Effects of previous myocardial infarction on measurements of reactive hyperemia and the coronary vascular reserve

Abstract

The measurement of coronary vascular reserve by the reactive hyperemic response to ischemia has been advocated as a practical method of assessing the physiologic significance of coronary stenoses. Because the concept of measuring coronary blood flow during maximal vasodilation assumes a normal arteriolar network and viable myocardium, the presence of previous myocardial infarction may cause a significant decrease in the coronary reserve unrelated to the severity of a coronary stenosis itself. To determine the potential importance of this effect, rest and hyperemic coronary blood flow were measured in 14 dogs in the regions subtended by the left anterior descending and left circumflex coronary arteries. One hour occlusion of the left anterior descending artery followed by reperfusion was performed in 10 dogs; the 4 remaining dogs in which no occlusion was performed served as control animals (group 3). One week later, rest and hyperemic blood flow measurements were repeated in all 14 dogs. Of the 10 dogs undergoing left anterior descending artery occlusion, 5 had a large infarct (group 1) and 5 had a small infarct (group 2). In group 1 in the 1 week study, both the coronary reserve in the left anterior descending artery zone and the ratio of the coronary reserve in this zone and the left circumflex artery zone decreased compared with values before occlusion (from 425 +/- 134 to 150 +/- 34% and from 1.56 +/- 0.40 to 0.68 +/- 0.31, respectively; both p = 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Coronary Stenosis on Adjacent Bed Flow Reserve

“…[2][3][4][5][6][7][8][9] We used a canine model of LAD stenosis that slightly reduced resting epicardial LAD flow but did not affect LAD bed microsphere flow so that ischemia was not present. We evaluated LCx coronary flow reserve with and without concurrent LAD stenosis using an adenosine A 2A receptorspecific agonist 23 ; thus, hypotension, which might confound the measurement of flow reserve, was avoided.…”

“…[2][3][4][5][6][7][8][9] Wu et al 2 evaluated myocardial perfusion in canines with varying coronary stenosis using radiolabeled microspheres. Similar to our findings, a negative linear relationship was found between stenosis severity and extent of adjacent bed flow reserve reduction, supporting the hypothesis that the coronary stenosis and reduction in adjacent bed flow reserve are causally linked.…”

“…1 In addition to the effects of a stenosis on flow reserve within its own bed, coronary stenosis and occlusion also decrease flow reserve in adjacent nonstenotic beds in both experimental animal models and clinical populations. [2][3][4][5][6][7][8][9] …”

Mean transit time for the assessment of myocardial perfusion by videodensitometry.

“…Inverse appearance time (l/Tapp), Dmax, DmaxlTapp, inverse time of maximal intensity (1I/T), and 1fTmn were calculated and the relations of these parameters to measured flow were investigated. Tm0 proved to be the most reliable parameter for this purpose (r=0.97+0.02; mean± SD), followed by Tmax [26][27][28][29][30][31][32][33][34][35][36] kg) were anesthetized with sodium pentobarbital 25 mg/kg i.v., a left thoracotomy was performed, and epicardial pacing electrodes were sutured on the left atrium. The proximal part of the left circumflex artery (LCx) was gently dissected free, over a distance of 1.0-1.5 cm proximal of the origin of the first large obtuse marginal branch.…”

Protection by superoxide dismutase from myocardial dysfunction and attenuation of vasodilator reserve after coronary occlusion and reperfusion in dog.

“…21 - 23 This reduction in vasodilator reserve may be due to the loss of EDRF, reduction in microvascular cross-sectional area by accumulation of neutrophils, 21 - 22 loss of myocardial function, 23 and to a variety of other factors. The present study was designed to examine if use of a scavenger of superoxide anion, superoxide dismutase (SOD), would modify reperfusion-induced myocardial dysfunction and attenuation of coronary vasodilator reserve in the anesthetized dogs.…”