Hemodynamic and neurohormonal predictors and consequences of the development of atrial fibrillation in dogs with chronic heart failure.

BACKGROUND

Heart failure increases the risk of atrial fibrillation (AF), which frequently results in heart failure progression. This prospective study examined the contribution of hemodynamic and neurohormonal activation to the spontaneous occurrence of AF in heart failure, and assessed the effects of AF on left ventricular (LV) function and neurohormonal activation.

METHODS AND RESULTS

Heart failure (LV ejection fraction [LVEF] 25%-30%) was induced in 27 dogs via sequential coronary microembolizations. Hemodynamic and neurohormonal measurements were performed at 1 month (prior to development of AF) and 4 months post-embolization. During the time between measurements, 10 dogs developed spontaneous AF. Plasma norepinephrine concentration (PNE) at 1 month was higher in animals that subsequently developed AF (576 + 101 vs. 425 + 197 pg/mL, P = .03). There were no significant differences between the groups in 1-month LV end-diastolic pressure (LVEDP), pulmonary artery wedge pressure (PAWP), cardiac output, end-diastolic volume (EDV), LVEF, or plasma renin activity (PRA). At 4 months, cardiac output was lower (2.1 + .4 vs. 2.6 + .6 L/h, P = .02) and PNE was higher (1036 + 857 vs. 508 + 288 pg/mL, P = .03) in dogs with AF versus those in sinus rhythm. There were no significant differences between groups in 4-month LVEDP, PAWP, EDV, LVEF, or PRA.

CONCLUSION

Spontaneous AF in heart failure was preceded by a significant increase in PNE. In animals that developed AF, there was a further decline in cardiac output and increase in PNE.