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

The majority of wide complex tachycardias are secondary to VT. The differential diagnosis of wide complex tachycardia also includes SVT with aberrancy or underlying bundle branch block and antegrade SVT conduction over an accessory pathway (antidromic SVT). VT is usually the result of reentry and most commonly arises in an area of diseased myocardium in the setting of previous myocardial infarction or cardiomyopathy. VT, however, can also occur in patients with structurally normal hearts. Criteria useful in diagnosis of wide complex tachycardia include clinical criteria (presence of structural heart disease or a history of previous myocardial infarction) and electrocardiographic criteria (the presence of capture or fusion beats, relation of atrial or ventricular activity, QRS duration and axis, and morphology). The acute management of wide complex tachycardia includes cardioversion and intravenous pharmacologic therapy. Almost all patients with VT require chronic therapy, although in rare patients treatment of acute precipitating factors may be sufficient. While pharmacologic therapy has been the mainstay of treatment for these patients, there have been many exciting advances using surgical, device, and ablative therapies.
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PMID:Wide complex tachycardias. Differential diagnosis and management. 181 68

Fetal echocardiographic examination was performed on 945 pregnant women (normal pregnancy: 291, high risk pregnancy: 654) since 1980. Of these, 39 fetuses (4.1%) were diagnosed as having cardiac arrhythmia. Fifteen fetuses had bradycardia, 7 tachycardia and 17 had an ectopic beat. These had been followed from 1 day to 8 years (mean 1 year and 6 months) soon after birth. Of the 15 cases with bradycardia (complete AV block; 8, 2:1 AV block; 3 and sinus bradycardia; 4), four resulted in an intrauterine fetal death, one was terminated and 5 died soon after birth. The remaining 5 cases are alive and 3 of these 5 have received an implanted pacemaker. Of these 15 cases with bradycardia 7 were associated with congenital heart disease, 6 of which died. Seven cases had tachycardia (supraventricular tachycardia: 3 and atrial flutter with 2:1 AV block: 3). Transplacental antiarrhythmic drug (digoxin and/or verapamil) administration was instituted in 5 cases and a conversion of the arrhythmia was achieved in 4. Paroxysmal tachycardia still remained after delivery in the other 3 cases. Two cases with supraventricular tachycardia (one of them with WPW syndrome type B) were resolved. One case has had persistent chaotic atrial rhythm for 7 years after birth. Of the 17 with an ectopic beat, 11 cases were diagnosed to have a supraventricular ectopic beat and 6 cases with a ventricular ectopic beat. A remaining arrhythmia was observed in 10 cases after delivery but all of these were resolved within 3 months after birth. Fetal tachycardia had relatively favorable prognosis because usually the intrauterine treatment was effective. However, fetal bradycardia had poor prognosis and further investigations to establish more effective treatments are essential.
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PMID:Fetal arrhythmias; intrauterine diagnosis and treatment. 184 Nov 76

The potential for proarrhythmic responses to the class IC sodium channel-blocking drugs encainide and flecainide has not been well described in young patients. Therefore, data were retrospectively collected from 36 institutions regarding 579 young patients who were administered encainide or flecainide for treatment of supraventricular tachycardias (encainide 86 patients, flecainide 369 patients) or ventricular arrhythmias (encainide 21 patients, flecainide 103 patients) to assess the frequency of proarrhythmia, cardiac arrest and death during therapy (adverse events). The two drugs were similar in regard to efficacy (flecainide 71.4%, encainide 59.8%) and rate of proarrhythmic responses (flecainide 7.4%; encainide 7.5%). However, patients receiving encainide more frequently experienced cardiac arrest (encainide 7.5% vs. flecainide 2.3%, p less than 0.05) or died during treatment (encainide 7.5% vs. flecainide 2.1%, p less than 0.05). Detailed data were provided for 44 patients experiencing one or more adverse events. Patient age, previous drug trials, concomitant therapy and days of inpatient monitoring were similar for patients receiving encainide or flecainide. However, echocardiographic left ventricular shortening before treatment was lower among patients receiving encainide (0.23 +/- 0.09) than among those receiving flecainide (0.34 +/- 0.06, p less than 0.05). Plasma drug concentrations were rarely elevated. Cardiac arrest (12 patients) and deaths (13 patients) occurred predominantly among patients with underlying heart disease, particularly among patients receiving flecainide for supraventricular tachycardia (8.3% vs. 0.3%, p less than 0.001). Fifteen patients with an ostensibly normal heart and normal ventricular function experienced proarrhythmia during treatment for supraventricular tachycardia, but only 3 of the 15 had a cardiac arrest or died. The relatively high incidence of adverse events should be considered when contemplating treatment with encainide or flecainide, particularly among patients with underlying heart disease.
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PMID:Proarrhythmia, cardiac arrest and death in young patients receiving encainide and flecainide. The Pediatric Electrophysiology Group. 190 3

