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Thrombosis in one coronary artery causes generalized coronary vasoconstriction in a dog model of unstable angina
M Mansaray1, J W Hynd, I Vergroesen
1Department of Cardiovascular Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF, UK.
Insights
Thrombosis in one coronary artery increases vascular resistance in another. This suggests unstable angina is a global coronary vascular disease, possibly due to circulating factors or neural reflexes.
Area of Science:
- Cardiovascular Physiology
- Thrombosis Research
- Ischemic Heart Disease
Background:
- Previous studies observed increased resistance downstream from coronary artery thrombus.
- Vasoconstriction of collateral vessels was noted in animal models of unstable angina.
Purpose of the Study:
- To investigate the impact of thrombosis in one coronary artery on the vascular resistance of a non-thrombosed artery.
- To determine if coronary artery thrombosis affects myocardial blood flow in a separate vascular bed.
Main Methods:
- Induced thrombosis in the left circumflex coronary artery (LCx) of 16 beagle dogs.
- Measured myocardial blood flow in the left anterior descending artery (LAD) territory using the radioactive microsphere technique.
- Monitored coronary vascular pressures (arterial to coronary sinus).
Main Results:
- Blood flow to the LAD-supplied myocardium significantly decreased following LCx thrombosis (P = 0.005).
- Coronary vascular resistance in the LAD bed increased significantly (from 147 to 172 mmHg/ml/sec/g, P = 0.02).
- No significant changes in coronary vascular pressures were observed.
Conclusions:
- Coronary artery thrombosis in one vessel can increase vascular resistance in a non-affected artery.
- This effect may be mediated by circulating vasoconstrictors released from the thrombus or neural reflex activation.
- Unstable angina involving coronary thrombosis appears to be a systemic coronary vascular disease.
Abstract:
We investigated the effect of thrombosis in one coronary artery upon the vascular resistance of another coronary artery. In previous investigations, using an animal model of unstable angina, we have observed increased resistance downstream from thrombus within a left circumflex coronary artery (LCx) stenosis and vasoconstriction of collateral vessels from the left anterior descending artery (LAD) supplying the distal LCx vascular bed. In the present paper, we induced thrombosis within a stenosis of the LCx of 16 beagle dogs, and observed the changes in blood flow to the myocardium supplied by the LAD using the radioactive microsphere technique. This blood flow decreased with thrombosis (P = 0.005) in these animals, whereas it did not do so in three time-control experiments. The pressures across the coronary vascular bed, i.e. arterial pressure to coronary venous pressure (coronary sinus catheter), did not change. Thus the vascular resistance of the LAD bed increased significantly from 147 +/- ll.5 mmHg/ml/sec/g of tissue to 172 +/- 13.4 mmHg/ml/sec/g of tissue (P = 0.02). As the LAD territory is not perfused with blood from the artery containing thrombus, we conclude that the effect observed is caused either by release of vasoconstrictors from the thrombus into the general circulation, or by activation of a neural reflex vasoconstriction. The study suggests that unstable angina involving thrombosis in one coronary artery is a global coronary vascular disease.
