Author + information
- Received September 7, 1982
- Revision received December 7, 1982
- Accepted December 10, 1982
- Published online May 1, 1983.
- Joseph J. Marcella, MD*,
- Allen B. Nichols, MD, FACC1,
- Lynne L. Johnson, MD,
- John Owen, MD,
- Dennis S. Reison, MD, FACC,
- Karen L. Kaplan, MD and
- Paul J. Cannon, MD, FACC
- ↵*Address for reprints: Joseph J. Marcella, MD, Cardiovascular Laboratory, Presbyterian Hospital, 630 West 168 Street, New York, New York 10032.
The hypothesis that exercise-induced myocardial ischemia is associated with abnormal platelet activation and fibrin formation or dissolution was tested in patients with coronary artery disease undergoing upright bicycle stress testing. In vivo platelet activation was assessed by radioimmunoassay of platelet factor 4, beta-thrombo-glob-ulin and thromboxane B2. In vivo fibrin formation was assessed by radioimmunoassay of fibrinopeptide A, and fibrinolysis was assessed by radioimmunoassay of throm-bin-increasable fibrinopeptide B which reflects plasmin cleavage of fibrin I. Peripheral venous concentrations of these substances were measured in 10 normal subjects and 13 patients with coronary artery disease at rest and during symptom-limited peak exercise. Platelet factor 4, beta-thromboglobulin and thromboxane B2concentrations were correlated with rest and exercise catecholamine concentrations to determine if exercise-induced elevation of norepinephrine and epinephrine enhances platelet activation. Left ventricular end-diastolic and end-systolic volumes, ejection fraction and segmental wall motion were measured at rest and during peak exercise by first pass radionuclide angiography. All patients with coronary artery disease had documented exercise-induced myocardial ischemia manifested by angina pectoris, ischemic electrocardiographic changes, left ventricular segmental dyssynergy and a reduction in ejection fraction.
Rest and peak exercise plasma concentrations were not significantly different for platelet factor 4, beta-thromboglobulin, thromboxane B2, fibrinopeptide A and thrombin-increasable fibrinopeptide B. Peripheral venous concentrations of norepinephrine and epinephrine increased significantly (p < 0.001) in both groups of patients. The elevated catecholamine levels did not lead to detectable platelet activation. This study demonstrates that enhanced platelet activation, thromboxane release and fibrin formation or dissolution are not detectable in peripheral venous blood of patients with coronary disease during exercise-induced myocardial ischemia.
↵1 Dr. Nichols is a Senior Investigator of the New York Heart Association, and Dr. Kaplan was a Senior Investigator of the New York Heart Association during the course of this study.
This work was supported in part by U.S. Public Health Service Grants HL-15486, HL-21006 and HL14148 from the National Institutes of Health, Bethesda, Maryland.
- Received September 7, 1982.
- Revision received December 7, 1982.
- Accepted December 10, 1982.
- American College of Cardiology Foundation