Effects of heart rate on hemodynamic severity of coronary artery stenosis in the dog.

In 14 open-chest mongrel dogs, the effects of heart rate on hemodynamic severity of proximal coronary artery stenosis were studied. Stenosis was produced by a circumferential wire snare on left circumflex coronary artery. An intermediate stenosis was defined by reduction of peak reactive hyperemia response to 200% of control flow, a critical stenosis by prevention of any reactive hyperemia flow to a 15-s occlusion. Heart rate was increased stepwise from control to 160 and 200 beats/min by left atrial pacing. In intermediate stenosis, increased pacing rate reduced peripheral coronary pressure distal to the stenosis from 77 +/- 3 to 73 +/- 4 to 65 +/- 3 mm Hg (p less than 0.05) and increased stenosis resistance from 0.30 +/- 0.05 to 0.34 +/- 0.05 to 0.35 +/- 0.05 resistance units (p less than 0.05). In critical stenosis, increased heart rate changed peripheral coronary pressure from 45 +/- 5 to 49 +/- 5 to 48 +/- 5 mm Hg (p less than 0.01) and reduced stenotic resistance from 1.24 +/- 0.19 to 1.08 +/- 0.18 to 1.15 +/- 0.19 resistance units (p less than 0.005). A significant correlation between changes in stenotic resistance and peripheral coronary pressure was obtained (r = -0.71, p less than 0.001). In maximally dilated coronary arteries, a circumferential stenosis decreased circumflex artery flow to 50%. Increased pacing rate up to nearly 200 beats/min raised peripheral coronary pressure distal to the stenosis from 51 +/- 4 to 56 +/- 4 mm Hg (p less than 0.005) and changed stenotic resistance from 0.41 +/- 0.13 to 0.30 +/- 0.06 to 0.33 +/- 0.10 resistance units (p less than 0.05). It is assumed that the changes in peripheral coronary pressure alter the luminal area of the stenosis and hence calculated stenotic resistance. Other possible mechanisms like turbulent streaming, vasomotion or platelet aggregation appear to be of minor importance in the present experimental conditions.