Further investigation of BMP8A using the Genotype Tissue Expression Database revealed multiple variants with nominally significant (P < 0.05) interaction P-values in our EA cohort were significant BMP8A eQTLs in tissue types highlight relevant for PAD such as rs755249 (tibial nerve, eQTL P = 3.6x10-6) and rs1180341 (tibial artery, eQTL P = 5.3x10-6).
The combined presence of DM+CKD may be associated with MAC severity in PAD plaques more so than DM or CKD alone, as illustrated in this study, where levels of calcification mediators BMP-2 and fetuin-A protein were related most robustly to DM+CKD.
Further investigation revealed several variants in BMP genes associated with PAD via an interaction with traffic exposure in both the EA and AA cohorts; this included interactions with non-synonymous variants in BMP2, which is regulated by air pollution exposure.
Lipoprotein apheresis in patients with peripheral artery disease and lipoprotein(a)-hyperlipoproteinemia: 2-year follow-up of a prospective single center study.
The highest ranked hazard ratios for continuous factors in coronary heart disease were those for age, total cholesterol, high-sensitivity troponin, NT-pro-BNP, cotinine, apolipoprotein A, and waist circumference (plus 10 more); in PAD they were age, high-sensitivity C-reactive protein, systolic blood pressure, expired carbon monoxide, cotinine, socioeconomic status, and lipoprotein (a) (plus 5 more).
The LPA gene C93T polymorphism influences plasma lipoprotein(a) levels and is independently associated with susceptibility to peripheral arterial disease.
Moreover, the presence of high levels of lipoprotein(a) and another metabolic risk factor raised the likelihood of PAD symptoms (dyslipidemia and elevated lipoprotein[a]: odds ratio [OR], 29; 95% confidence interval [CI], 6.2 to 136.2; P <.0001; hyperhomocysteinemia and elevated lipoprotein[a]: OR, 37.7; 95% CI, 3.7 to 381.5; P <.0001).
The objective of the study was to determine the association of ABO blood type with ankle brachial index (ABI) as well as prevalent and incident PAD in a multi-ethnic cohort.
The aim of this study was to investigate the association between the transcription factor 7-like 2 gene (<i>TCF7L2</i>) rs7903146 polymorphism and peripheral arterial disease in type 2 diabetes.
Our study showed higher frequency of heterozygous form of Leiden mutation in diabetic patients with unsuccessful outcome of PTA in comparison with patients with successful PTA and diabetic patients without PAD.
In conclusion, we confirmed that fasting B48 is an independent marker of PAD in patients with DM2, unrelated to the preheparin LPL mass, statin therapy or glucose lowering treatment.
Although factor V Leiden is strongly associated with deep venous thrombosis, additional cofactors such as hyperhomocysteinemia may predispose to an increased risk of acute arterial thrombosis in areas of pre-existing peripheral arterial disease.
Two common coding sequence mutations of lipoprotein lipase (serine447-ter, producing a carboxy terminal truncation; and asp9-asn variants) were studied in 329 Caucasian subjects, of whom 243 had angiographic features of premature atheroscelerosis (220 with coronary artery disease; 23 with coronary and peripheral artery disease).
The main objective of this study was to evaluate the levels of VEGF-A/sVEGFR-1 and VEGF-A/sVEGFR-2-presented using a novelty acronym VASCULAR-1 and VASCULAR-2-in patients with IC and CLI, as well as displayed in 4 classes of severity of PAD.
The values of C-reactive protein, white blood cell and neutrophil-to-lymphocyte ratio values were found to be statistically significantly higher in study group versus control group, but none of them were considered as an independent predictor of peripheral arterial disease according to multivariate logistic regression analysis.