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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chagas' disease is a chronic parasitosis affecting most Latin American countries. Its most important clinical manifestation is a late developing chronic myocarditis and, much less frequently, an early acute myocarditis. Chagasic myocardial damage is microfocal and disseminated throughout the heart. In most cases, the coexistence of areas of myocytic degeneration, inflammatory infiltration, and fibrosis suggests a permanent evolving process. Commonly, chronic chagasic myocarditis resembles a dilated cardiomyopathy, with characteristic ECG abnormalities (atrial and ventricular extrasystoles, intraventricular and/or AV conduction disturbances, and primary ST-T wave changes). Since myocardial damage is scattered throughout the heart, the ECG abnormalities (arrhythmias, conduction disturbances, and repolarization changes) are also representative of the widespread cardiac involvement. Thus, sick sinus syndrome, atrial extrasystoles, intraatrial conduction disturbances, and atrial fibrillation or flutter are common findings in different stages of the disease. At the ventricular level, both conduction disturbances and arrhythmias are conspicuous expressions of the myocardial damage. Right bundle branch block alone or in combination with left anterior hemiblock are the most common conduction defects. Further compromise of the conduction system can lead to different degrees of AV block. Chagas' disease is the main cause of bundle branch block and AV block in endemic areas. In advanced cases of Chagas' heart disease, ventricular premature contractions are extremely frequent, multiform, and repetitive (couplets and runs of ventricular tachycardia), and show R on T phenomenon. These arrhythmias are usually aggravated by increased sympathetic tone, implying an enhanced risk of cardiac sudden death among chagasic patients, which is sometimes the first manifestation of the illness. Chronic chagasic myocarditis is the leading cause of cardiovascular death, mostly as a consequence of heart failure and sudden death, in areas where the disease is endemic.
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PMID:Cardiac arrhythmias in Chagas' heart disease. 826 25

A total of 38 patients with syncope in whom a cause was not assigned or suggested by the initial history, physical examination and electrocardiography (ECG) were studied. Twenty-four patients underwent cardiac examination with Holter ECG, electrophysiologic testing with programmed ventricular stimulation (EPS) and/or coronary arteriography including ergonovine provocation (ergonovine CAG). The study with Holter ECG, EPS and ergonovine CAG yielded a presumptive diagnosis in 36 patients (36/38 = 95%), 11 with vasopastic angina, 7 with ventricular tachycardia, 4 with ischemic heart disease, 9 with sick sinus syndrome (SSS), 1 with drug induced SSS, 3 with A-V block, 1 with supraventricular tachycardia, 1 with hypertrophic cardiomyopathy, 1 with aortic valve stenosis and 1 with carotid sinus syndrome (included are 1 patient with ventricular tachycardia+ischemic heart disease, 1 with SSS+vasopastic angina and 1 with ventricular tachycardia+vasospastic angina). Therapy based on these findings provided complete symptomatic relief in all patients during a mean follow up of 25 +/- 10 months (range 5-45 months). In conclusion, EPS and ergonovine CAG are useful in the diagnosis and therapy of unexplained syncope.
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PMID:Electrophysiologic study and ergonovine provocation of coronary spasm in unexplained syncope. 831 14

The left ventricular (LV) systolic and diastolic functions in 31 patients with sick sinus syndrome (types I and II) were analyzed using LV time activity curves obtained by a 99mTc-RBC cardiac pool scintigraphy-forward and backward multiple gated study (FBMG) and compared with those in controls. On A-V sequential pacing (rate, 70 bpm; A-V delay, 150 msec), LV-peak ejection rate (PER) and peak filling rate (PFR) were significantly decreased compared to those in normal controls. As pacing rate was increased, PFR decreased significantly in patients in whom PER was decreased. The etiology of disturbed LV systolic and diastolic functions in patients with sick sinus syndrome remains unknown. No patient had significant organic coronary artery disease or other cardiac disorder. On the other hand, the frequency of vasospastic angina was higher in this group than in the controls. We suspect that sick sinus syndrome and vasospastic angina probably share a common pathophysiology. In patients with sick sinus syndrome, LV systolic and diastolic functions are impaired at rest and during A-V sequential pacing.
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PMID:[Left ventricular hemodynamics in patients with sick sinus syndrome: analysis by 99mTc-RBC cardiac pool scintigraphy with forward and backward multiple gated method (FBMG)]. 846

A 26-year-old man underwent an electrophysiological study for evaluation of a history of congenital heart disease, presyncope, and wide complex tachycardia. During the study the patient developed sustained atrial fibrillation with a rapid ventricular response. A 17-year-old man with a history of sick sinus syndrome developed sustained atrial fibrillation. Both patients failed four attempts at external cardioversion with a maximum delivered energy of 360 J. Low energy cardioversion was successful in both patients using biphasic waveforms and internal transvenous defibrillation electrodes. Internal cardioversion using a transvenous electrode system can be successful in patients with atrial fibrillation refractory to external cardioversion.
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PMID:Internal cardioversion in two patients with atrial fibrillation refractory to external cardioversion. 873 59

