 64

The incidence of multifocal atrial tachycardia (MAT) is very low and accounts for less than 1% of supraventricular tachycardia in infants and children. In this report, the clinical characteristics, medical treatment and outcome of MAT in 2 children are described. The first patient presented with tachycardia and respiratory failure since the day after birth. First, he received amiodarone, propranolol, and digoxin and then amiodarone alone. The heart rhythm converted to sinus rhythm 2 weeks after hospitalization. Although nonsustained MAT was occasionally observed when the infant suffered from pulmonary infection, the frequency of recurrent MAT decreased as the infant grew up. The second patient was a 5-year-old girl. She had congenital heart disease with double outlets of right ventricle (DORV), patent ductus arteriosus, coarctation of aorta, and ventricular and atrial septal defects. She underwent total correction at the age of 4 years. MAT was noted 3 months after the operation with the presentation of congestive heart failure. The heart rate slowed down and returned to normal sinus rhythm within several hours after amiodarone use. The symptoms and signs of congestive heart failure also disappeared. The patient took amiodarone regularly, and no tachycardia was detected during the follow-up period. MAT is considered to be a relatively benign arrhythmia with likely good outcome if there is no severe underlying illness. It can be well controlled under appropriate drugs, and a long period of follow-up is suggested. If pharmacologic intervention is required, we suggest that amiodarone may be an excellent choice.
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PMID:Multifocal atrial tachycardia in 2 children. 1705 56