To investigate the mechanism by which muscular coronary overbridging can cause myocardial ischaemia, we studied the effect of systolic compression (SC) of the proximal left circumflex coronary artery in ten anaesthetised dogs, with both intact autoregulation and maximally dilated coronary arteries. Systolic compression was produced by a mechanical device adjusted to interrupt circumflex coronary flow only during the aortic ejection period and we measured left ventricular, aortic and distal circumflex coronary pressures, phasic coronary blood flow, regional myocardial blood flow (RMBF), myocardial oxygen consumption (MVO2), and myocardial lactate extraction (MLE). During both autoregulation and maximal coronary vasodilatation, there was a diastolic time lag after SC to restart phasic circumflex coronary blood flow (34 +/- 3 vs 31 +/- 3 ms) and to increase distal circumflex coronary pressure (69 +/- 4 vs 79 +/- 6 ms). With autoregulation, SC reduced the diastolic circumflex coronary: systolic left ventricular pressure time ratio (DPTIc:SPTI) and there were no changes in the other measured variables. During maximal coronary vasodilatation and SC, the coronary vasodilator reserve, the DPTIc:SPTI ratio and the inner:outer myocardial blood flow distribution were decreased in the territory of the left circumflex coronary artery; a linear relationship was observed between the DPTIc:SPTI and the inner:outer myocardial blood flow ratio. Systolic compression during vasodilatation also produced a reduction in myocardial oxygen consumption of the whole heart and a production of lactate in the coronary sinus. These results suggest that myocardial ischaemia with a myocardial bridge is due to the combined effects of a diastolic time lag to repressurise the coronary vascular bed, of tachycardia and of coronary vasodilatation.
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