Patients With Glanzmann Thrombasthenia Lacking Platelet Glycoprotein α IIb β 3 (GPIIb/IIIa) and α v β 3 Receptors Are Not Protected From Atherosclerosis

Abstract

Background — Platelets have been suggested to play a role in the early development of atherosclerosis. As one test of this hypothesis, we assessed whether patients with Glanzmann thrombasthenia who lack platelet glycoprotein α IIb β 3 (GPIIb/IIIa) complexes or both α IIb β 3 and the more ubiquitous α v β 3 cell membrane complexes are protected from development of atherosclerosis. Methods and Results — Seven patients with Glanzmann thrombasthenia, 45 to 66 years of age, underwent bilateral carotid artery ultrasonography and screening for risk factors of atherosclerosis. Findings consistent with early atherosclerosis evaluated by measurement of intima-media thickness and presence of atherosclerotic plaques were observed in 6 of the 7 patients. Intima-media thickness values higher than the 75th and 90th percentiles of age- and sex-matched white control subjects of the Atherosclerosis Risk in Communities (ARIC) study were observed in 30 and 8 of 56 carotid artery measurements, respectively. Five of the 6 patients with signs consistent with early atherosclerosis lacked both α IIb β 3 and α v β 3 complexes and 1 only lacked α IIb β 3 . Conclusions — Glanzmann thrombasthenia does not protect affected individuals from development of atherosclerosis.