Blood Coagulation After Cardioversion of Atrial Fibrillation

ABSTRACT & COMMENTARY

Synopsis: A more agressive strategy of early anticoagulation may be appropriate in patients undergoing cardioversion.

Source: Oltrona L, et al. Circulation 1997;95:2003-2006.

Oltrona and colleagues investigated changes in coagulation parameters that occur coincident with pharmacologic conversion of short duration atrial fibrillation. They identified 23 patients with atrial fibrillation of less than 48-hour duration who were candidates for pharmacologic cardioversion. Venous plasma samples were drawn at entry, at the time of conversion to sinus rhythm, and after one month for measurement of two markers of thrombin generation and activity—thrombin-antithrombin complex (TAT) and fibrinopeptide A (FPA). Patients received either amiodarone, flecainide, or propafenone intravenously for cardioversion. Eighteen patients converted within 24 hours of drug administration and three within the next 48 hours. Median plasma TAT levels increased from 2.8 ng/mL to 3.5 ng/mL after conversion and returned to 2.5 ng/mL after one month.

When compared to TAT levels in normal blood donors without atrial fibrillation, patient TAT levels were abnormal in 24% at baseline, 43% after conversion, and in 10% at one month. Median FPA levels showed a similar pattern. They increased from 1.1 ng/mL at baseline to 1.8 ng/mL after cardioversion and fell to 0.8 ng/mL one month later. Abnormal values were noted in 10% at baseline, 18% after cardioversion, and in only 5% after one month. Oltrona et al conclude that there is a significant increase in plasma markers for thrombin generation after pharmacologic cardioversion of acute atrial fibrillation that suggests induction of a hypercoaguable state.

COMMENT BY JOHN DiMARCO, MD, PhD

In recent years, increasing emphasis has been placed on the role of atrial fibrillation as a causal factor in stroke and systemic embolism. Current guidelines recommend 3-4 weeks of warfarin anticoagulation prior to elective cardioversion of atrial fibrillation of more than 48 hours duration but do not recommend anticoagulation for episodes of less than 48 hours. Recent studies using transesophageal echocardiography have raised the possibility that a number of processes leading to clot formation begin very early after the onset of atrial fibrillation. It is also well known that after cardioversion, recovery of atrial contractility may be delayed, and this phenomena also contributes to the thrombogenic risk of cardioversion. In this paper, Oltrona et al show that almost 50% of patients with recent onset atrial fibrillation will show activation of two markers of thrombogenesis, early after pharmacologic cardioversion. These data suggest that an even more aggressive strategy of early anticoagulation may be appropriate in patients undergoing cardioversion. If a patient is to be hospitalized either to await electrical cardioversion or for a pharmacologic attempt at conversion, heparin therapy would seem reasonable. Since recovery of atrial function in short duration atrial fibrillation occurs relatively rapidly, continuation of long-term anticoagulation should probably not be necessary.