Double-blind study of intravenous propafenone for paroxysmal supraventricular reentrant tachycardia.

Propafenone was administered during electrophysiologic testing to determine its efficacy and safety for terminating and preventing reinduction of paroxysmal supraventricular reentrant tachycardia. Four men and 10 women (mean age 50 years, range 28 to 69) were studied. Five patients had Wolff-Parkinson-White syndrome with orthodromic atrioventricular (AV) reentrant tachycardia, three had a concealed accessory pathway with AV reentrant tachycardia and six had tachycardia due to reentry within the AV node. In the five patients with Wolff-Parkinson-White syndrome, propafenone terminated reentrant tachycardia in three (the tachycardia was reinducible in one) and had no effect in two. In the three patients with a concealed accessory pathway, propafenone terminated reentrant tachycardia in all three and prevented reinduction of the tachycardia in two. In the six patients with tachycardia due to reentry within the AV node, propafenone terminated and prevented reinduction of reentrant tachycardia. Propafenone had no effect on blood pressure, heart rate, PA interval, AV node refractoriness or rate of reentrant tachycardia. Propafenone significantly (p less than 0.05) prolonged the AH, HV, QRS and ventriculoatrial intervals and decreased the AV node Wenckebach rate. Of the nine patients receiving long-term oral propafenone therapy, eight had a reduction of at least 90% in reentrant tachycardia during a mean follow-up period of 14.5 months (range 11 to 22); all eight patients had had noninducible reentrant tachycardia after intravenous propafenone. One patient had increased frequency of reentrant tachycardia; this patient had had inducible reentrant tachycardia after intravenous propafenone. In conclusion, intravenously administered propafenone terminated reentrant tachycardia in 85% of patients and prevented reinduction in 71%, with no adverse hemodynamic effects.

Cardiac histologic findings in patients with life-threatening ventricular arrhythmias of unknown origin.

Percutaneous endomyocardial biopsy (right ventricle in 10, left ventricle in 2) was performed in 12 patients, aged 9 to 57 years, with serious ventricular arrhythmias occurring in the setting of normal cardiac anatomy and mechanical function. Light microscopic examination of tissue revealed histologic abnormalities in 11 patients, including myocardial cellular hypertrophy in 7, interstitial fibrosis in 5, endocardial fibrosis in 2, myocardial degenerative changes in 1 and increased interstitial cellularity in 1. One patient had histologic evidence of acute lymphocytic myocarditis. Thus, a majority of patients with serious ventricular arrhythmias and normal cardiac anatomy had histologic abnormalities, bringing into question the concept of primary electrical heart disease or idiopathic ventricular tachycardia.

Electrophysiologic testing in the upright position: improved evaluation of patients with rhythm disturbances using a tilt table.

Patients are traditionally evaluated in the supine position in the electrophysiology laboratory, although symptoms due to a cardiac rhythm disturbance are often maximal clinically during standing. The assumption of the upright position results in dependent displacement of blood, followed by prompt vasoconstriction to maintain arterial pressure. This normal response may aggravate tachyarrhythmias by increasing catecholamine levels or may precipitate vasodepressor syncope if the vasoconstrictor response is absent. The use of a tilt table during electrophysiologic testing was evaluated over a 12 month period in 104 patients having a mean age of 60 years (range 37 to 81): 59 with supraventricular tachycardia, 6 with vasovagal syncope and 39 with carotid sinus hypersensitivity. Twenty-three patients (22%) had significant abnormalities when upright that were not present when supine: eight patients with supraventricular tachycardia who had their clinical syndromes of palpitation and syncope reproduced when upright, but only minimal symptoms when supine; two patients with supraventricular tachycardia who had sustained atrioventricular reentry when upright, but only two to eight beats of tachycardia when supine; six patients with syncope and a normal cardiac evaluation before electrophysiologic testing who had their typical spells only after being placed upright during a vasovagal event and seven patients with carotid sinus hypersensitivity who had their clinical syndromes reproduced with carotid sinus massage only when upright, developing hypotension despite maintaining their heart rate with sinus rhythm or pacing (vasodepressor response). In 22% of patients, electrophysiologic testing in the upright position provided clinically important information that was not evident during standard testing in the supine position.

Surgical treatment of accessory atrioventricular pathways and symptomatic tachycardia in children and young adults.

Twenty-seven patients aged 21 years or younger (mean 15) with symptomatic tachycardia underwent operation for ablation of an accessory atrioventricular pathway. Six patients had associated Ebstein's malformation of the tricuspid valve. Supraventricular tachycardia had been present for a mean of 5 years. At electrophysiologic study, 4 patients were found to have 2 accessory pathways. Left ventricular free wall pathways were found in 14 patients, right ventricular free wall pathways in 10 and septal pathways in 6. Successful initial ablation of all the pathways was achieved in 26 of the 27 patients. No patient died perioperatively and none had persistent complete heart block. During a mean follow-up of 11 months, no patient had recurrence of an arrhythmia related to the accessory pathway. Thus, the surgical treatment of children and young adults with accessory atrioventricular pathways and symptomatic supraventricular tachycardia is safe and effective. For these patients, unless the tachycardia can be easily controlled with a minimal number of drugs and adverse effects, surgical ablation should be considered early in the clinical course.

Refractory supraventricular tachycardia in the neonate: treatment with temporary antitachycardial pacing.

