Dataset Information

Activation recovery interval imaging of premature ventricular contraction.

ABSTRACT: Dispersion of ventricular repolarization due to abnormal activation contributes to the susceptibility to cardiac arrhythmias. However, the global pattern of repolarization is difficult to assess clinically. Activation recovery interval (ARI) has been used to understand the properties of ventricular repolarization. In this study, we developed an ARI imaging technique to noninvasively reconstruct three-dimensional (3D) ARI maps in 10 premature ventricular contraction (PVC) patients and evaluated the results with the endocardial ARI maps recorded by a clinical navigation system (CARTO). From the analysis results of a total of 100 PVC beats in 10 patients, the average correlation coefficient is 0.86±0.05 and the average relative error is 0.06±0.03. The average localization error is 4.5±2.3 mm between the longest ARI sites in 3D ARI maps and those in CARTO endocardial ARI maps. The present results suggest that ARI imaging could serve as an alternative of evaluating global pattern of ventricular repolarization noninvasively and could assist in the future investigation of the relationship between global repolarization dispersion and the susceptibility to cardiac arrhythmias.

SUBMITTER: Yang T

PROVIDER: S-EPMC6003683 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Activation recovery interval imaging of premature ventricular contraction.

Yang Ting T Yu Long L Jin Qi Q Wu Liqun L He Bin B

PloS one 20180615 6

Dispersion of ventricular repolarization due to abnormal activation contributes to the susceptibility to cardiac arrhythmias. However, the global pattern of repolarization is difficult to assess clinically. Activation recovery interval (ARI) has been used to understand the properties of ventricular repolarization. In this study, we developed an ARI imaging technique to noninvasively reconstruct three-dimensional (3D) ARI maps in 10 premature ventricular contraction (PVC) patients and evaluated t ...[more]

PMID: 29906289

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Project description:BACKGROUND:The presence and significance of neural remodeling in premature ventricular contraction-induced cardiomyopathy (PVC-CM) remain unknown. OBJECTIVES:This study aimed to characterize cardiac sympathovagal balance and proarrhythmia in a canine model of PVC-CM. METHODS:In 12 canines, the investigators implanted epicardial pacemakers and radiotelemetry units to record cardiac rhythm and nerve activity (NA) from the left stellate ganglion (SNA), left cardiac vagus (VNA), and arterial blood pressure. Bigeminal PVCs (200 ms coupling) were applied for 12 weeks to induce PVC-CM in 7 animals then disabled for 4 weeks to allow complete recovery of left ventricular ejection fraction (LVEF), versus 5 sham controls. RESULTS:After 12 weeks of PVCs, LVEF (p = 0.006) and dP/dT (p = 0.007) decreased. Resting SNA (p = 0.002) and VNA (p = 0.04), exercise SNA (p = 0.01), SNA response to evoked PVCs (p = 0.005), heart rate (HR) at rest (p = 0.003), and exercise (p < 0.04) increased, whereas HR variability (HRV) decreased (p = 0.009). There was increased spontaneous atrial (p = 0.02) and ventricular arrhythmias (p = 0.03) in PVC-CM. Increased SNA preceded both atrial (p = 0.0003) and ventricular (p = 0.009) arrhythmia onset. Clonidine suppressed SNA and abolished all arrhythmias. After disabling PVC for 4 weeks, LVEF (p = 0.01), dP/dT (p = 0.047), and resting VNA (p = 0.03) recovered to baseline levels. However, SNA, resting HR, HRV, and atrial (p = 0.03) and ventricular (p = 0.03) proarrhythmia persisted. There was sympathetic hyperinnervation in stellate ganglia (p = 0.02) but not ventricles (p = 0.2) of PVC-CM and recovered animals versus sham controls. CONCLUSIONS:Neural remodeling in PVC-CM is characterized by extracardiac sympathetic hyperinnervation and sympathetic neural hyperactivity that persists despite normalization of LVEF. The altered cardiac sympathovagal balance is an important trigger and substrate for atrial and ventricular proarrhythmia.

Project description:Mechanisms behind development of premature ventricular contraction (PVC)-induced cardiomyopathy remain unclear. PVCs may adversely modulate the autonomic nervous system to promote development of heart failure. Afferent neurons in the inferior vagal (nodose) ganglia transduce cardiac activity and modulate parasympathetic output. Effects of PVCs on cardiac parasympathetic efferent and vagal afferent neurotransmission are unknown. The purpose of this study was to evaluate effects of PVCs on vagal afferent neurotransmission and compare these effects with a known powerful autonomic modulator, myocardial ischemia. In 16 pigs, effects of variably coupled PVCs on heart rate variability (HRV) and vagal afferent neurotransmission were evaluated. Direct nodose neuronal recordings were obtained in vivo, and cardiac-related afferent neurons were identified based on their response to cardiovascular interventions, including ventricular chemical and mechanical stimuli, left anterior descending (LAD) coronary artery occlusion, and variably coupled PVCs. On HRV analysis before versus after PVCs, parasympathetic tone decreased (normalized high frequency: 83.6?±?2.8 to 72.5?±?5.3; P < 0.05). PVCs had a powerful impact on activity of cardiac-related afferent neurons, altering activity of 51% of neurons versus 31% for LAD occlusion (P < 0.05 vs. LAD occlusion and all other cardiac interventions). Both chemosensitive and mechanosensitive neurons were activated by PVCs, and their activity remained elevated even after cessation of PVCs. Cardiac afferent neural responses to PVCs were greater than any other intervention, including ischemia of similar duration. These data suggest that even brief periods of PVCs powerfully modulate vagal afferent neurotransmission, reflexly decreasing parasympathetic efferent tone.NEW & NOTEWORTHY Premature ventricular contractions (PVCs) are common in many patients and, at an increased burden, are known to cause heart failure. This study determined that PVCs powerfully modulate cardiac vagal afferent neurotransmission (exerting even greater effects than ventricular ischemia) and reduce parasympathetic efferent outflow to the heart. PVCs activated both mechano- and chemosensory neurons in the nodose ganglia. These peripheral neurons demonstrated adaptation in response to PVCs. This study provides additional data on the potential role of the autonomic nervous system in PVC-induced cardiomyopathy.

Dataset Information

Activation recovery interval imaging of premature ventricular contraction.

Publications

Activation recovery interval imaging of premature ventricular contraction.

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