Daigo Yagishita1, Ray W Chui1, Kentaro Yamakawa1, Pradeep S Rajendran1, Olujimi A Ajijola1, Keijiro Nakamura1, Eileen L So1, Aman Mahajan1, Kalyanam Shivkumar1, Marmar Vaseghi2. 1. From the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles. 2. From the UCLA Cardiac Arrhythmia Center (D.Y., R.W.C., P.S.R., O.A.A., K.N., E.L.S., K.S., M.V.), UCLA Neurocardiology Center of Excellence (D.Y., R.W.C., K.Y., P.S.R., O.A.A., K.N., E.L.S., A.M., K.S., M.V.), and Department of Cardiac Anesthesia (K.Y., A.M.), University of California, Los Angeles. mvaseghi@mednet.ucla.edu.
Abstract
BACKGROUND: T-peak to T-end interval (Tp-e) is an independent marker of sudden cardiac death. Modulation of Tp-e by sympathetic nerve activation and circulating norepinephrine is not well understood. The purpose of this study was to characterize endocardial and epicardial dispersion of repolarization (DOR) and its effects on Tp-e with sympathetic activation. METHODS AND RESULTS: In Yorkshire pigs (n=13), a sternotomy was performed and the heart and bilateral stellate ganglia were exposed. A 56-electrode sock and 64-electrode basket catheter were placed around the epicardium and in the left ventricle (LV), respectively. Activation recovery interval, DOR, defined as variance in repolarization time, and Tp-e were assessed before and after left, right, and bilateral stellate ganglia stimulation and norepinephrine infusion. LV endocardial and epicardial activation recovery intervals significantly decreased, and LV endocardial and epicardial DOR increased during sympathetic nerve stimulation. There were no LV epicardial versus endocardial differences in activation recovery interval during sympathetic stimulation, and regional endocardial activation recovery interval patterns were similar to the epicardium. Tp-e prolonged during left (from 40.4±2.2 ms to 92.4±12.4 ms; P<0.01), right (from 47.7±2.6 ms to 80.7±11.5 ms; P<0.01), and bilateral (from 47.5±2.8 ms to 78.1±9.8 ms; P<0.01) stellate stimulation and strongly correlated with whole heart DOR during stimulation (P<0.001, R=0.86). Of note, norepinephrine infusion did not increase DOR or Tp-e. CONCLUSIONS: Regional patterns of LV endocardial sympathetic innervation are similar to that of LV epicardium. Tp-e correlated with whole heart DOR during sympathetic nerve activation. Circulating norepinephrine did not affect DOR or Tp-e.
BACKGROUND: T-peak to T-end interval (Tp-e) is an independent marker of sudden cardiac death. Modulation of Tp-e by sympathetic nerve activation and circulating norepinephrine is not well understood. The purpose of this study was to characterize endocardial and epicardial dispersion of repolarization (DOR) and its effects on Tp-e with sympathetic activation. METHODS AND RESULTS: In Yorkshire pigs (n=13), a sternotomy was performed and the heart and bilateral stellate ganglia were exposed. A 56-electrode sock and 64-electrode basket catheter were placed around the epicardium and in the left ventricle (LV), respectively. Activation recovery interval, DOR, defined as variance in repolarization time, and Tp-e were assessed before and after left, right, and bilateral stellate ganglia stimulation and norepinephrine infusion. LV endocardial and epicardial activation recovery intervals significantly decreased, and LV endocardial and epicardial DOR increased during sympathetic nerve stimulation. There were no LV epicardial versus endocardial differences in activation recovery interval during sympathetic stimulation, and regional endocardial activation recovery interval patterns were similar to the epicardium. Tp-e prolonged during left (from 40.4±2.2 ms to 92.4±12.4 ms; P<0.01), right (from 47.7±2.6 ms to 80.7±11.5 ms; P<0.01), and bilateral (from 47.5±2.8 ms to 78.1±9.8 ms; P<0.01) stellate stimulation and strongly correlated with whole heart DOR during stimulation (P<0.001, R=0.86). Of note, norepinephrine infusion did not increase DOR or Tp-e. CONCLUSIONS: Regional patterns of LV endocardial sympathetic innervation are similar to that of LV epicardium. Tp-e correlated with whole heart DOR during sympathetic nerve activation. Circulating norepinephrine did not affect DOR or Tp-e.
Authors: Jesus Castro Hevia; Charles Antzelevitch; Francisco Tornés Bárzaga; Margarita Dorantes Sánchez; Francisco Dorticós Balea; Roberto Zayas Molina; Miguel A Quiñones Pérez; Yanela Fayad Rodríguez Journal: J Am Coll Cardiol Date: 2006-04-17 Impact factor: 24.094
Authors: David Hamon; Pradeep S Rajendran; Ray W Chui; Olujimi A Ajijola; Tadanobu Irie; Ramin Talebi; Siamak Salavatian; Marmar Vaseghi; Jason S Bradfield; J Andrew Armour; Jeffrey L Ardell; Kalyanam Shivkumar Journal: Circ Arrhythm Electrophysiol Date: 2017-04
Authors: Tarek A N Ahmed; Amr A Abdel-Nazeer; Ayman K M Hassan; Hosam Hasan-Ali; Amr A Youssef Journal: Ann Noninvasive Electrocardiol Date: 2019-02-09 Impact factor: 1.468