Key result
In a porcine model, short episodes of atrial fibrillation increased left atrial appendage mean outflow velocity compared to baseline (41 vs 35 cm/s, P<0.05), with further enhancement after termination.
Why the study?
Do short paroxysms of atrial fibrillation alter left atrial appendage contractility in a porcine model?
Do short paroxysms of atrial fibrillation alter left atrial appendage contractility in a porcine model?
Short paroxysms of atrial fibrillation induce a postfibrillatory enhancement of left atrial appendage contractility, likely mediated by increased calcium influx through L-type calcium channels.
Answers are grounded in this paper and cite their sources.
Animal data indicate post-AF LAA flow enhancement; hypothesis-generating and should not alter clinical practice.
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 an increased Ca(2+) influx through the L-type Ca(2+) channel.
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Zarse et al. (2004) studied Atrial Fibrillation (n=28). Induced atrial fibrillation vs. Baseline sinus rhythm was evaluated on Mean outflow velocity of the left atrial appendage (LAA-V(outmean)) (p=<0.05). In a porcine model, short episodes of atrial fibrillation increased left atrial appendage mean outflow velocity compared to baseline (41 vs 35 cm/s, P<0.05), with further enhancement after termination.
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