title: Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy.
abstract: When angina occurs in patients with hypertension, it is usually attributed to coronary artery disease or left ventricular hypertrophy. To determine the contribution of coronary microvascular abnormalities to angina in patients with hypertension, we evaluated hypertensive patients without coronary artery disease or left ventricular hypertrophy by measuring the coronary responses to rapid atrial pacing before and after administration of ergonovine. We compared 12 hypertensive patients who had pacing-induced angina with 13 normotensive subjects without such angina. The two groups had similar coronary flow (in the great cardiac vein) at rest; however, pacing increased coronary flow less in hypertensive patients with angina than in normotensive subjects (48 vs. 83 percent; P = 0.05). In the hypertensive patients with angina, pacing after ergonovine increased coronary flow by only 32 percent (as compared with 48 percent before ergonovine; P less than 0.05) and decreased coronary resistance by 15 percent (as compared with 28 percent before ergonovine; P less than 0.05), indicating the presence of ergonovine-induced vasoconstriction. In normotensive subjects, in contrast, cardiac pacing after ergonovine increased coronary flow by 112 percent (P less than 0.001), and its effect on coronary resistance was not different from that of pacing before ergonovine. The hypertensive patients with angina had a significant increase in myocardial oxygen extraction during pacing after ergonovine and less of an increase in myocardial lactate consumption - a response consistent with the presence of myocardial ischemia. Thus, angina in hypertensive patients without epicardial coronary disease may be caused by myocardial ischemia, which appears to be due to an abnormally elevated resistance of the coronary microvasculature.
authors.affiliation: Cardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, Md.
authors.forename: J E
authors.initials: JE
authors.lastname: Brush
authors.forename: R O
authors.initials: RO
authors.lastname: Cannon
authors.forename: W H
authors.initials: WH
authors.lastname: Schenke
authors.forename: R O
authors.initials: RO
authors.lastname: Bonow
authors.forename: M B
authors.initials: MB
authors.lastname: Leon
authors.forename: B J
authors.initials: BJ
authors.lastname: Maron
authors.forename: S E
authors.initials: SE
authors.lastname: Epstein
mesh_terms: D000787:Angina Pectoris / Q000209:etiology*; D002304:Cardiac Pacing, Artificial; D003326:Coronary Circulation; D003327:Coronary Disease / Q000150:complications* / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology; D004874:Ergonovine; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D014655:Vascular Resistance
chemical_list: D004874:Ergonovine