Why the study?
Does procainamide alter the excitable gap composition in patients with common atrial flutter?
Does procainamide alter the excitable gap composition in patients with common atrial flutter?
Procainamide prolongs atrial flutter cycle length and excitable gap duration but fails to eliminate fully excitable tissue at the wavefront head, which may explain its inefficacy in acutely terminating common atrial flutter.
Answers are grounded in this paper and cite their sources.
Does not support excitable gap proportion change as termination mechanism; leaves open procainamide efficacy in common atrial flutter from case data.
The composition of the excitable gap (EG) in common atrial flutter (AF1) was determined before and during infusion of procainamide (PA) in 9 patients (6 men and 3 women; age 70 +/- 7 years). The EG was determined by introducing a premature stimulus after every 20th AF1 complex detected using a quadripolar electrode catheter placed just above the tricuspid valve. Diastole was scanned in 2- to 4-ms decrements to the atrial effective refractory period (ERP). The relationship between the coupling interval and the return cycle length (CL) determined a reset-response curve (RRC), which described the EG. PA (15 mg/kg) was administered during AF1 over 30 minutes and RRC was repeated at maximum AF1 CL. PA prolonged AF1 CL from 227 +/- 29 to 296 +/- 62 ms (P < 0.01) but did not terminate AF1. ERP during AF1 prolonged from 169 +/- 24 to 219 +/- 41 ms (P < 0.01). Control EG was 57 +/- 16 ms or 25% +/- 6% of AF1 CL and on PA EG was 77 +/- 30 ms (P = 0.01), which was still 26% +/- 7% of the CL. Without drug, RRC was mixed in eight cases demonstrating an EG composed of fully excitable tissue (10 +/- 4 ms or 19% +/- 10% of the EG) and partially refractory tissue (48 +/- 18 ms). PA did not change the duration of the fully excitable region (13 +/- 10 ms or 19% +/- 15% of EG). Peak PA plasma concentration was 47 +/- 20 mumol/L. PA prolonged AF1 CL, ERP, and EG duration but did not change the proportion of AF1 CL occupied by the EG. The persistance of fully excitable tissue at the head of the wavefront in the presence of PA may largely explain its inefficacy in the acute termination of common AF1.
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Jalil et al. (1998) studied this question.
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