The Journal of Thoracic and Cardiovascular Surgery, Vol 94, 904-910, Copyright © 1987 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Myocardial protective effects of the class Ic antiarrhythmic agent flecainide
LA Brunsting, ME Jessen, AS Abd-Elfattah, WK Mask, CK Godwin and AS Wechsler
Department of Surgery, Duke University Medical Center, Durham, NC 27710.
The class Ic antiarrhythmic agent flecainide has recently become available
in this country for management of ventricular arrhythmias. The
pharmacologic and electrophysiologic features of this class of drug-
-marked sodium channel blockade producing inhibition of phase 0 of the
myocardial action potential, moderate blockade of slow inward (calcium)
channels, and general lack of systemic toxicity--suggest that these agents
may exert significant myocardial protective effects. This hypothesis was
tested in isolated, perfused rat hearts subjected to 30 minutes of global
normothermic ischemia followed by 30 minutes of reperfusion after
pretreatment with (1) Krebs-Henseleit buffer (n = 7); (2) Krebs-Henseleit
buffer with potassium adjusted to 20.9 mmol/L with potassium chloride (n =
10); and (3) Krebs-Henseleit buffer plus flecainide acetate 50 mg/L (0.12
mmol/L) (n = 11). Severity of ischemic injury was assessed by time to
ischemic contracture: 9.9 +/- 1.3 (Krebs- Henseleit buffer), 18.4 +/- 1.1
(potassium chloride), and 25.4 +/- 1.0 (flecainide) minutes (mean +/-
standard error of the mean) (p less than 0.05 among all groups). Functional
recovery after ischemia and reperfusion was measured by developed pressure
(expressed as percent of preischemic control): 19.6 +/- 5.4
(Krebs-Henseleit buffer), 70.8 +/- 3.2 (potassium chloride), and 67.3 +/-
2.7 (flecainide). These results suggest that class Ic agents afford
significant myocardial protection from global normothermic ischemia.
