Chronic Heart Failure Markedly Attenuates the Low Pressure Baroreflex in Regulating Sympathetic Function in Rats

Background: We aimed to elucidate the prognostic impacts of atrial fibrillation (AF) in patients with chronic heart failure ( CHF). Methods and Results: We examined 4,818 consecutive patients with Stage C/D CHFregistered in our CHART-2 Study (N510,219). Among them, 1,859 (38.6%) had AF at enrollment. As compared with the remaining 2,953 patients with sinus rhythm at enrollment, patients with AF were characterized by higher age (71 vs. 68 yrs.), lower esti- mated glomerular filtration rate (58.9 vs. 61.9 ml/min/1.73m 2 ), higher brain natri- uretic peptide (BNP) levels (152 vs. 74.5 pg/ml), comparable LVEF (56.8 vs 56.5%) and similar prescription rate of beta-blocker(48.1 vs. 50.6%) and renin- angiotensin system (RAS) inhibitor (72.9 vs. 71.6%). Among the patients with si- nus rhythm at enrollment, 106 (3.6%) developed de-novo AF (dnAF) during the median follow-up for 3.2 years, which was associated with an increased mortality (adjusted hazard ratio (HR) 1.72, P50.013). In contrast, neither paroxysmal AF (pAF) nor chronic AF (cAF) at enrollment was associated with mortality (pAF, adjusted HR 1.10, P50.491; cAF, adjusted HR 1.00, P 50.992). IPTW analysis revealed that neither beta-blockersnor RAS inhibitors was associated with reduced mortality in AF patients, regardless of pAF or cAF. Conclusions: These results indicate that development of dnAF, but not pAF or cAF at enrollment, was associated with increased mortality in CHFpatients. Background: We previously reported that the activation of low-pressure baroreflex(LBARO) by volume infusion biphasically altered sympathetic nerve activity (SNA). We examined whether chronic heart failure ( CHF) changed LBARO. Methods: In 14 anesthetized Sprague-Dawley rats, we created CHFby myocardial infarction. We isolated carotid sinuses to abolish the arterial baroreflex. We infused blood stepwise to activate LBARO, and recorded SNA and hemodynamics. Result: In the normal group (n56), volume loading increased both central venous pressure(CVP) and left ventricular end-diastolic pressure (LVEDP) and biphasically changed SNA with a maximal response of 48621%. In contrast, CHF(n58) markedly reduced the maximum response (1567%, p!0.05) and abolished the biphasic change of SNA (Figure). Conclusions: CHFinduces the L-BARO failure. How the LBARO failure impacts the pathophysiology of CHFremains to be investigated.