CORONARY VENOUS HYPERTENSION PREVENTS THE FORMATION OF THE ELECTROPHYSIOLOGICAL ARRHYTHMOGENIC SUBSTRATE OF ACUTE-ISCHEMIA IN THE DOG - SALUTARY EFFECTS OF PRESERVED MYOCARDIAL HYDRATION

Coronary venous hypertension induced by partial coronary sinus obstruc tion (CSO) in the dog, prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia. Also, CSO acti ng presumably through enhanced myocardial hydration, normalizes the in homogenous extracellular potassium ([K+](o)) accumulation, a major fac tor in producing the electrophysiological disparities, characteristic of arrhythmogenic substrate, To further clarify the mechanism of early ischemic VF prevention in dogs, radioactive microspheres were used to evaluate regional perfusion changes, resulting from CSO sufficient to raise the coronary sinus pressure to 40 mmHg, before and during ische mia induced by double coronary artery occlusion (CAO) (n = 5). Also, g lobal or regional unipolar electrogram mapping was used to assess chan ges of epicardial ventricular activation times (AT) and sequence and a ctivation recovery intervals (ARI) during CSO, CAO and combined CSO an d CAO, induced in random order (n = 8). CSO did not affect regional pe rfusion nor improved collateral blood flow during ischemia, With CSO, AT shortened modestly over time (0.41 +/- 1.1 ms/min, r=0.85, P<0.05) and ARI transiently decreased by up to 5.5%. With CAO, AT became varia bly delayed and isochrone map distortions were indicative of localized conduction delays or blocks, consistent with elevated [K+](o). In con trast, when CAO was preceded by CSO, AT delays were homogenous and nor mal activation sequence was preserved, Also, whereas with CAO, ARI sho rtened unequally over the ischemic region by as much as 43% at individ ual sites (average of 38.3 +/- 6.8 ms, P < 0.001), with combined CSO a nd CAO, ARI shortening was less pronounced and more homogenous (26.1 /- 5.6 ms, P < 0.05), not exceeding 29% at any site. Thus, in accordan ce with previous findings of enhanced [K+](o) homogeneity, coronary ve nous hypertension reduces the disparities of activation and refractori ness of ischemia attributable, at least in part, to disparate [K+](o) accumulation, Since no collateral blood now improvement could be ident ified, the salutary electrophysiological effects of CSO may reflect a more homogenous extracellular environment, due to preservation of norm al microvascular pressure (P-mv) and sustained filtration and lymph fl ow. (C) 1998 Academic Press Limited.