| Summary: | In patients with coronary artery disease, we postulate that dysfunction of the coronary resistive vessels may cause or contribute to myocardial ischaemia. Thus, impaired myocardial perfusion may be due to the abnormal behaviour of collateral and resistive vessels rather than to epicardial disease alone. We propose that this alteration in resistive vessel function occurs, not only in regions subtended by epicardial disease, but is present in remote myocardium and may be altered by coronary intervention such as coronary angioplasty (PTCA) and after myocardial infarction (MI). To investigate coronary resistive vessel function, position emission tomography (PET) may be used to evaluate regional MBF using the flow tracer <SUP>15</SUP>O-labelled water. Using vasodilator (or vasoconstrictor) stimuli, the coronary vasodilator response (CVT=maximal/basal coronary [myocardial] blood flow), an index of coronary resistive vessel function, may be measured and compared in regions of interest and in remote myocardium. In summary, there is coronary resistive vessel dysfunction after PTCA which recovers over 3 months due to acute impairment of the response to dipyridamole and a longer increase in basal flow, possibly due to the previous stenosis. This impairment is not due to altered production or release of NO in the microcirculation. In stable disease, there is both an impaired CVR and altered metabolism during pacing in regions subtended by a normal artery. This remote alteration is impaired acutely by myocardial infarction elsewhere, with only incomplete recovery over at least 6 months. In addition to reduced vasodilator function, resistive vessels in patients with atherosclerosis, have an increased tendency to vasoconstrict to a sympathetic stimulus. Thus, the atherosclerotic process and the sympathetic nervous system may both play a role in determining the degree of resistive vessel dysfunction, which may cause or contribute to myocardial ischaemia in patients with coronary artery disease.
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