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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1703.)
© 2003 American Heart Association, Inc.

Letters to the Editor

Increased Platelet Reactivity Due to Platelet Receptor Polymporphisms? Not in the Real World

Italo Porto; Antonio Maria Leone; Alessandro Sciahbasi; Felicita Andreotti

Dipartimento di Medicina Cardiovascolare, Istituto di Cardiologia, Universitá Cattolica del Sacro Cuore, Roma, Italy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with interest the article by Pontiggia et al,¹ discussing the possible functional implications of double homozygosity for two "prothrombothic" platelet glycoprotein receptor polymorphisms (Pl^A1/A2 of GpIIIa and C807T of GpIa) in a family with a strong history of premature cardiovascular events. We would like to report our experience in 90 stable coronary artery disease (CAD) patients, studied in the "real world" while taking their usual medications, in whom we tried to recognize environmental and genetic determinants of high-shear platelet aggregation, measured by collagen-ADP PFA-100 closure time (mimicking the high-shear conditions of diseased arteries).

Using a multivariate analysis approach, we recorded clinical variables such as age, sex, smoking, diabetes, previous myocardial infarction, and drug therapy, including use of thyenopiridines (aspirin use was not considered as it is known not to influence collagenADP PFA-100 values). We also measured laboratory variables (platelet and white blood cell count, mean platelet volume, cholesterol, triglycerides, von Willebrand factor activity as Ristocetin Cofactor Activity [vWf RCA]) and determined GpIIIa Pl^A1/A2 and GpIa C807T genotypes.

On univariate analysis, increased vWf RCA (r=-0.372, P=0.0001) and platelet count (r=-0.207, P=0.04), reduced triglyceride levels (r=0.318, P=0.002), male sex (89±18 vs 105±23 s, P=0.003) and nonusage of thyenopiridines (84±16 vs 96±20 s, P=0.02) were associated with increased platelet reactivity (ie, reduced PFA-100 closure times). In contrast, the genetic polymorphisms were not. No double homozygotes for the variant genotypes were observed in our population, and double heterozygotes . . . [Full Text of this Article]

Juerg H. Beer; Luca Pontiggia; Riitta Lassila

Department of Medicine (J.H.B., L.P.), Kantonspital Baden, Switzerland; Helsinki University Central Hospital (R.L.), Finland