The use of oral propafenone was assessed in 57 children. Mean age was 4.8 +/- 5.2 years (range 1 day to 17 years). Twenty-three patients were less than 1 year of age (40%) and 10 were less than 1 month of age (18%). Arrhythmias included supraventricular tachycardia in 32 patients (57%), atrial flutter in six (10%), and ventricular tachycardia in 19 (33%). Cardiac diagnoses included: an otherwise normal heart in 30 (53%); unoperated congenital heart defect in 11 (19%); cardiomyopathy in nine (16%); and an operated congenital heart defect in seven (12%). Mean dose of propafenone was 13.1 mg/kg/day (range 8 to 15). Success (assessed by relief of symptoms and serial 24-hour ECGs) was achieved in 16 of 32 patients with supraventricular tachycardia (50%), three of six with atrial flutter (50%), and 8 of 19 with ventricular tachycardia (42%). Drug efficacy in patients with and without organic heart disease was 30% (8 of 27) and 63% (19 of 30), respectively (p less than 0.05). Mean duration of therapy in patients in whom the drug was effective was 22.9 +/- 13.2 months (range 6 to 60). Growth was unimpaired in all patients. A neonate with nonsustained monomorphic ventricular tachycardia had sustained ventricular tachycardia during the second day of propafenone therapy at a dose of 13 mg/kg/day. Sustained ventricular tachycardia disappeared when the drug was discontinued. Another patient had an asymptomatic and transient increase in the glutamic pyruvic transaminase level. No adverse hemodynamic effects were observed. In conclusion, propafenone is an effective antiarrhythmic drug in children with normal hearts; it is less effective in patients with heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral propafenone therapy for children with arrhythmias: efficacy and adverse effects in midterm follow-up. 192 53

Emergency physicians may be called on to resuscitate acute complications in pediatric patients with congenital heart disease. Supraventricular tachycardia, with or without hemodynamic decompensation, is one of the most serious complications. We present the case of a 22-month-old boy with a history of single ventricle who presented to our institution with a history of syncope and hemodynamically stable supraventricular tachycardia. Initial attempts at pharmacologic conversion with propranolol and verapamil failed. The arrhythmia was terminated in response to an IV fluid bolus and dopamine infusion and probably resulted from a combination of anemia, hypovolemia, and impaired contractility. Appropriate evaluation and management relating to the cre of acute supraventricular tachycardia in children are discussed.
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PMID:Evaluation and management of supraventricular tachycardia in children. 198 28

In 450 cases of structural heart disease diagnosed prenatally, 38 fetuses (8.5%) had either a dysplastic or a displaced tricuspid valve. The tricuspid valve was dysplastic in 22 fetuses, all of which had evidence of tricuspid regurgitation resulting in right atrial dilation and increased cardiothoracic ratio. An associated abnormality of the pulmonary valve occurred in 16 fetuses. The remaining 16 fetuses had Ebstein's malformation, 14 with evidence of tricuspid incompetence at presentation and 10 with an associated abnormality of the pulmonary valve. Of the 38 cases, the pregnancy was interrupted in 17, spontaneous intrauterine fetal death occurred in 8, 11 infants died postnatally and 2 infants are still alive; additional abnormalities were found in 8 cases (chromosomal anomalies in 2, ventricular septal defects in 2, corrected transposition in 2, the Chiari malformation in 2, supraventricular tachycardia in 1 case and coarctation of the aorta in 1). Fetuses with severe abnormalities are selected for fetal echocardiography by the four chamber screening program and a high rate of natural loss both in intrauterine life and immediately after birth was observed in the 21 cases in which pregnancy was continued. This would explain the higher incidence of tricuspid valve disease in our prenatal compared with postnatal series. Although increased cardiothoracic ratio and associated lesions of the right ventricular outflow tract contribute to the poor outcome in the cases detected prenatally, the absence of these features does not always indicate a good prognosis because progression of disease can occur with advancing gestational age. No absolute measurement or single echocardiographic feature emerged as a consistent predictive factor of prognosis.
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PMID:Tricuspid valve dysplasia or displacement in intrauterine life. 199 32

In order to evaluate the incidence and significance of inducible supra-ventricular (SVTA) in patients with chronic myocardial infarction (MI), the results of systematic programmed atrial stimulation were compared in two groups of patients: 150 patients (group I) without MI or underlying heart disease, studied for syncope or conduction disturbances, 296 patients (group II) studied after an acute Mi (greater than 1 month). None of them had spontaneous SVTA, and 24-h Holter monitoring showed no SVTA. The atrial stimulation programme used one and two extra stimuli delivered during sinus rhythm and atrial pacing (600 ms and 10% less than the sinus cycle length). A sustained (S) (greater than 30 s) supraventricular tachycardia (SVT) (atrial flutter, fibrillation, tachycardia) was induced in 17 patients in group I (11%) and in 120 patients in group II (40.5%). In group II inducible SVTA could not be correlated with the occurrence of a SVT during acute MI, the location of MI, the value of LV ejection fraction (EF), the incidence of inducible sustained ventricular tachycardia (VT), or fibrillation (VF). However, inducible SVTA could be correlated with a significantly shorter effective atrial refractory period (197 +/- 23 ms vs 220 +/- 35 ms, P less than 0.001) and a shorter retrograde block cycle length (518 +/- 215 vs 585 +/- 215 ms, P less than 0.03). The patients in group II were followed-up for at least 6 months; 12 of them developed sustained episodes of supraventricular tachycardia; 11 of them had inducible SVTA (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incidence and significance of inducible supraventricular tachyarrhythmias in patients with chronic myocardial infarction. 204 Mar 23

