The DOI matches its Crossref record.
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.
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Citations
Cited by
Rakusan, K., Flanagan, M. F., Geva, T., Southern, J., & Van Praagh, R. (1992) · Circulation · doi:10.1161/01.cir.86.1.38 · Cited by 327
Antony, I., Nitenberg, A., Foult, J.-M., & Aptecar, E. (1993) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(93)90058-9 · Cited by 147
Coronary flow reserve and myocardial diastolic dysfunction in arterial hypertension
Galderisi, M., Cicala, S., Caso, P., De Simone, L., D’Errico, A., Petrocelli, A., & de Divitiis, O. (2002) · The American Journal of Cardiology · doi:10.1016/s0002-9149(02)02708-x · Cited by 140
The Role of the Autonomic Nervous System in Hypertension.
Amerena, J., & Julius, S. (1995) · Hypertension Research · doi:10.1291/hypres.18.99 · Cited by 63
Coronary microvascular dysfunction
Sucato, V., Novo, G., Saladino, A., Evola, S., & Galassi, A. R. (2020) · Minerva Cardioangiologica · doi:10.23736/s0026-4725.20.05070-7 · Cited by 30
Metadata
- Authors
- Brush, J. E., Cannon, R. O., Schenke, W. H., Bonow, R. O., Leon, M. B., Maron, B. J., & Epstein, S. E.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 1988-11-17
- Volume
- 319
- Issue
- 20
- Pages
- 1302-1307
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2050061293
- Cited by
- 435
- References
- 0
- FWCI
- 13.24
- Type
- journal article
- Language
- en
- Open access
- closed
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