The purpose of the study was to report the prevalence of inducible supraventricular tachyarrhythmias (SVTA) in 827 consecutive patients aged 17 to 90 years who did not have spontaneous documented SVTA and who had unexplained presyncope and/or syncope. The electrophysiologic study (EPS) included programmed atrial and ventricular stimulation up to two extrastimuli at three cycle lengths, and the study of sino-atrial and AV conduction. The results were as follows. EPS was normal in 386 patients. Inducible junctional tachycardia or atrial flutter and fibrillation was the only finding in 187 patients (23%). In the remaining patients we found ventricular tachycardia in 103 (12%), heart block in 67 (8%), sick sinus syndrome in 56 (7%) and increased vagal tone in 28 (3%). The presence of an underlying heart disease (47%) and salvos of atrial premature beats on Holter monitoring (39%) were significantly correlated with the induction of SVTA. However, the comparison with similar groups without syncope indicates that only the induction of SVTA in patients with hypertrophic cardiomyopathy and mitral valve prolapse was significantly correlated with the history of syncope. In patients without heart disease or with prior myocardial infarction or decreased left ventricular function, the induction of SVTA, which is not associated with hypotension in the supine position, could require an induction after head-up tilting, because of the lack of specificity of programmed stimulation in these patients. Programmed atrial stimulation should be systematically performed in patients with unexplained syncope, in particular in those with hypertropic cardiomyopathy and mitral valve prolapse, who require a specific treatment, if a SVTA is induced. In other patients the results of programmed atrial stimulation should be interpreted cautiously.
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PMID:Significance and prevalence of inducible atrial tachyarrhythmias in patients undergoing electrophysiologic study for presyncope or syncope. 877 79

Sick sinus syndrome is a rare but potentially important cardiac disorder in patients with myotonic dystrophy. We evaluated 3 patients with myotonic dystrophy complicated with sick sinus syndrome using intracardiac electrocardiography and endomyocardial biopsy. Electrocardiography identified sinus arrest, atrial flutter and right bundle-branch block in 2 cases and marked sinus bradycardia and first-degree atrioventricular block in 1 case. Their sinus node recovery times were significantly prolonged as demonstrated by the overdrive suppression test. Two patients had Adams-Stokes syndrome and one had tachycardia with severe palpitations. Therefore permanent pacemaker implantation was indicated in all 3 cases. Light microscopic analysis of right ventricular endomyocardial biopsies showed vacuolar degeneration and nuclear deformity of cardiomyocytes in all cases and endocardial and interstitial fibrosis in 1 case. These findings indicate that pathological changes may occur in any part of the myocardium in patients with myotonic dystrophy.
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PMID:Association of myotonic dystrophy and sick sinus syndrome, with special reference to electrophysiological and histological examinations. 878 50

Atrial tachycardias, in particular atrial flutter after surgery for congenital heart disease, is associated with a high mortality. Treatment with various antiarrhythmic drugs and/or antitachycardia pacemakers is not very successful. Sotalol, a Class III drug, has shown to be a promising drug in adults with atrial tachycardias. However, the experience with sotalol in children after surgery for congenital heart disease is limited. Therefore, we describe our results here. Between December 1990 and February 1997, 26 children with atrial tachycardias, most of them with atrial flutter or fibrillation (n = 20), after surgery for congenital heart disease were treated with sotalol orally. The age of the children at the start of treatment was 7.5 +/- 5.8 years (mean +/- SD). The time interval between surgery and the start of atrial tachycardia ranged from 1 day to 14.3 years (3.8 +/- 3.8 years). Conversion to sinus rhythm was achieved in 16 out of 22 hemodynamically stable children with a dosage of 4.0 +/- 1.6 mg/kg per day. The six children without sinus rhythm on sotalol and four hemodynamically unstable patients were treated prophylactically with sotalol after DC cardioversion for their tachycardias. Two children complained of mild transient fatigue. Heart rate decreased during therapy (95 +/- 33 vs 81 +/- 21 beats/min; P = 0.01). QTc-intervals did not change. Proarrhythmias such as torsades de pointes were not encountered. Two children with a preexistent sick sinus syndrome showed aggravation of bradycardia and needed pacemaker implantation. The percentage of children with a recurrence-free interval of 1 and 2 years was 96% and 81%, respectively, for all atrial tachycardias, and 92% and 66% for atrial flutter. The recurrences of atrial tachycardias during the follow-up period, which ranged from 0.1-6.1 years (2.5 +/- 1.8 years) could be treated with only an increase of the dosage of sotalol in all but one patient. We conclude that sotalol is an effective drug for the treatment and prevention of atrial tachycardia in children after surgery for congenital heart disease.
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PMID:Sotalol for atrial tachycardias after surgery for congenital heart disease. 927 23