Ventricular fibrillation (VF) is a well-known but rare complication of the Wolff-Parkinson-White syndrome (WPW). Clinical and electrophysiological data of 23 patients with spontaneous VF were compared with data from 100 consecutive patients with WPW without VF but with symptomatic supraventricular tachycardia. The 23 patients were collected in a multicentre retrospective study in seven European centres. VF occurred in only one patient who was receiving antiarrhythmic drugs, and was the first manifestation of the syndrome in six. No significant differences were found between those with VF and without VF in age, complaints of palpitations, syncope, and presence of structural heart disease. The retrograde effective refractory period of the accessory pathway, the atrial refractory period and the fastest atrial pacing rate with 1:1 anterograde conduction over the accessory pathway were similar in both groups. Significant differences were found for sex, permanent pre-excitation on the electrocardiogram, type of documented supraventricular tachyarrhythmias, shortest RR interval less than or equal to 220 ms during spontaneous atrial fibrillation (AF), inducibility of supraventricular tachycardias, ventricular effective refractory period less than or equal to 190 ms, mean shortest RR interval during induced AF less than or equal to 180 ms and presence of multiple accessory pathways.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventricular fibrillation in the Wolff-Parkinson-White syndrome. 204 47

The authors report a case of fetal supraventricular tachycardia with the heart rate of 400/min diagnosed in the 34th week of pregnancy. Congestive heart failure forming non immun hydrops fetalis was occurred by this rhythm disturbance. With digitalis and beta receptor blocker propranolol therapy administered to the mother the rhythm disturbance has stopped, ascites and hydrothorax secondary to fetal congestive heart failure have been abolished. Congenital heart disease and cardiomyopathy were excluded by fetal echocardiography. In the 40th week a healthy newborn was delivered by cesarean section and after delivery congenital heart disease, rhythm disorder, infection or metabolic disturbance couldn't be verified. The authors reviewing the literature demonstrate the suggested investigating procedures and the possibilities of therapy in the case of fetal supraventricular tachycardia.
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PMID:[Intrauterine treatment of fetal tachycardia causing circulatory failure]. 218 48

These findings permit the following conclusions on cardiac changes induced by high-performance sports and high levels of training. Sinus bradycardia and AV block can frequently be observed in athletes, but they do not require attention as long as they are asymptomatic or do not produce pauses exceeding 4 seconds. Persistent rather than transient second-degree AV block or Mobitz second- or third-degree AV block is an extremely unusual finding even in athletes and should be considered a sign of organic lesions until proved otherwise. Supraventricular and AV node ectopic beats are not more frequent in athletes than in the general population except for atrial fibrillation. WPW syndrome is of particular importance, since rapid conduction to the ventricle via the accessory AV pathway is possible, especially if there is a tendency toward atrial fibrillation. Likewise caution is required in athletes with hypertrophic cardiomyopathy. Here hemodynamic deterioration must be anticipated with the occurrence of supraventricular tachycardia. Simple ventricular arrhythmias occur among athletes with the same frequency as in the general population, but they usually disappear with exercise. The occurrence of complex ventricular forms of arrhythmia should always prompt cardiologic examination in search of underlying cardiac disease, particularly hypertrophic or dilated cardiomyopathy. The presence of ventricular arrhythmias without evidence of underlying heart disease does not indicate a special or increased risk of sudden cardiac death. A higher incidence of right and/or left ventricular hypertrophy, exercise-reversible ST elevation, and exercise-reversible changes in T waves (T negativity, sharp and/or excessive T waves) can be considered physiologic changes in the ECGs of athletes. These changes correlate closely with the type of sports activity and degree of training and are reversible when the activity is stopped. Horizontal ST segment depression are by contrast very rare in athletes and should always be clarified by cardiologic examination. Exercise-induced sudden cardiac death in athletes is unusual without preexisting heart disease. The cause of sudden cardiac death among athletes less than 40 years of age can be predominantely ascribed to congenital heart diseases (such as hypertrophic cardiomyopathy or coronary anomalies). In athletes more than 40 years of age and with increasing age, coronary heart disease is the most frequent autopsy finding. A corresponding risk stratification should take these partial dangers into account.
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PMID:ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. 219 78


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