Postfibrillatory enhancement of left atrial contractility after short paroxysms of atrial fibrillation

Implantable cardioverter defibrillators and pacemakers detect an increasing number of silent episodes of AF. In a porcine model, the study evaluated the contractility of the left atrial appendage (LAA) during, AF paroxysms as they may occur in patients. Peak outflow velocity of the LA and mean outflow velocity of the LAA (LAA-V (outmean)) (n = 17) were measured before, during, and after induction of self-terminating AF. LAA-V (outmean) was also measured during incremental pacing from different atrial sites using epicardial Doppler probes (n = 6) and during continuous recordings (n = 5) of 40 minutes of pacing maintained AF Compared to baseline sinus rhythm, LAA-V (outmean) increased during short AF episodes (41 +/- 3 vs 35 +/- 2 cm/s, P < 0.05). After termination of the AF episodes, LAA-V (outmean) further increased (69 +/- 15 cm/s, P < 0.001 vs baseline). This "postfibrillatory enhancement" maintained after repeated induction of short AF paroxysms. During prolonged AF episodes lasting 40 minutes, an initial hypercontractility (44 +/- 2 vs 38 cm/s, P < 0.01) was followed by a hypocontractility after 20 minutes (29 +/- 12 P < 0.05 vs SR) and a postfibrillatory enhancement after cessation of AF (56 +/- 12 vs 27 +/- 9 cm/s at 40 minutes AF, P < 0.001). L-type Ca channel blockade abolished the initial hypercontractility during AF and the postfibrillatory enhancement. Repetitive AF paroxysms up to 2 minutes did not decrease left atrial contractility During maintained AF up to 40 minutes an initial hypercontractility and a consecutive hypocontractility, which is overcompensated by a postfibrillatory enhancement of atrial inotropy after cessation of AF, are present. The observed phenomenon seems to be related to on increased Ca2+ influx through the L-type Ca2+ channel.