Key result
An acute increase in right atrial pressure from 2 to 10 cm H2O significantly increased atrial fibrillation inducibility in sham rats (5% to 50%, P<0.01) but not in LVH rats with chronic atrial dilation (20% to 25%, NS).
Why the study?
Does an acute increase in atrial pressure increase the inducibility of AF in diseased rat hearts with chronic atrial dilation compared to normal hearts?
Does an acute increase in atrial pressure increase the inducibility of AF in diseased rat hearts with chronic atrial dilation compared to normal hearts?
Absolute Event Rate: 25% vs 50%
In a rat model, chronic atrial dilation prevents the increased inducibility of AF caused by acute atrial pressure elevation, suggesting a role for electrophysiological remodeling in compensated states.
Acute pressure rise may not heighten AF inducibility in chronically dilated atria; hypothesis-generating in rats and leaves human relevance open.
Although acute atrial dilation facilitates the induction of atrial fibrillation (AF) in the normal heart, little is known about whether the induction of AF due to acute atrial dilation increases in the diseased heart. To clarify this, we compared the inducibility of AF by an acute increase of atrial pressure with and without chronic atrial dilation induced by volume- and pressure-overload in rats. Eight weeks after creating abdominal aortocaval shunt and aortic constriction rats (LVH rats, n = 8) or sham rats (n = 8), the hearts were perfused in Langendorff's manner. Right atrial (RA) pressure was increased from 2 cm H(2)O to 10 cm H(2)O by the height of the reservoir. Inducibility of AF was evaluated by 5 times burst pacing from the right atrium, and mean cycle length of AF (CL) and the atrial effective refractory period (AERP) were also measured. The inducibility of AF increased from 5 ± 3% at 2 cm H(2)O to 50 ± 5% at 10 cm H(2)O RA pressure in sham rats (P < 0.01), but not in LVH rats (20 ± 7% to 25 ± 6%, NS). Mean CL and AERP in LVH rats were longer than those in sham rats. In addition, the AERP decreased with an increase in RA pressure from 2 cm H(2)O to 10 cm H(2)O in sham rats, but not in LVH rats. The inducibility of AF caused by an acute increase of RA pressure did not increase in the diseased heart, suggesting that electrophysiological remodeling may play a role, at least in a compensated state, for the prevention of AF due to an acute increase of atrial pressure.
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Suzuki et al. (2012) studied Chronic atrial dilation / Left ventricular hypertrophy (n=16). Left ventricular hypertrophy (LVH) induced by volume- and pressure-overload vs. Sham operation was evaluated on Inducibility of atrial fibrillation at 10 cm H2O right atrial pressure. An acute increase in right atrial pressure from 2 to 10 cm H2O significantly increased atrial fibrillation inducibility in sham rats (5% to 50%, P<0.01) but not in LVH rats with chronic atrial dilation (20% to 25%, NS).
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