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The Journal of Thoracic and Cardiovascular Surgery, Vol 83, 563-568, Copyright © 1982 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Increased regional myocardial perfusion after intracoronary papaverine in patients after coronary artery bypass grafting

S Goldman, R Henry, MJ Friedman, T Ovitt, A Rosenfeld, N Salomon and J Copeland

The objective of coronary artery bypass grafting (CABG) is to increase blood flow to ischemic areas of the myocardium. To determine if this was achieved, anterior wall myocardial perfusion was measured at rest and during intracoronary papaverine (5 mg), with the use of xenon-133 washout in 35 patients. Twelve control patients had no significant diameter narrowing (0% to 25%) of the left anterior descending coronary artery (LAD), 13 patients had greater than 50% narrowing of the LAD, and 10 patients had greater than 50% narrowing of the LAD with patent saphenous vein bypass grafts to the LAD. There was no significant difference in age. LVEDP, and global ejection fraction among the patients. There was no significant difference in anterior wall myocardial perfusion at rest between control subjects (61.0 +/- 3.7 ml/min/100 gm) and non-CABG LAD patients (60.2 +/- 5.4 ml/min/100 gm), or CABG LAD patients (63.4 +/- 4.8 ml/min/100 gm). After coronary arteriolar vasodilatation with papaverine, anterior wall perfusion increased in the CABG patients to 140.6 +/- 6.8 ml/min/100 gm. This was significantly greater (p less than 0.001) than the increase in the non- CABG LAD patients (72.8 +/- 8.1 ml/min/100 gm) but not different from the increase in the control subjects (145.3 +/- 8.4 ml/min/100 gm). In three cases, the same patients were studied before and after CABG with identical results. These data indicate that in patients with coronary disease, increases in myocardial perfusion are limited by the resistance of the proximal stenosis independent of vasodilatation distal to the stenosis. After successful CABG, the patent vein graft restores control of myocardial perfusion to the arteriolar bed.