Effects of transient myocardial ischemia on the ventricular defibrillation threshold

被引:23
作者
Anastasiou-Nana, MI [1 ]
Tsagalou, EP [1 ]
Charitos, C [1 ]
Siafakas, KX [1 ]
Drakos, S [1 ]
Terrovitis, JV [1 ]
Ntalianis, A [1 ]
Doufas, A [1 ]
Mavrikakis, J [1 ]
Nanas, JN [1 ]
机构
[1] Univ Athens, Sch Med, Dept Clin Therapeut, Alexandra Hosp, GR-11527 Athens, Greece
来源
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY | 2005年 / 28卷 / 02期
关键词
defibrillation; ventricular fibrillation; ventricular ischemia;
D O I
10.1111/j.1540-8159.2005.09303.x
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Background: Acute myocardial ischemia and the mode of ventricular fibrillation (VF) induction influence the ventricular defibrillation threshold (DFT). Methods: Ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT), and DFT were measured under nonischemic conditions (control) in 26 pigs weighing 25-35 kg. Myocardial ischemia was then induced by occlusion of the mid left anterior descending coronary artery, and measurements of ERP and VFT were repeated after 2 minutes of Occlusion. The coronary artery ligation was released immediately after the onset of VF and DFT was measured. Results: LV ERP was unchanged by ischemia (199 +/- 19 ms at control vs. 200 22 Ins under ischemic conditions, P=0.799), whereas VFT was significantly lower during coronary Occlusion (10.7 +/- 15.4 mA vs. 37.7 +/- 13 mA, P = 0.000). Brief myocardial ischemia caused a significant increase in DFT (13.5 +/- 12.6 J after coronary occlusion vs. 6.8 +/- 6.8 J at control, P = 0.023). The duration of coronary occlusion was not Correlated with the amounts of energy required to defibrillate (P = 0.526). Conclusions: This experimental study shows that transient myocardial ischemia markedly increases the DFT suggesting that specific defibrillation algorithms should be designed for recipients of implantable defibrillators at risk of myocardial ischemia.
引用
收藏
页码:97 / 101
页数:5
相关论文
共 21 条
[1]
ARREDONDO MT, 1982, MED PROG TECHNOL, V8, P175
[2]
VULNERABILITY TO VENTRICULAR-FIBRILLATION DURING ACUTE CORONARY ARTERIAL-OCCLUSION AND RELEASE [J].
AXELROD, PJ ;
VERRIER, RL ;
LOWN, B .
AMERICAN JOURNAL OF CARDIOLOGY, 1975, 36 (06) :776-782
[3]
BABBS CF, 1983, MED INSTRUM, V17, P18
[4]
Effects of myocardial ischemia on ventricular fibrillation inducibility and defibrillation efficacy [J].
Behrens, S ;
Li, CL ;
Franz, MR .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1997, 29 (04) :817-824
[5]
Prediction of defibrillation outcome by epicardial activation patterns following shocks near the defibrillation threshold [J].
Chattipakorn, N ;
Fotuhi, PC ;
Ideker, RE .
JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, 2000, 11 (09) :1014-1021
[6]
ACTIVATION DURING VENTRICULAR DEFIBRILLATION IN OPEN-CHEST DOGS - EVIDENCE OF COMPLETE CESSATION AND REGENERATION OF VENTRICULAR-FIBRILLATION AFTER UNSUCCESSFUL SHOCKS [J].
CHEN, PS ;
SHIBATA, N ;
DIXON, EG ;
WOLF, PD ;
DANIELEY, ND ;
SWEENEY, MB ;
SMITH, WM ;
IDEKER, RE .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 77 (03) :810-823
[7]
Effect of antithrombotic therapy on risk of sudden coronary death in patients with congestive heart failure [J].
Dries, DL ;
Domanski, MJ ;
Waclawiw, MA ;
Gersh, BJ .
AMERICAN JOURNAL OF CARDIOLOGY, 1997, 79 (07) :909-913
[8]
Efimov IR, 1998, CIRC RES, V82, P918
[9]
EFFECT OF ISCHEMIA, HYPERTROPHY, HYPOXIA, ACIDOSIS, AND ALKALOSIS ON CANINE DEFIBRILLATION [J].
KERBER, RE ;
PANDIAN, NG ;
HOYT, R ;
JENSEN, SR ;
KOYANAGI, S ;
GRAYZEL, J ;
KIESO, R .
AMERICAN JOURNAL OF PHYSIOLOGY, 1983, 244 (06) :H825-H831
[10]
RELATIONSHIP BETWEEN SYMPATHETIC NEURAL ACTIVITY, CORONARY DYNAMICS, AND VULNERABILITY TO VENTRICULAR-FIBRILLATION DURING MYOCARDIAL ISCHEMIA AND REPERFUSION [J].
LOMBARDI, F ;
VERRIER, RL ;
LOWN, B .
AMERICAN HEART JOURNAL, 1983, 105 (06) :958-965