Changes in platelet size and count in unstable angina compared to stable angina or non-cardiac chest pain.

AIMS An increase in platelet aggregability is associated with unstable angina and myocardial infarction. Platelet size and activity correlate and mean platelet volume was found to be increased before acute myocardial infarction. We measured the mean platelet volume and platelet count in patients with stable angina, unstable angina and non-cardiac chest pain. METHODS AND RESULTS We studied 981 patients (734 men; 247 women) defined clinically as stable angina (n = 688), unstable angina (n = 108) and unstable angina requiring immediate angioplasty (n = 52). After coronary angiography the patients were subdivided into single (n = 269), double (n = 304) and triple-vessel disease (n = 311) and the control group of non-cardiac chest pain (n = 97). There was no significant difference in platelet count between the control group and patients with 1, 2, or 3-vessel disease. However, the platelet size in patients with coronary artery disease was significantly larger (single: 8.7 +/- 1.19 fl; double: 8.7 +/- 1.12 fl; triple-vessel disease: 8.8 +/- 1.18 fl) than the control group (8.2 +/- 0.95 fl) (P < 0.01). Patients with stable angina similarly had no, significant difference in platelet count compared to the control group but did have a significantly increased mean platelet volume (8.7 +/- 1.13; P < 0.01). In contrast, patients with unstable angina had a decreased platelet count (245 +/- 56 x 10/l) compared to either stable angina (262 +/- 62 x 10/l; P < 0.05) or the control group (261 +/- 58 x 10/l; P < 0.05); furthermore, the mean platelet volume (9.4 +/- 1.23 fl) was significantly greater than for stable angina (P < 0.01). Patients with unstable angina requiring immediate PTCA had an even lower platelet count (231 +/- 55 x 10/l) and higher mean platelet volume (10.4 +/- 1.03 fl) (P < 0.01) than the rest of the population with unstable angina. CONCLUSIONS In stable angina the platelet count is unchanged compared to patients with normal coronary arteries but the platelet size is increased. However, in unstable angina there is a decrease in platelet count and an even larger increase in platelet size. We interpret this as meaning that unstable angina might be associated or preceded by an increase in platelet destruction rate that is not completely compensated for by an increase in platelet production rate. The large, more reactive platelets might be causally related to an ongoing coronary artery obstruction in unstable angina.