Basic Res Cardiol 97: 445 – 451 (2002) DOI 10.1107/s00395-002-0376-5 ORIGINAL CONTRIBUTION José A. Barrabés David Garcia-Dorado Ferran Padilla Luis Agulló Lourdes Trobo Julio Carballo Jordi Soler-Soler Ventricular fibrillation during acute coronary occlusion is related to the dilation of the ischemic region  Abstract Myocardial stretch induces several electrophysiological changes and arrhythmias, but little is known on its possible role in triggering ventric- ular fibrillation (VF) during acute coronary occlusion. In thiopental-anes- thetized, open-chest pigs submitted to a 40-min ligation of the left anterior descending coronary artery, the association between the early increase in end-diastolic length (measured by means of ultrasonic crystals) in the ischemic region and subsequent VF was analyzed. Animals received no treat- ment (n = 35) or intravenous nitroglycerin (2.5 µg/kg/min for 20 min, start- ing 10 min after coronary occlusion, n = 8) or Gd 3+ (80 µM/kg for 35 min, starting 5 min before occlusion, n = 15). Twenty-four animals (41 %) had VF, 16 to 39 min after coronary occlusion. The magnitude of ischemic dilation and the incidence of VF were similar among groups. End-diastolic length in the ischemic region 15 min after coronary occlusion was 115.7 ± 1.2 % of baseline in animals with VF and 111.4 ± 0.9 % in those without (P = 0.007), and was the strongest predictor of this arrhythmia (P = 0.003) after adjusting for treat- ment and other possible confounding variables. Thus, the dilation of the ischemic region is closely and independently associated with VF following coronary occlusion. Although the interventions tested in the present study failed to protect against this arrhythmia, the results strongly suggest an influ- ence of ischemic dilation on VF.  Key words Ventricular arrhythmias – ischemia – stretch – mechanoelec- trical coupling – coronary occlusion BRC 376 J. A. Barrabés · D. Garcia-Dorado, M.D. () F. Padilla · L. Agulló · L. Trobo J. Carballo · J. Soler-Soler Servicio de Cardiolog´ ıa Hospital Universitari Vall d’Hebron Pg. Vall d’Hebron 119–129 08035 Barcelona, Spain Tel.: +34 93 489 4038 Fax: +34 93 489 4032 E-Mail: dgdorado@hg.vhebron.es Received: 11 April 2002 Returned for revision: 21 May 2002 Revision received: 12 June 2002 Accepted: 27 June 2002 Introduction Acute myocardial ischemia is frequently associated with ventricular arrhythmias and sudden death (11), but the mechanisms of these arrhythmias remain unclear (15). There is uncertainty on the determinants of the Ib phase of ischemic ventricular arrhythmias, which takes place approximately 12 to 30 min after interruption of coro- nary flow (18). Phase Ib arrhythmias have been related to the deterioration of intercellular communication, which might cause inhomogeneous conduction favoring micro- reentry (21, 31), and to the release of endogenous cate- cholamines, which might induce abnormal automaticity (23, 29). Moreover, these arrhythmias are especially sen- sitive to neural influences, being facilitated by decreased vagal tone (7, 27) or by increased sympathetic activity (16, 30). On the other hand, it is well known that coronary occlusion (CO) causes the dilation of the ischemic region in a few minutes (2, 33). Hypothetically, this rapid regional left ventricular distension could favor the devel- opment of ventricular arrhythmias by triggering a car- diac autonomic reflex (7, 24, 30) or through activation