Adaptive mechanisms of arterial and venous coronary bypass grafts to an increase in flow demand

Objective-To compare the mechanisms by which arterial and venous grafts inc rease their flow during pacing induced tachycardia, early and later after c oronary bypass surgery. Design-43 grafts (13 epigastric artery, 15 mammary artery, 15 saphenous vei n) evaluated early (9 (3) days (mean (SD)) after bypass surgery were compar ed with 41 other grafts (15 epigastric, 11 mammary, 15 saphenous vein) eval uated later after surgery (mean 23 months, range 6 to 168 months) by quanti tative angiography and intravascular Doppler velocity analysis during atria l pacing. Controls were 17 normal coronary arteries. Results-Baseline graft flow tended to be lower later after surgery than ear ly (41 (16) v 45 (21) ml/min, NS). Blood flow increased during pacing by 30 (16)% early after surgery, less than later after surgery (+46 (18)%, p < 0 .001) and less than in normal coronary arteries (+54 (27)%, p < 0.001 v ear ly grafts; NS v late grafts). There was no difference between venous and ar terial grafts. No significant vasodilatation was observed during pacing ear ly after surgery in arterial and venous grafts. Later after surgery, signif icant vasodilatation was observed only in arterial grafts (mammary and epig astric grafts), from 2.41 (0.37) to 2.53 (0.41) mm (+5.1% v basal, p < 0.00 1). Early after surgery and in venous grafts later after surgery, the incre ase in flow was entirely due to an increase in velocity. In later arterial grafts, the relative contribution of the increase in velocity to the increa se in flow during pacing was lower in arterial grafts (70 (22)%) than in ve nous grafts (102 (11)%, p < 0.001) and similar to normal coronary arteries (68 (28)%). Conclusions-Early and later after surgery, arterial grafts and venous graft s both increase their flow similarly during pacing. Early arterial grafts a nd venous grafts increase their flow only through an increase in velocity. Later after surgery, arterial grafts act as more physiological conduits and increase their flow in the same way as normal coronary arteries, through a n increase in velocity and calibre mediated by the endothelium.