- 作者：José ; A. Barrabé ; s ; jabarrab@vhebron.net ; Jaume Figueras ; Jaume Candell-Riera ; Luis Agulló ; Javier Inserte ; David Garcia-Dorado
- 关键词：EDL ; end-diastolic segment length ; LAD ; left anterior descending coronary artery ; VF ; ventricular fibrillation
- 刊名：Revista Española de Cardiología (English Edition)
- 出版年：2013
- 出版时间：March, 2013
- 年：2013
- 卷：66
- 期：3
- 页码：171-176
- 全文大小：562 K
Introduction and objectives
Distension of the ischemic region has been related to an increased incidence of spontaneous ventricular arrhythmias following coronary occlusion. This study analyzed whether regional ischemic distension predicts increased ventricular fibrillation inducibility after coronary occlusion in swine.Methods
In 18 anesthetized, open-chest pigs, the left anterior descending coronary artery was ligated for 60 min. Myocardial segment length in the ischemic region was monitored by means of ultrasonic crystals. Programmed stimulation was applied at baseline and then continuously between 10 and 60 min after coronary occlusion.
Results
Coronary occlusion induced a rapid increase in end-diastolic length in the ischemic region, which reached 109.4 % (0.9 % ) of baseline values 10 min after occlusion (P<.001). On average, 6.6 (0.5) stimulation protocols were completed and 5.4 (0.6) ventricular fibrillation episodes induced between 10 and 60 min of coronary occlusion. Neither baseline serum potassium levels nor the size of the ischemic region were significantly related to ventricular fibrillation inducibility. In contrast, the increase in end-diastolic length 10 min after coronary occlusion was associated directly (r=0.67; P=.002) with the number of induced ventricular fibrillation episodes and inversely (r=-0.55; P=.018) with the number of extrastimuli needed for ventricular fibrillation induction.
Conclusions
Regional ischemic expansion predicts increased ventricular fibrillation inducibility following coronary occlusion. These results highlight the potential influence of mechanical factors, acting not only on the triggers but also on the substrate, in the genesis of malignant ventricular arrhythmias during acute ischemia.