Neural mechanism of angiotensin-converting enzyme inhibitors in improving heart rate variability and sleep disturbance after myocardial infarction.

BACKGROUND: Sympathetic hyperactivity and poor sleep quality are reported in myocardial infarction (MI) patients and angiotensin-converting enzyme inhibitors (ACEI) can improve long-term survival in these patients. We aimed to evaluate ACEI effects on cardiac autonomic activity (CAA) and disordered sleep patterns in ambulatory rats after MI. METHODS: Polysomnographic recording was performed in sham (n = 8) and MI (n = 9) male rats during normal daytime sleep before and after captopril treatment. Spectral analyses of the electroencephalogram and electromyogram were evaluated to define active waking (AW), quiet sleep (QS), and paradoxical sleep (PS). Central sleep apnea (CSA) events were measured by analyzing the electromyogram of the diaphragm. CAA was measured by power spectrum analyses of heart rate variability (HRV). RESULTS: In the MI group, there was a higher low frequency/high frequency ratio during sleep, which reduced significantly after captopril treatment, especially at the QS stage compared to that before captopril treatment. The frequency of sleep interruption was higher in the MI group than the sham group. Increased AW and PS, and decreased QS times were noted in the MI group compared to the sham group. These changes were restored to baseline after captopril treatment in the MI group. CSA events were significantly increased in the MI group, and were restored to the normal level after captopril treatment. CONCLUSIONS: Our results demonstrate significant sleep fragmentation with sympathetic hyperactivity after MI, and that captopril restores the autonomic dysfunction and sleep disorder. These findings suggest that ACEI improved sleep-related respiration disorder after MI by restoring autonomic homeostasis, and provide a hypothesis generating for future studies in humans.

The autonomic neural mechanism of right ventricular outflow tract tachycardia.

BACKGROUND: Ventricular tachycardia (VT) and ventricular premature complexes (VPCs) originating from the right ventricular outflow tract (RVOT) are generally considered as benign arrhythmias, with ECG morphology showing LBBB pattern and inferior axis. Pathogenic mechanisms in the genesis of RVOT VT/VPC remain largely unknown. We aimed to investigate the neural mechanism in RVOT ventricular arrhythmias in canine model. METHODS: Twelve mongrel dogs (13.7 ±â€¯1.3 kg, 5 male dogs) were studied through midline thoracotomies. High-frequency stimulation (HFS) was applied to the proximal pulmonary artery (PA) to induce RVOT VT/VPC. An EnSite Array and a mapping catheter were used for electroanatomical mapping. The RVOT and PA were surgically excised for immunohistochemistry studies, including tyrosine hydroxylase (TH) stain for sympathetic nerves and choline acetyltransferase (ChAT) stain for parasympathetic nerves. RESULTS: In nine (75%) out of twelve dogs, HFS of the proximal PA induced RVOT VT/VPC. The density of TH-positive nerves was significantly higher than that of ChAT-positive nerves (6803 ±â€¯700 vs. 670 ±â€¯252 µm2/mm2, p < 0.001). Furthermore, the density of TH-positive nerves was also significantly higher in the VT/VPC origin sites than that in the non-origin sites (18,044 ±â€¯2866 vs. 5554 ±â€¯565 µm2/mm2, p = 0.002). Catheter ablation of the proximal PA eliminated the inducibility of RVOT VT/VPC successfully. CONCLUSIONS: HFS of the proximal PA could induce RVOT VT/VPC. The sympathetic nerves were densely innervated to the origin of RVOT VT/VPC, indicating the critical role of sympathetic hyperactivity in the initiation and perpetuation of RVOT VT/VPC.