Pathophysiology and Natural History Coronary Artery Disease

نویسندگان

  • DAVID T. KAWANISHI
  • HERBERT J. MEISELMAN
چکیده

We investigated several rheologic variables in 17 patients (11 men, six women, mean age = 52. 1 + 9.8 years) with chronic stable angina. None took any medication except for sublingual nitroglycerin for 2 weeks before the study, and all had angiographically proven coronary artery disease with no history of myocardial infarction. Rheologic measurements included hematocrit, whole blood and plasma viscosity (750 and 1500 sec'), degree of red cell aggregation via the zeta sedimentation ratio, and the extent and rate of red cell aggregation after stasis (Myrenne aggregometer). Compared with normal control donors, salient observations in the patients as a group included: (1) a small (6%) but significant increase in hematocrit, (2) a significant elevation in plasma viscosity (9%), (3) significant increases in whole blood viscosity at both shear rates (14% and 16%), (4) significant increases in the degree (12%), the extent (41 %), and the rate (28% faster time constant) of red cell aggregation, (5) an elevated a2 level (15% increase) and a significantly increased fibrinogen concentration (25% increase), both of which correlated with the enhanced red cell aggregation. Rheologic abnormalities were evident when patients with disease in either one vessel or two to three vessels were compared with controls, but differences between these subgroups of patients were not significant. We conclude that patients with angina have rheologic abnormalities that are compatible with disturbed blood flow and an enhanced tendency for coronary arterial thrombosis. Circulation 76, No. 1, 15-20, 1987. THE RELATIONSHIPS between myocardial function, coronary artery disease, and blood rheology continue to be of interest to both basic science and clinical investigators. Compared with healthy control subjects, previous reports have indicated that patients with angina pectoris and ischemic heart disease (i.e., coronary artery disease) have increased whole blood viscosity,'" 2 plasma viscosity that is unaltered,3'4 or, in the presence of unstable angina, elevated,3 elevated plasma fibrinogen levels,' and either increased' or decreased5 red blood cell flexibility. Lowe et al.4 have reported that patients with twoor three-vessel disease have significantly higher blood viscosity and plasma From the Department of Physiology and Biophysics and the Section of Cardiology, Department of Medicine, University of Southern California School of Medicine, Los Angeles. Supported by NIH Research Grants HL 15722 and HL 15162 and by American Heart Association-Greater Los Angeles Afiliate, Award 537 IG. Address for correspondence: Dr. Herbert J. Meiselman, Department of Physiology and Biophysics, University of Southern California School of Medicine, 2025 Zonal Ave., Los Angeles, CA 90033. Received March 25, 1986; revision accepted April 2, 1987. fibrinogen levels than patients with no or one-vessel disease, whereas the data of Low et al.6 demonstrate differences in blood viscosity but not fibrinogen level in these two patient groups. Although fibrinogen is known to be a major determinant of red cell aggregation7 and thus of the rheologic behavior of human blood.'8'9 only limited data exist with respect to red cell aggregation in coronary artery disease; while patients with significant stenosis of at least one coronary artery have been shown to exhibit increased red cell aggregation, '0 correlations with either fibrinogen levels or the extent of coronary artery disease have not been presented. The present study was thus designed to examine blood rheology in patients with stable angina pectoris as a result of coronary artery disease, with particular emphasis on the extent and dynamics of red cell aggregation. Materials and methods Patients. The patients selected for this study were among those participating in an ongoing long-term study of chronic Vol. 76, No. 1, July 1987 15 by gest on M ay 8, 2017 http://ciajournals.org/ D ow nladed from

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تاریخ انتشار 2005