Is the arterial baroreflex control of cardiac sympathetic nerve activity altered in heart failure?

Abstract

The increase in cardiac sympathetic nerve activity (CSNA) in heart failure (HF) is detrimental because it causes arrhythmias that can lead to sudden death. The causes of this sympathetic activation are not well understood. Aim: To determine the changes in CSNA by direct recording in conscious normal sheep and in sheep with HF and to determine whether the arterial baroreflex control of CSNA is desensitised in HF. Methods: Studies were performed on conscious sheep with carotid artery loops. In six sheep HF was induced by rapid ventricular pacing for 4–8 weeks at 200 beats/min. Development of heart failure was monitored weekly by echocardiography. When ejection fraction had fallen to <40%, recording electrodes were implanted in the left cardio-thoracic sympathetic nerves. At least 3 days after surgery, CSNA and arterial pressure were recorded with the pacing switched off. Arterial baroreceptor curves were constructed by infusion of phenylephrine and sodium nitroprusside. Results: The basal level of CSNA was dramatically increased in HF sheep (n =6) compared with normal sheep (n =6), burst frequency increased from 64T7 to 92T2 bursts/ 100 heart beats. The maximum gain of the arterial baroreceptor relationship between diastolic blood pressure (dBP) and heart rate was significantly depressed in HF animals compared to normal animals, but the relationship between dBP and CSNA did not differ between the two groups. Conclusions: In sheep with HF, directly measured CSNA was significantly elevated. The gain of the arterial baroreflex was unchanged, indicating baroreceptor desensitization is not responsible for the elevation of CSNA seen in HF.