The angiotensin-converting-enzyme insertion/deletion polymorphism is not a risk factor for peripheral arterial disease.

BACKGROUND: An insertion/deletion (I/D) polymorphism of the gene for angiotensin-converting-enzyme (ACE) is associated with ACE plasma levels and activity. Conflicting results have been reported about the relevance of this polymorphism for atherosclerotic vascular disease. The aim of the present study was to analyze the role of this polymorphism for peripheral arterial disease (PAD). METHODS: The study was designed as a case-control study including 522 patients with documented PAD and 522 sex- and age-matched controls. ACE genotype was determined by size-analysis of polymerase chain reaction products. RESULTS: ACE genotype frequencies were similar between patients (II: 23.4%; ID: 44.8%; DD: 31.8%) and controls (II: 23.8%; ID: 48.3%; DD: 27.9%, P=0.37). The adjusted odds ratio of carriers of the DD genotype for PAD was 1.29 (95% confidence interval 0.95-1.75). The polymorphism was furthermore not associated with age at onset of PAD (P=0.56), Fontaine stage of the disease (P=0.68) or ankle/brachial index of patients (P=0.86). CONCLUSION: The ACE I/D polymorphism is not a significant risk factor for PAD.

Two polymorphisms in the fracalkine receptor CX3CR1 are not associated with peripheral arterial disease.

OBJECTIVE: CX(3)CR1 is a novel chemokine receptor located on monocytes. Recently, two polymorphisms were linked to coronary artery disease (CAD), V249I and T280M. Carriers of at least one I-allele or one M-allele were found less frequently among patients with CAD compared to controls. The aim of the present study was to investigate the influence of these polymorphisms on the development of peripheral arterial disease (PAD). METHODS: 522 human subjects with documented PAD and 522 age and sex matched controls were genotyped by polymerase chain reaction followed by restriction digestion. RESULTS: Adjusted odds ratio (OR) of carriers of the I-allele for PAD was 1.34 (95% confidential interval (CI) from 0.86 to 2.09; P=0.19). The OR associated with the M-allele for PAD was 0.65 (95% CI from 0.41 to 1.04; P=0.07), when tested in the same regression analysis with the V249I genotypes. The genotypes were not linked to age at onset or severity of the disease. A subgroup of 137 CAD patients of whom 131 could be genotyped and who did not differ in baseline parameters from the remaining PAD patients, showed VV-genotype in 52.0%, VI in 42.7% and II in 5.3% CAD (OR associated with the I-allele for CAD: 1.29; 95% CI: 0.66-2.51; P=0.46). The distribution of the T280M genotypes was 67.1, 29.8, 3.1% (TT, TM, MM) also showing no association with CAD (OR=0.77; 95% CI 0.36-1.46; P=0.37). CONCLUSION: In this study we could not detect a difference in genotype frequencies of the V249I and T280M polymorphisms in CX(3)CR1 between PAD patients and controls. CAD concomitant with PAD was also not affected by the I- or the M-allele.

Crimping and repositioning of a maldeployed balloon-expandable arterial stent using a gooseneck snare.

PURPOSE: To describe a technique for repositioning a fully deployed iliac stent from the infrarenal aorta into the common iliac artery (CIA). CASE REPORT: A 58-year-old man was undergoing treatment for a significant right CIA stenosis when a 7x24-mm Palmaz Genesis medium stent was mistakenly deployed in the infrarenal aorta. With the stent still over the guidewire, an 8x60-mm balloon catheter was placed coaxially in the stent. Via a left groin access, a 6-F vascular sheath was introduced retrograde, and a 2.5-cm Amplatz gooseneck snare was advanced into the infrarenal abdominal aorta and pulled back over the stent. The snare was tightly closed to crimp the stent onto the collapsed balloon; this maneuver was repeated several times until the stent was contracted along its entire length. The balloon/stent assembly was carefully pulled back into the right CIA, and the stent was deployed across the target lesion, although there was overlap of the left CIA. Color duplex sonography at 1 year showed no signs of significant iliac arterial stenoses on either side. The patient reported no claudication. CONCLUSIONS: Using a gooseneck snare, fully deployed balloon-expandable iliac stents can be recrimped on a balloon.

Effects of folate treatment and homocysteine lowering on resistance vessel reactivity in atherosclerotic subjects.

Hyperhomocysteinemia is associated with arterial hypertension and endothelial dysfunction in healthy humans. Placebo-controlled vitamin intervention studies cannot distinguish intrinsic actions of homocysteine (tHcy) and folate concentrations on the endothelium. The present two-period crossover study investigates the effects of tHcy lowering through oral folic acid on antioxidant status and resistance vessel reactivity in patients with established coronary artery disease (CAD). We investigated 27 male patients with angiographically documented multivessel CAD aged 50 (range 46-56) years. Resistance vessel reactivity was assessed by measurement of postischemic reactive hyperemia (RH) in the forearm using venous occlusion plethysmography at baseline, after 6 weeks of treatment with 5 mg of oral folic acid, and after a washout period of another 6 weeks. Plasma folate increased 3.49-fold with a mean tHcy reduction of 21.3%. Peak reactivity of resistance vessels improved significantly (18.97-23.60 ml/min(-1) per 100 ml; P = 0.01) with unchanged total antioxidant status (TAS; 0.912-0.944 microM; P = 0.4). This effect was limited to subjects (n = 14) with a tHcy reduction >2 microM (median reduction, 14.4-9.6 microM, P < 0.001). In the 13 subjects with a below-median reduction, tHcy remained unaltered (9.7-9.6 microM, P = 0.88) and TAS increased significantly (0.923-1.055 microM, P = 0.006), whereas RH peak flow was not affected (20.22-22.99 ml/min(-1) per 100 ml, P = 0.28). Homocysteine lowering >2 microM through folic acid supplementation improves resistance vessel reactivity in patients with CAD. Our data support the hypothesis that homocysteine lowering may have intrinsic vasoprotective effects largely independent of folate.