Monitoring aspirin 100 mg and clopidogrel 75 mg therapy with the PFA-100 device in patients with peripheral arterial disease.

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.

Factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations are not associated with chronic limb ischemia: the Linz Peripheral Arterial Disease (LIPAD) study.

OBJECTIVE: Factor V G1691A (Leiden), prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations are considered risk factors for venous thromboembolism. It remains to be characterized whether the presence of these relatively common mutations poses a risk for peripheral arterial disease (PAD). Therefore, we intended to test, by conducting a case-control study, the hypothesis that PAD was associated with an increased prevalence of factor V G1691A, prothrombin G20210A, and MTHFR C677T mutations. METHODS: The study comprised 433 patients admitted for inpatient diagnostics and treatment of PAD in patients with chronic limb ischemia. Patients with acute ischemia or malignancy were excluded. A total of 433 control subjects matched to the patients with PAD in a 1:1 design by sex, age (+/-2 years), and diabetes mellitus status were recruited. Factor V G1691A, prothrombin G20210A, and MTHFR C677T genotypes were assessed by polymerase chain reaction. RESULTS: For the factor V G1691A polymorphism, the genotype frequencies in PAD patients were 92.8% GG (normal homozygotes = wild type) and 7.2% GA (mutant heterozygotes), and in control subjects they were 94.0% GG and 6.0% GA (chi 2 test; P = .493). The distribution of the prothrombin G20210A genotypes was 96.3% GG (normal homozygotes = wild type) and 3.7% GA (mutant heterozygotes) in PAD patients and was 97.2% GG and 2.8% GA in control subjects (chi 2 test; P = .442). Genotype frequencies for the MTHFR C677T polymorphism were 47.8% CC (normal homozygotes = wild type), 43.4% CT (mutant heterozygotes), and 8.8% TT (mutant homozygotes) in PAD patients, compared with 47.1% CC, 44.1% CT, and 8.8% TT in control subjects (chi 2 test; P = .977). Accordingly, as determined by logistic regression analysis, no significant odds ratios for heterozygous or homozygous genotypes of the three polymorphisms could be observed. CONCLUSIONS: PAD was not associated with an increased prevalence of factor V G1691A, prothrombin G20210A, and MTHFR C677T mutations in the population studied. Thus, there is no indication that of one of these mutations may be a risk factor for chronic limb ischemia. However, the role of these mutations in acute limb ischemia remains to be clarified.

Erythrocyte mean corpuscular volume associated with severity of peripheral arterial disease: an angiographic evaluation.

Elevated erythrocyte mean corpuscular volume (MCV) may be a risk factor for peripheral arterial disease (PAD). The aim of the present study was to evaluate whether MCV was associated with the severity of atherosclerotic findings in the lower limbs of PAD patients, as measured by an angiographic scoring system based on vessel lumen reduction. One hundred male patients with symptomatic PAD were studied. MCV was significantly correlated with the angiographic score (rs = 0.247, p = 0.013). PAD patients with an angiographic score in the lower third were compared to those with values in the upper third using a logistic regression model with age, smoking, hypertension, MCV, homocysteine, and total cholesterol and triglycerides as independent variables. This model revealed significant odds ratios (OR) for MCV (OR = 2.02 for an increment of 5 fl, 95% CI = 1.08-3.8) and for age (OR = 2.41 for an increment of 10 years, 95% CI = 1.21-4.81) and facilitated classification of 71% of all subjects correctly. In conclusion, MCV may be associated with angiographically determined disease severity in patients with PAD. This finding supports the hypothesis that MCV is a risk factor for PAD, although the mechanism by which MCV may contribute to the presence and severity of the disease is not yet determined.