Studies of platelet factor 4 and beta thromboglobulin release during exercise: lack of relationship to myocardial ischemia.

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Abstract
Platelet activation, which results in release of the platelet-specific proteins platelet factor 4 (PF4) and .beta. thromboglobulin (.beta.TG), may participate in exercise-induced myocardial ischemia by the formation of intravascular platelet aggregates or the generation of vasoactive substances such as thromboxane A2. Whether platelet release occurs during exercise-induced myocardial ischemia and its relationship to exercise-induced catecholamine release in 10 normal males (mean age 29 .+-. 6 yr) and 25 males with proved coronary artery disease (mean age 60 .+-. 8 yr) who performed maximal, symptom-limited treadmill exercise tests. None of the subjects took drugs known to modify platelet behavior; 17 coronary artery disease patients took .beta.-blocking agents. Plasma and urine PF4, plasma .beta.TG and plasma catecholamines were measured before and immediately after exercise. Plasma PF4 and .beta.TG were also measured 30 min after exercise. Ischemia, defined as angina or 1 mm or more of horizontal or downsloping ST depression, developed in 14 coronary artery disease patients. In young normal subjects during exercise, plasma PF4 increased from 2.1 .+-. 1.2 at rest to 4.7 .+-. 2.6 ng/ml at maximal exercise (P < 0.01 rest vs. exercise) and plasma .beta.TG increased from 11.7 .+-. 5.4 to 16.7 .+-. 7.7 ng/ml (P < 0.01 rest vs. exercise). Among the 25 coronary artery disease patients, plasma PF4 during exercise increased slightly but significantly, from 2.1 .+-. 1.4 at rest to 2.6 .+-. 2.2 ng/ml at exercise (P < 0.01); plasma .beta.TG did not change significantly, from 13.3 .+-. 6.0 at rest to 14.1 .+-. 5.8 ng/ml during exercise. The small exercise-induced elevations in plasma PF4 and .beta.TG in all 25 coronary artery disease patients were significantly less than those in the 10 young normal subjects (both P < 0.01 vs. normals). Among the subset of 14 coronary artery disease patients with exercise-induced ischemia, neither plasma PF4 nor .beta.TG increased significantly (PF4 from 2.6 .+-. 1.7 at rest to 3.0 .+-. 2.9 ng/ml with exercise; plasma .beta.TG from 13.6 .+-. 6.4 to 14.1 .+-. 7.1 ng/ml). The 14 coronary artery disease patients with ischemia had less exercise-induced elevation in both plasma PF4 and .beta.TG than normal subjects (both P < 0.05). Plasma PF4 and .beta.TG levels 30 min after exercise were not significantly different from rest levels in any subject group. Mean rest, peak exercise and 30-min postexercise plasma PF4 and .beta.TG values did not differ significantly between the 17 coronary disease patients taking .beta.-blocking agents and the 8 coronary disease patients not taking .beta.-blocking drugs. Urinary PF4 did not change significantly with exercise in either normal subjects or in any of the coronary artery disease groups. Among all 35 subjects, exercise-induced increases in plasma epinephrine correlated with increases in plasma PF4 (r = 0.35; P = 0.04) and .beta.TG (r = 0.40; P = 0.02). Increases in norepinephrine did not correlate with either increases in plasma PF4 (r = 0.24, P = 0.2) or .beta.TG (r = 0.23, P = 0.2). Exercise-induced release of plasma PF4 and .beta.TG, as measured by sampling peripheral venous blood, is not a marker of myocardial ischemia. The small elevations in plasma PF4 and .beta.TG induced in normal subjects and in coronary artery disease patients by exercise are nonspecific for myocardial ischemia and may be related to the magnitude of epinephrine release.