Bradyarrhythmias are the cause of syncope in 3 to 10% of cases. Marked bradycardia or asystole can be due to impaired function of the sinus node (sick sinus syndrome), high degree AV block or neurocardiogenic disorders (carotid sinus syndrome, vasovagal syncope). A precise history, ECG and 24-h. Holter recordings are the most helpful tools in diagnosis of bradyarrhythmia-induced syncope. An association between symptoms and documented ECG is essential for proper diagnosis. Sometimes an event-recorder may be helpful for this purpose. If a patient has normal physical examination, ECG, Holter, stress test, tilt-table test and echocardiography, no further electrophysiological investigation is needed. If the noninvasive tests show pathologic results that do not clearly explain the cause of syncope (sinus bradycardia, first-degree AV block, fascicular block, structural heart disease), then electrophysiological studies are recommended, which will also rule out ventricular tachyarrythmias in the differential diagnosis. If all diagnostic tests in a patient with syncope are normal, the prognosis is fairly good despite 30% recurrence rate. Treatment for symptomatic bradyarrhythmias is implantation of a pacemaker. The selection of an appropriate pacemaker system is very important. Dual-chamber systems (DDD) provide physiological stimulation by maintaining AV synchrony; thus, they should be preferred whenever possible.
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PMID:[Bradycardia-induced syncope]. 933 79

We examined the incidence of long P wave duration in lead II and increased P terminal force in lead V1 (PTFV1), and their relationship to electrophysiological findings of atrial muscle in 34 patients with sick sinus syndrome (SSS). Patients were divided into three groups: Group I, consisting of 20 patients with various cardiac arrhythmias other than SSS and paroxysmal atrial fibrillation (PAF) who served as controls; Group II, consisting of 18 patients with SSS but without PAF; and Group III consisted of 16 patients with SSS and PAF. P wave duration was significantly longer in Group III (122 +/- 11 ms, mean +/- SD, P < 0.0001) and Group II (111 +/- 15 ms, P < 0.002) than in Group I (98 +/- 10 ms). PTFV1 was greater in Group III (0.052 +/- 0.025 ms) than in Group I (0.028 +/- 0.011 ms, P < 0.05). P wave duration and PTFV1 had significantly and/or borderline correlations with longest duration of right atrial electrograms (r = 0.84, P < 0.0001 and 0.47, P < 0.02, respectively), maximal number of fragmented deflections of atrial electrograms (r = 0.69, P < 0.0001 and r = 0.51, P < 0.02, respectively), repetitive atrial firing zone (RAFZ) (r = 0.81, P < 0.0001 and 0.48, P < 0.05, respectively) and fragmented atrial activity zone (FAAZ)(r = 0.53, P < 0.01 and r = 0.45, P = 0.06, respectively). We concluded that long P wave duration and increased PTFV1 are electrocardiographic indicators for coexistence of electrophysiological abnormalities in the atria in SSS without recognizable heart disease.
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PMID:Abnormalities of electrocardiographic P wave morphology and their relation to electrophysiological parameters of the atrium in patients with sick sinus syndrome. 947 51

A multicenter, retrospective study was undertaken to determine the prevalence of and risk factors for thromboembolism and efficacy of therapy in patients with atrial fibrillation. The primary prevention group consisted of 1,819 Japanese patients (mean age 64 years). During the mean follow-up period of 4.6 years. 158 patients developed cerebral thromboembolism or peripheral embolism (1.9%/year). The annual rate of thromboembolic complications was 0.9% for patients without underlying heart disease which was significantly lower compared with that for patients with underlying heart disease (p < 0.001). The annual rate was 1.4% among patients treated with aspirin (alone and in combination with other drugs except for warfarin), 1.4% with warfarin (alone and in combination with other drugs) and 1.1% with ticlopidine. The risk was lower for patients receiving these drugs (2.2%/year, p < 0.001). Among 801 patients not receiving treatment for thromboembolism, the annual rate was 0.9% for patients without underlying heart disease, which was significantly lower compared with patients with underlying heart diseases (e.g., 2.5% for ischemic heart disease and 2.1% for mitral valve disease, p < 0.001). Multivariate analysis using quantification method II revealed hypertension, sick sinus syndrome and left ventricular dysfunction (> or = NYHA class II) as risk factors for embolism. Although limited due to its retrospective nature, the present study suggests that the risk for embolism seems low in patients with atrial fibrillation but is not associated with underlying heart diseases or other risk factors, and antiplatelet treatment seems beneficial for these patients.
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PMID:[Atrial fibrillation and thromboembolism: a multicenter cooperative study. Research Group for Antiarrhythmic Drug Therapy]. 959 72


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