Association of plasma homocysteine with restenosis after percutaneous coronary angioplasty.

AIMS: Restenosis after percutaneous coronary angioplasty remains an important limitation of this procedure. This study evaluates whether elevated total plasma homocysteine levels contribute to the development of restenosis after coronary angioplasty. METHODS AND RESULTS: Two hundred and five patients were recruited after successful angioplasty of at least one coronary stenosis (> or =50%). End-points were restenosis (> or =50%) and a composite of major adverse cardiac events. Of the 205 patients, 183 (89.3%) underwent 6 months angiographic follow-up. Patients with restenosis had significantly higher homocysteine levels than those without (10.9+/- 3.9 micromol x l(-1) vs 9.3+/-3.8 micromol x l(-1), P<0.01). Homocysteine levels were significantly correlated to follow-up diameter stenosis (r=0.24, P=0.0001), especially in small vessels (<3 mm) treated with balloon angioplasty only (r=0.40, P<0.0005). Late lumen loss at follow-up was significantly smaller with homocysteine levels below 9 micromol x l(-1) (0.62+/-0.82 mm vs 0.90+/-0.77 mm, P<0.01). Restenosis rate (25.3% vs 50.0%, P<0.001) and major adverse cardiac events (15.7% vs 28.4%, P<0.05) were also significantly lower in patients with homocysteine levels below 9 micromol x l(-1). Multivariate analysis did not weaken these findings. CONCLUSION: Total plasma homocysteine is a strong predictor of restenosis and major adverse cardiac events after coronary angioplasty. Thus, plasma homocysteine appears to be an important cardiovascular risk factor influencing outcome after successful coronary angioplasty.

Common femoral artery anatomy is influenced by demographics and comorbidity: implications for cardiac and peripheral invasive studies.

We assessed the angiographic size of the common femoral artery (CFA) and the influence of demographics and comorbidites. In addition, the location of the CFA bifurcation and the site of femoral puncture were also assessed. Consecutive CFA angiograms (n = 200) were prospectively analyzed. CFA diameter was 6.9 +/- 1.4 mm and length 43.3 +/- 16.2 mm. By multivariate analysis, only diabetes (P < 0.001), female gender (P < 0.0005), and small body surface area (P < 0.01) predicted small vessel size. Vessel length correlated with patient height (P < 0.0005). CFA bifurcation occurred at or below the femoral head center in 98.5%. The femoral puncture was into a vessel other than the CFA in 13%, and 54% of punctures were in a less than ideal anatomical location. In conclusion, the CFA is a relatively small diameter vessel, particularly in diabetics and women. Puncture above the femoral head center and below the superior margin of the acetabulum accurately predicts an ideal puncture site. Thus, routine fluoroscopic guidance should be considered. Cathet Cardiovasc Intervent 2001;53:289-295.

Decreased rate of coronary restenosis after lowering of plasma homocysteine levels.

BACKGROUND: We have previously demonstrated an association between elevated total plasma homocysteine levels and restenosis after percutaneous coronary angioplasty. We designed this study to evaluate the effect of lowering plasma homocysteine levels on restenosis after coronary angioplasty. METHODS: A combination of folic acid (1 mg), vitamin B12 (400 microg), and pyridoxine (10 mg)--referred to as folate treatment--or placebo was administered to 205 patients (mean [+/-SD] age, 61+/-11 years) for six months after successful coronary angioplasty in a prospective, double-blind, randomized trial. The primary end point was restenosis within six months as assessed by quantitative coronary angiography. The secondary end point was a composite of major adverse cardiac events. RESULTS: Base-tine characteristics and initial angiographic results after coronary angioplasty were similar in the two study groups. Folate treatment significantly lowered plasma homocysteine levels from 11.1+/-4.3 to 7.2+/-2.4 micromol per liter (P<0.001). At follow-up, the minimal luminal diameter was significantly larger in the group assigned to folate treatment (1.72+/-0.76 vs. 1.45+/-0.88 mm, P=0.02), and the degree of stenosis was less severe (39.9+/-20.3 vs. 48.2+/-28.3 percent, P=0.01). The rate of restenosis was significantly lower in patients assigned to folate treatment (19.6 vs. 37.6 percent, P=0.01), as was the need for revascularization of the target lesion (10.8 vs. 22.3 percent, P=0.047). CONCLUSIONS: Treatment with a combination of folic acid, vitamin B12, and pyridoxine significantly reduces homocysteine levels and decreases the rate of restenosis and the need for revascularization of the target lesion after coronary angioplasty. This inexpensive treatment, which has minimal side effects, should be considered as adjunctive therapy for patients undergoing coronary angioplasty.

Connexin37 in normal and pathological development of mouse heart and great arteries.

Cx37 is a member of the connexin family of gap junction proteins, whose distribution in heart remains controversial. We have generated novel antibodies against Cx37 to investigate this distribution during normal and pathological development in mouse. Using these affinity-purified antibodies, we have detected Cx37 in hearts and aortas of mouse embryos from day 11 ed. onwards. Immunostaining revealed that during prenatal development Cx37 predominated in endothelial and endocardial cells but was also detectable in small amounts in the trabeculated and compact layers of ventricular myocardium, as well as in the mesenchyme of conotruncal ridges and atrioventricular cushions. Cx37 was also differentially expressed in the ascending and descending portions of the embryonic aorta, according to a pattern which differed in the three layers of the vessel wall. Cx37 distribution was altered in both heart and aorta of mice that had been exposed to all-trans retinoic acid at the beginning of foetal development, whether or not these animals subsequently developed a transposition of great arteries. The data indicate that Cx37 is widely distributed in multiple compartments of cardiovascular system, in patterns which are modulated during development, by retinoic acid.