Background The ability of the coronary vascular bed to dilateand thus increase blood flow to the myocardium may be impairedin coronary artery disease, even in regions of myocardium suppliedby an angiographically normal coronary artery. If this kindof vasomotor dysfunction was present or accentuated after acutemyocardial infarction, it might influence the extent of ischemiaand necrosis in areas not directly injured by the infarction.
Methods We studied 13 patients (mean [±SD] age, 62 ±11years) with single-vessel coronary artery disease after theyhad received thrombolytic therapy for myocardial infarction.Using positron-emission tomography (PET) with oxygen-15-labeledwater, we measured regional myocardial blood flow under basalconditions and after the intravenous administration of dipyridamole(0.5 mg per kg of body weight over a period of four minutes)8 ±3 days after infarction in all 13 patients (1-weekstudy) and 6 ±2 months after infarction in 9 of the 13(6-month study). On both occasions we measured blood flow bothin the infarcted region and in a region of myocardium that wasremote from the infarcted region and supplied by a normal artery.
Results At the one-week PET study, the coronary vasodilatorresponse (the ratio of the myocardial blood flow after the administrationof dipyridamole to basal blood flow) was 1.12 ±0.50 inthe infarct-related artery and 1.53 ±0.36 in the remoteregion (P = 0.015). At the six-month study, the coronary vasodilatorresponse was 1.42 ±0.37 in the infarcted region and 2.19±0.69 in the remote region (P = 0.004 for the comparisonwith the infarcted region; P = 0.011 for the comparison withthe remote region at the one-week study). The value in remotemyocardium remained lower than that in similar regions in 10control patients, who had single-vessel coronary artery diseasebut no evidence of myocardial infarction (3.17 ±0.72;P = 0.009).
Conclusions After acute myocardial infarction, there is a severevasodilator abnormality involving not only resistance vesselsin infarcted myocardium, but also those in myocardium perfusedby normal coronary vessels. This dysfunction may affect theextent of myocardial ischemia and necrosis after coronary occlusion.
Source Information
From the Division of Cardiology (N.G.U., T.C., D.C.L., G.J.D., A.M.) and the Medical Research Council Cyclotron Unit, Hammersmith Hospital, London (R.S.).
Address reprint requests to Dr. Uren at the Department of Cardiology, Glenfield General Hospital, Groby Rd., Leicester LE3 9QF, United Kingdom.
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