Regression of Left Ventricular Hypertrophy With Captopril Restores Normal Ventricular Action Potential Duration, Dispersion of Refractoriness, and Vulnerability to Inducible Ventricular Fibrillation

Circulation ◽  
1997 ◽  
Vol 96 (4) ◽  
pp. 1330-1336 ◽  
Author(s):  
Seth J. Rials ◽  
Ying Wu ◽  
Xiaoping Xu ◽  
Roland A. Filart ◽  
Roger A. Marinchak ◽  
...  
1990 ◽  
Vol 67 (2) ◽  
pp. 501-509 ◽  
Author(s):  
A L Taylor ◽  
R Winter ◽  
F Thandroyen ◽  
S Murphree ◽  
L M Buja ◽  
...  

2007 ◽  
Vol 293 (4) ◽  
pp. H2530-H2536 ◽  
Author(s):  
Jian Huang ◽  
Kang-An Cheng ◽  
Derek J. Dosdall ◽  
William M. Smith ◽  
Raymond E. Ideker

During ventricular fibrillation (VF) only 39% of the variation in action potential duration (APD) is accounted for by the previous diastolic interval [DI( n−1)], i.e., restitution, and the previous APD [APD( n−1)], i.e., memory. We tested the hypothesis that a characteristic of the AP upstroke, the maximum rate of depolarization ( V̇max), also helps account for its APD. A floating microelectrode was used to make transmembrane recordings at 16,000 samples/s from the anterior left ventricular wall during four 20-s episodes of VF in each of six pigs. V̇max, time from V̇max to 60% repolarization (APD60), and DI were calculated throughout all episodes. Stepwise linear regression was used to determine how well each APD60 (APD60 n) was predicted by V̇max of that AP, the four previous DIs ( n−1, n − 2, n − 3, n − 4), and the three previous APD60s ( n−1, n − 2, n − 3). V̇max entered in the regression equation significantly more often (86% of VF episodes) than either APD( n−1) (47% of episodes) or DI( n−1) (58% of episodes). When these three variables entered first or second, their coefficients were almost always positive, consistent with a longer APD associated with 1) a larger V̇max, 2) a longer APD( n−1), and 3) a longer DI( n−1). R2 of the regression for all entered variables was 0.51 ± 0.01 (mean ± SD). During the first 20 s of VF in swine, V̇max is a more important determinant of APD than the previous DI (restitution) or the previous APD (memory). All variables together account for only one-half of APD variation during VF.


Author(s):  
Joseph S. Piktel ◽  
Yi Suen ◽  
Shalen Kouk ◽  
Danielle Maleski ◽  
Gary Pawlowski ◽  
...  

Background Amiodarone is administered during resuscitation, but its antiarrhythmic effects during targeted temperature management are unknown. The purpose of this study was to determine the effect of both therapeutic hypothermia and amiodarone on arrhythmia substrates during resuscitation from cardiac arrest. Methods and Results We utilized 2 complementary models: (1) In vitro no‐flow global ischemia canine left ventricular transmural wedge preparation. Wedges at different temperatures (36°C or 32°C) were given 5 µmol/L amiodarone (36‐Amio or 32‐Amio, each n=8) and subsequently underwent ischemia and reperfusion. Results were compared with previous controls. Optical mapping was used to measure action potential duration, dispersion of repolarization (DOR), and conduction velocity (CV). (2) In vivo pig model of resuscitation. Pigs (control or targeted temperature management, 32–34°C) underwent ischemic cardiac arrest and were administered amiodarone (or not) after 8 minutes of ventricular fibrillation. In vitro: therapeutic hypothermia but not amiodarone prolonged action potential duration. During ischemia, DOR increased in the 32‐Amio group versus 32‐Alone (84±7 ms versus 40±7 ms, P <0.05) while CV slowed in the 32‐Amio group. Amiodarone did not affect CV, DOR, or action potential duration during ischemia at 36°C. Conduction block was only observed at 36°C (5/8 36‐Amio versus 6/7 36‐Alone, 0/8 32‐Amio, versus 0/7 32‐Alone). In vivo: QTc decreased upon reperfusion from ischemia that was ameliorated by targeted temperature management. Amiodarone did not worsen DOR or CV. Amiodarone suppressed rearrest caused by ventricular fibrillation (7/8 without amiodarone, 2/7 with amiodarone, P =0.041), but not pulseless electrical activity (2/8 without amiodarone, 5/7 with amiodarone, P =0.13). Conclusions Although amiodarone abolishes a beneficial effect of therapeutic hypothermia on ischemia‐induced DOR and CV, it did not worsen susceptibility to ventricular tachycardia/ventricular fibrillation during resuscitation.


Sign in / Sign up

Export Citation Format

Share Document