Evaluation of the reentry vulnerability index to predict ventricular tachycardia circuits using high-density contact mapping.

BACKGROUND: Identifying arrhythmogenic sites to improve ventricular tachycardia (VT) ablation outcomes remains unresolved. The reentry vulnerability index (RVI) combines activation and repolarization timings to identify sites critical for reentrant arrhythmia initiation without inducing VT. OBJECTIVE: The purpose of this study was to provide the first assessment of RVI's capability to identify VT sites of origin using high-density contact mapping and comparison with other activation-repolarization markers of functional substrate. METHODS: Eighteen VT ablation patients (16 male; 72% ischemic) were studied. Unipolar electrograms were recorded during ventricular pacing and analyzed offline. Activation time (AT), activation-recovery interval (ARI), and repolarization time (RT) were measured. Vulnerability to reentry was mapped based on RVI and spatial distribution of AT, ARI, and RT. The distance from sites identified as vulnerable to reentry to the VT site of origin was measured, with distances <10 mm and >20 mm indicating accurate and inaccurate localization, respectively. RESULTS: The origins of 18 VTs (6 entrainment, 12 pace-mapping) were identified. RVI maps included 1012 (408-2098) (median, 1st-3rd quartiles) points per patient. RVI accurately localized 72.2% VT sites of origin, with median distance of 5.1 (3.2-10.1) mm. Inaccurate localization was significantly less frequent for RVI than AT (5.6% vs 33.3%; odds ratio 0.12; P = .035). Compared to RVI, distance to VT sites of origin was significantly larger for sites showing prolonged RT and ARI and were nonsignificantly larger for sites showing highest AT and ARI gradients. CONCLUSION: RVI identifies vulnerable regions closest to VT sites of origin. Activation-repolarization metrics may improve VT substrate delineation and inform novel ablation strategies.

In vivo human left-to-right ventricular differences in rate adaptation transiently increase pro-arrhythmic risk following rate acceleration.

Left-to-right ventricular (LV/RV) differences in repolarization have been implicated in lethal arrhythmias in animal models. Our goal is to quantify LV/RV differences in action potential duration (APD) and APD rate adaptation and their contribution to arrhythmogenic substrates in the in vivo human heart using combined in vivo and in silico studies. Electrograms were acquired from 10 LV and 10 RV endocardial sites in 15 patients with normal ventricles. APD and APD adaptation were measured during an increase in heart rate. Analysis of in vivo electrograms revealed longer APD in LV than RV (207.8 ± 21.5 vs 196.7 ± 20.1 ms; P<0.05), and slower APD adaptation in LV than RV (time constant τ(s) =47.0 ± 14.3 vs 35.6 ± 6.5 s; P<0.05). Following rate acceleration, LV/RV APD dispersion experienced an increase of up to 91% in 12 patients, showing a strong correlation (r(2) =0.90) with both initial dispersion and LV/RV difference in slow adaptation. Pro-arrhythmic implications of measured LV/RV functional differences were studied using in silico simulations. Results show that LV/RV APD and APD adaptation heterogeneities promote unidirectional block following rate acceleration, albeit being insufficient for establishment of reentry in normal hearts. However, in the presence of an ischemic region at the LV/RV junction, LV/RV heterogeneity in APD and APD rate adaptation promotes reentrant activity and its degeneration into fibrillatory activity. Our results suggest that LV/RV heterogeneities in APD adaptation cause a transient increase in APD dispersion in the human ventricles following rate acceleration, which promotes unidirectional block and wave-break at the LV/RV junction, and may potentiate the arrhythmogenic substrate, particularly in patients with ischemic heart disease.

Oscillatory patterns of respiration: consequences for the stability and control of cardiac electrophysiology.

Periodic breathing patterns known as Central Sleep Apnea (CSA) are often observed in congestive heart failure. This phenomenon is associated with increased risk of sudden cardiac death, but the mechanism for that outcome has not been exposed. Endocardial electrograms were recorded during spontaneous episodes of CSR and PB in patients in conscious and unconscious states. Analysis exposed a regular bidirectional phase-walk in the relationship between respiration and arterial blood pressure. Recently developed signal processing techniques revealed that respiration also modulates cardiac repolarization properties at multiple simultaneous frequencies, and the effect was heterogeneous across measurement sites in both ventricles. These measurements offer unique evidence of the electro-physiological manifestations of these breathing patterns. Analysis of phase relationships suggested a mechanism by which the behavior may predispose patients to cardiac arrhythmias. Such predisposition would be easily measured to direct treatment priorities and improve risk stratification.

The circumferential loading of a direct cardiac compression assist device.

Heart disease is the developed world's largest killer. Transplantation of the failing heart remains the most effective treatment currently employed, but demand far exceeds donor supply. In a bid to address this imbalance, the use of mechanical circulatory support has been explored since the mid-1960s. This paper utilizes one such device, which achieves assistance by mechanically compressing the epicardial surface of the failing heart. The circumferential normal loading of the device is investigated, showing how frictional effects inherent to the device's operation affect localized surface pressure. Results showed that as distance from the device's actuator increased, assistive systolic force reduced, whilst device constriction to ventricular filling detrimentally increased. Active device relaxation was shown to limit the diastolic effect outlined above, providing the simulated diseased heart with an improved cardiac output. The results also raise questions concerning device in-vivo positioning and short-comings with the current heart simulator.