Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entrainment of the tachycardia

To test the hypothesis that an area of slow conduction is present during reentrant ventricular tachycardia in man, and that the earliest activation site during ventricular tachycardia is within or orthodromically just distal to the area of slow conduction in the reentry loop, we studied 12 episodes of ventricular tachycardia (mean rate 185 +/- 32 beats/min) that were induced in nine patients with ischemic heart disease. Rapid ventricular pacing was performed at selected sites during ventricular tachycardia while recording electrograms from an early activation site relative to the onset of the QRS complex (site A) and from a site close to the pacing site (site B). Rapid pacing from the right ventricular apex during ventricular tachycardia with a right bundle branch block pattern and from selected left ventricular sites during ventricular tachycardia with a left bundle branch block pattern (mean pacing rate 202 +/- 38 beats/min) resulted in constant ventricular fusion beats on the electrocardiogram except for the last captured beat (i.e., the ventricular tachycardia was entrained) in 11 of 12 episodes. During entrainment: sites A and B were activated at the pacing rate, conduction time from the last pacing impulse to the last captured ventricular electrogram at site A (St-A interval) was 359 +/- 69 msec and spanned the diastolic interval, while that at site B (St-B interval) was only 28 +/- 13 msec, site A had the same ventricular electrogram morphology as that during ventricular tachycardia, while site B had a different electrogram morphology, indicating that site A was activated in the same direction during entrainment as during ventricular tachycardia. Eight episodes of ventricular tachycardia were entrained at two or more different pacing rates. The St-A interval increased during pacing at the faster rate(s) in four of eight episodes, while the St-B interval remained unchanged. Rapid ventricular pacing performed from the same site during sinus rhythm (mean pacing rate 201 +/- 37 beats/min) resulted in an St-A interval of 103 +/- 37 msec (p less than .001 vs the value during entrainment) and an St-B interval of 31 +/- 15 msec (p = NS vs the value during entrainment). It is concluded that an area of slow conduction not demonstrable during sinus rhythm exists during ventricular tachycardia, and that the earliest activation site during ventricular tachycardia is at or orthodromically distal to this area of slow conduction.     

Electrophysiological delineation of the specialized A-V conduction system in patients with corrected transposition of the great vessels and ventricular septal defect.

The specialized atrioventricular (A-V) conduction system was electrophysiologically delineated during open-heart surgery in four patients with congenitally corrected transposition of the great vessels and associated ventricular septal defect and one patient with single ventricle. Two consistent observations were made: 1) In no case was the specialized A-V conduction system found in the right atrium, whether or not there was a coronary sinus ostium present. 2) Specialized A-V conduction system electrograms were never delineated posterior to the ventricular septal defect, in contradistinction to this usual location in hearts having ventricular septal defects associated with other congenital lesions. In three of five patients, the initial course of the A-V conduction system of the ventricles was delineated between the anterior aspect of the ventricular septal defect and the pulmonary artery. In one patient the proximal portion of the A-V conduction system was delineated on the anterior aspect of the pulmonary conus. The course and extent of the A-V conduction system delineated in the morphological left ventricle suggests it is a left bundle branch. The surgical implications of the ectopic location of the A-V conduction system anterior to the ventricular septal defect, and the variability of the more proximal portion of the A-V conduction system are discussed.     

Flecainide acetate prevents recurrence of symptomatic paroxysmal supraventricular tachycardia. The Flecainide Supraventricular Tachycardia Study Group

Oral flecainide acetate was administered to 34 patients with documented symptomatic paroxysmal supraventricular tachycardia (PSVT) with a double-blind, placebo-controlled, 8-week crossover trial design. PSVT was defined as a regular tachycardia of at least 120 beats/min without evidence of atrioventricular dissociation. The study required considerable patient cooperation. Patients first entered a 4-week qualifying phase followed by a 3-week, open label, flecainide dose-ranging phase. They were then randomized in a blind fashion to receive either placebo or tolerated flecainide dose for an 8-week treatment period and then crossed over after four symptomatic documented episodes of PSVT or at the end of the treatment period. By all efficacy parameters analyzed, flecainide was superior to placebo. Flecainide was associated with an actuarial 79% freedom from symptomatic PSVT events compared with only 15% on placebo at 60 days (p less than 0.001). Of the 34 patients, 29 had recurrence of symptomatic PSVT at least once during the placebo phase; only eight patients had a recurrence during the flecainide phase (p less than 0.001). The median time to the first symptomatic PSVT event was 11 days in the placebo group and greater than 55 days in the flecainide group (p less than 0.001). Likewise, the interval between attacks was a median of 12 days on placebo compared with more than 55 days on flecainide (p less than 0.001). Finally, the flecainide slowed symptomatic PSVT heart rates to 143 +/- 12 beats/min from 178 +/- 12 on placebo (p less than 0.02) in the seven patients who had events in the placebo and flecainide treatment phases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Termination of a tachyarrhythmia by flunarizine is not a specific marker for a triggered mechanism

