Search

A tool to identify vascular patients who receive antiplatelet therapy nd to distinguish between responders and non-responders to antiplatelet therapy could be of clinical importance. The present observational study was designed to investigate whether the PFA-100 device (Dade Behring) is suitable to detect long-term therapy of aspirin (100 mg/d) and/or clopidogrel (75 mg/d) in a cohort of patients with peripheral arterial disease (PAD). A total of 150 consecutive patients with PAD were studied; 34 patients were excluded from the study due to irregular intake of antiplatelet therapy or due to method limitations. Of the remaining 116 patients, 42 had no antiplatelet therapy, 47 had daily aspirin (100 mg) intake, 19 were administered clopidogrel 75 mg daily, and 10 received a medication with 100 mg aspirin plus clopidogrel 75 mg daily, all for at least 10 days. Nonparametric Kruskal-Wallis test with post hoc comparisons showed that collagen plus epinephrine (CEPI) closure times of the patient group receiving aspirin and the group receiving aspirin plus clopidogrel were similar (p>0.05). In contrast, both patient groups exhibited prolonged CEPI values compared to patients without antiplatelet therapy and patients taking clopidogrel (p<0.001). Finally, both patients without antiplatelet therapy and patients with clopidogrel did not show marked differences with respect to their CEPI values (p>0.05). However, Kruskal-Wallis test results revealed that collagen plus adenosine-5'-diphosphate closure times were not significantly different in all four patient groups (p=0.257). In conclusion, the PFA-100 device may be a suitable tool for monitoring aspirin 100 mg therapy, but it is not appropriate for the detection of clopidogrel administration in its current setup. Although it appears plausible that patients with PAD could benefit from monitoring platelet inhibition, clear evidence for this concept is still lacking.

Elevated serum total homocysteine, an established risk factor for peripheral arterial disease, is influenced by the vitamin B12 and folate status. Since these vitamins are inversely correlated with erythrocyte mean corpuscular volume, an investigation of whether mean corpuscular volume is higher in patients with symptomatic peripheral arterial disease than in healthy subjects was performed. Furthermore, a determination of predictors of increased mean corpuscular volume levels in this population free of symptomatic coronary artery disease, cerebrovascular disease, and diabetes mellitus was carried out. From 469 consecutive patients with symptomatic peripheral arterial disease, 100 fulfilled study inclusion criteria. Peripheral arterial disease was confirmed by angiography. One hundred age-matched subjects without peripheral arterial disease as verified by ankle-brachial index measurements >0.9 served as control subjects. Patients with PAD displayed a significantly higher mean corpuscular volume level (94.5 fl) than control subjects (90.9 fl, p<0.001). Logistic regression analysis showed that current smoking status (p<0.001) and mean corpuscular volume (p=0.009), but not total homocysteine or lipid parameters discriminated case control status. In addition, logistic regression analysis revealed a relationship of mean corpuscular volume with smoking (p=0.001), gamma-glutamyltransferase (p<0.001), and total homocysteine (p=0.012). This model predicted mean corpuscular volume values with an accuracy of 83%. Elevated mean corpuscular volume is a predictor of symptomatic peripheral arterial disease in the sample studied. A deficiency of folate and/or vitamin B12 may be responsible for this observation, as indicated by the correlation of mean corpuscular volume with total homocysteine. Due to the additional association of mean corpuscular volume with smoking and gamma-glutamyltransferase, an unhealthy lifestyle with low vitamin intake may cause elevated mean corpuscular volume values in patients with PAD.