![]() To compare fixed with variable CI (short versus short and long versus long), at least one extrasystolic beat with a CI equal to the short as well as the long CI subtypes was induced in the last minute of variable CI sequences. ARIs and DORs were analyzed for the PVC and PAC beat delivered in the last minute, as well as the sinus beats following them (postextrasystolic sinus beat (PES-SB)) that were compared with baseline sinus beats (SBs) (average of 5 SBs before introduction of each extrasystolic subtype). 16, 17 Global dispersion of repolarization (DOR) was calculated as the variance across all electrodes. ARIs were calculated using a customized software ScalDyn (University of Utah, Salt Lake City, UT, USA) as previously described. Therefore, the purpose of this study was to evaluate in an in vivo porcine model the impact of PVC CI on: (1) intrinsic cardiac neuronal activity and (2) cardiac electrical and mechanical parameters using a novel cardio-neural mapping approach that utilizes direct neuronal recordings from a beating heart.Įpicardial activation recovery intervals (ARIs), a surrogate for action potential duration, were derived from unipolar electrograms recorded from a 56-electrode sock array placed over the ventricles (Prucka CardioLab, GE Healthcare) ( Figure 1A). 11, 14Īs both PVCs with variable CI and the ICNS have been linked to CMP and life-threatening arrhythmias, we hypothesized that variability in PVC CI could induce destabilizing changes in the ICNS. 15 Moreover, neural remodeling within the ICNS following cardiac injury has been correlated with arrhythmias. 12– 14 Even in normal states, disruptions of ICNS function are arrhythmogenic. ![]() 11 The ICNS, a distributed network of ganglia and interconnecting nerve fibers on the epicardial surface, represents the first level of the ANS directly impacted by cardiac injury. Processing and integration of this information at different levels of the ANS, including the intrinsic cardiac nervous system (ICNS), provides an elegant mechanism to ensure fine-tuned regulation of efferent neural signals to the heart. 11 Afferent sensory neurons provide beat-to-beat information regarding the cardiac milieu. The ANS regulates all aspects of cardiac function. 10 Of these mechanisms, the role of the autonomic nervous system (ANS) is not well understood. Precise mechanisms underlying the adverse effects of PVCs remain unknown, but are likely multifactorial including mechanical dyssynchrony, 7, 8 abnormalities in calcium handling and oxygen consumption, 9 and autonomic imbalance. ![]() Particularly, patients with PVCs showing high coupling interval (CI) variability are at a greater risk for cardiac events such as left ventricular (LV) dysfunction 4 and sudden cardiac death. 2, 3 Recent clinical studies have identified factors that predict worse outcomes in PVC patients. In structurally normal hearts, despite being referred to as “benign”, PVCs may lead to cardiomyopathy (CMP) 1 or even to sudden cardiac death. Premature ventricular contractions (PVCs) are common in clinical practice. ![]()
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