BACKGROUND: Prior studies have indicated that tachyarrhythmia termination by flunarizine demonstrates a triggered mechanism. This concept was not confirmed in atrial tachyarrhythmias. OBJECTIVE: The purpose of this study was to test the hypothesis that flunarizine will not terminate reentrant atrial flutter (AFL). METHODS: We administered flunarizine (2 mg/kg intravenously over 2 minutes) in 11 episodes of reproducibly inducible, sustained AFL in eight canines with sterile pericarditis. If flunarizine terminated AFL, we studied AFL reinducibility. We also studied pacing thresholds, refractoriness, and intra-atrial conduction time during closed-chest studies and pacing at selected cycle lengths (CLs) from selected sites before and after flunarizine administration. Atrial mapping (510 electrodes) assessed the epicardial activation sequence during AFL and its termination in six episodes. Four AFL episodes were studied in the closed-chest state. RESULTS: Flunarizine increased AFL CL in all episodes (mean 21 ms; range 7-49 ms), which is explained by slowing conduction in the AFL reentrant circuit, principally in the area of slow conduction. AFL was terminated in 10/11 episodes after drug initiation (mean 3.7 minutes; range 0.5-6.5 minutes) by block in the area of slow conduction. AFL was then not immediately reinducible until >20 minutes after drug administration. Flunarizine had no meaningful effect on atrial pacing thresholds for capture or refractoriness and only affected conduction time in the area of slow conduction in the reentrant circuit. CONCLUSIONS: Flunarizine (1) causes progressive slowing and block in the area of slow conduction of the AFL reentrant circuit in the canine sterile pericarditis model and (2) is effective in terminating reentrant AFL and so is not a specific marker for a triggered mechanism.     

A perspective on ventricular arrhythmias: patient assessment for therapy and outcome

Clinical management of patients with ventricular arrhythmias continues to evolve. It is generally accepted that patients with sustained ventricular tachyarrhythmias (ventricular tachycardia [VT] or fibrillation) require treatment. It is also generally accepted that patients with frequent or complex ventricular ectopy or nonsustained VT, in the absence of underlying heart disease, do not require treatment unless relief of symptoms is warranted. Whether patients with frequent or complex ventricular ectopy or nonsustained VT require treatment in the presence of underlying organic heart disease remains uncertain. The concern is that these ventricular arrhythmias may be a precursor for sustained, potentially life-threatening ventricular tachyarrhythmias. Available data suggest that patients with underlying heart disease, particularly coronary artery disease and a previous myocardial infarction, who manifest frequent or complex ventricular ectopy or nonsustained VT are at increased risk for sudden cardiac death. However, no studies have shown that treatment of these arrhythmias will affect outcome. Data are accumulating to suggest that use of the principles of risk stratification permits identification of patients at very high risk for developing sustained ventricular tachyarrhythmias. Carefully designed clinical trials are required before one can provide firm guidelines for the management of these patients. Nevertheless, when several risk factors for sudden cardiac death (e.g., abnormal ejection fraction, a late potential on a signal-averaged electrocardiogram, and frequent or complex ventricular ectopy or nonsustained VT) are present in a patient, especially after a recent myocardial infarction, invasive electrophysiologic testing may help identify those who need treatment (sustained VT is inducible) and those who do not (no sustained VT is inducible).     

Hospitalized patients with atrial fibrillation and a high risk of stroke are not being provided with adequate anticoagulation.

OBJECTIVES: The purpose of this study was to determine both treatment gaps and predictors of warfarin use in atrial fibrillation (AF) patients enrolled in a national multicenter study. BACKGROUND: The National Anticoagulation Benchmark Outcomes Report (NABOR) is a performance improvement program designed to benchmark anticoagulation prophylaxis, treatment, and outcomes among participating hospitals. METHODS: A retrospective cohort study of inpatients was performed at 21 teaching, 13 community, and 4 Veterans Administration hospitals in the U.S. Patients with an ICD-9-CM code for AF (427.31) were randomly selected. RESULTS: Among the 945 patients studied, the mean age was 71.5 (+/- 13.5) years; 43% were >75 years of age, 54.5% were men, and 67% had a history of hypertension. Most (86%) had factors that stratified them as at high risk of stroke, and only 55% of those received warfarin. Neither warfarin nor aspirin were prescribed in 21% of high-risk patients, including 18% of those with a previous stroke, transient ischemic attack, or systemic embolic event. Age >80 years (p = 0.008) and perceived bleeding risk (p = 0.022) were negative predictors of warfarin use. Persistent/permanent AF (p < 0.001) and history of stroke, transient ischemic attack, or systemic embolus (p = 0.014) were positive predictors of warfarin use, whereas high-risk stratification was not. CONCLUSIONS: This study confirms the under-use of warfarin, but also adds to published reports in several regards. It showed that risk stratification, the guidepost for treatment in international guidelines, had little effect on warfarin use, and that age >80 years and AF classification (permanent/persistent) are factors that influence warfarin use.