Although intracardiac antitachycardial pacing techniques are frequently used to terminate reentrant supraventricular tachycardia in adults, this approach has rarely been used in neonates. We describe two neonates, both of whom were in circulatory shock due to recurrent paroxysmal supraventricular tachycardia, who were treated with temporary antiatachycardial pacing. This approach allows repeated termination of the tachycardia at the bedside until an adequate therapeutic concentration of an effective drug regimen is achieved and obviates repeated direct-current cardioversion.

Severe hyperkalaemia with Moduretic.

Three patients with impaired renal function suffered complications of hyperkalaemia within 10 days of beginning therapy with hydrochlorothiazide and amiloride combination (Moduretic). The possible relationship between hyperkalaemia and this diuretic is discussed.

Oral tocainide versus disopyramide: a double-blind, randomized, crossover study of outpatients with stable ventricular premature beats.

Oral tocainide and disopyramide were compared in a double-blind, crossover trial in 10 outpatients with stable ventricular premature beats (VPBs). Efficacy was assessed by suppression of VPB activity and reduction of VPB grade during an exercise test and an 18-h Holter recording. An estimate of variance of VPB activity was obtained from two separate placebo periods, and a 95% confidence limit for VPB suppression was calculated. During Holter recording, both drugs produced a significant reduction in VPB frequency and grade (p less than 0.05). During the exercise challenge, tocainide produced a reduction in VPB frequency and grade, but this did not reach statistical significance; VPB frequency was unaltered by disopyramide, but VPB grade was significantly reduced (p less than 0.01).

Congestive cardiomyopathy and haemochromatosis--rapid progression possibly accelerated by excessive ingestion of ascorbic acid.

We describe rapidly fatal cardiomyopathy in a young man. He had for twelve months ingested large amounts of ascorbic acid and was admitted with severe heart failure having been symptomatic for two months. He died after eight days. Idiopathic haemochromatosis was diagnosed at autopsy. The clinical and laboratory features are discussed and the possible implications of ascorbic acid ingestion are explored.

Tachycardia induced myocardial dysfunction. A reversible phenomenon?

Four patients with myocardial dysfunction related to tachycardia underwent electrophysiological studies, which showed a re-entrant supraventricular tachycardia using an accessory atrioventricular connexion. Serial assessment of left ventricular function by echocardiography before and after control of the tachycardia indicated a variable degree of reversibility. Endomyocardial biopsy in two patients detected non-specific histological changes. Because of the possible role of ischaemia in this condition effective control of prolonged tachycardia is needed to prevent deterioration of myocardial function.

Out-of-hospital cardiac arrest in patients without clinically significant coronary artery disease: comparison of clinical, electrophysiological, and survival characteristics with those in similar patients who have clinically significant coronary artery disease.

Fifty nine survivors of out-of-hospital cardiac arrest unassociated with an acute myocardial infarction were referred for intracardiac electrophysiological study. Thirty patients who had no clinically significant coronary artery disease (group 1) were compared with 29 who did (group 2). Ventricular tachycardia or fibrillation was induced in significantly more patients in group 2 than in group 1 (69% vs 40%). Median duration of follow up, which was achieved in all patients, was 31 months in group 1 and 14 months in group 2. In group 1, an effective treatment was identified electrophysiologically in seven patients, and none died; an arrhythmia was induced, but no effective treatment was identified in five patients, and one patient died subsequently; an arrhythmia was not induced in 18 patients, 15 of whom were treated empirically with anti-arrhythmic drugs, and one died. In group 2, effective treatment was identified electrophysiologically in seven patients and three died (two of pump failure) during follow up. In 13 an arrhythmia was induced but no effective drug was identified, and six died or had a recurrence; in another nine patients without inducible arrhythmias, six subsequently died or had a recurrence. A Cox proportional hazards analysis identified previous myocardial infarction as the only predictor of recurrence. Patients without coronary artery disease who suffer an out-of-hospital cardiac arrest have a low inducibility rate at electrophysiological study and an excellent prognosis compared with patients who have coronary artery disease. Electrophysiological testing seemed to be of value in predicting the response to antiarrhythmic drugs, but non-inducibility of arrhythmias in patients with coronary artery disease was of no predictive value.

Increased vagal tone as an isolated finding in patients undergoing electrophysiological testing for recurrent syncope: response to long term anticholinergic agents.

Features suggestive of an isolated increase in vagal tone during electrophysiological study were found in 12 patients with recurrent near syncope or syncope. Results at neurological and cardiac evaluation were otherwise normal. The increased tone or heightened sensitivity to vagal tone was manifested by abnormal atrioventricular nodal refractoriness and conduction that were reversed with atropine. The patients underwent long term treatment with an anticholinergic agent (propantheline bromide) and 75% improved. Before treatment they had experienced a median of seven episodes (range 3-28) of near syncope or syncope during 10.5 months (range 1-60). During treatment these episodes decreased to a median of one (range 0-15) during 22.5 months (range 3-67); six patients experienced no further symptoms. Three patients continued to have syncope while on treatment, and one of these required permanent cardiac pacing. No additional cause for syncope was identified in any patient. During electrophysiological assessment of patients with syncope, evidence may be obtained pointing to an increase in vagal tone. In many of these patients treatment with anticholinergic drugs seemed to improve or eliminate the symptoms.