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Articles by E Larose
Total Records ( 2 ) for E Larose
  J Rodes Cabau , O. F Bertrand , E Larose , J. P Dery , S Rinfret , R Bagur , G Proulx , C. M Nguyen , M Cote , M. C Landcop , J. R Boudreault , J Rouleau , L Roy , O Gleeton , G Barbeau , B Noel , J Courtis , G. R Dagenais , J. P Despres and R. DeLarochelliere
 

Background— The presence of moderate saphenous vein graft (SVG) lesions is a major predictor of cardiac events late after coronary artery bypass grafting. We determined the effects of sealing moderate nonsignificant SVG lesions with paclitaxel-eluting stents (PES) on the prevention of SVG atherosclerosis progression.

Methods and Results— Patients with at least 1 moderate SVG lesion (30% to 60% diameter stenosis) were randomized either to stenting the moderate SVG lesion with a PES (n=30, PES group) or to medical treatment alone (n=27, medical treatment group). Patients had an angiographic and intravascular ultrasound evaluation of the SVG at baseline and at 12-month follow-up. The primary end points were (1) the ultrasound SVG minimal lumen area at follow-up and (2) the changes in ultrasound atheroma volume in an angiographically nondiseased SVG segment. Mean time from coronary artery bypass grafting was 12±6 years, and mean low-density lipoprotein cholesterol level was 73±31 mg/dL. A total of 70 moderate SVG lesions (39±7% diameter stenosis) were evaluated. Significant disease progression occurred in the medical treatment group at the level of the moderate SVG lesion (decrease in minimal lumen area from 6.3±3.0 to 5.6±3.1 mm2; P<0.001), leading to a severe flow-limiting lesion or SVG occlusion in 22% of the patients compared with none in the PES group (P=0.014). In the PES group, mean minimal lumen area increased (P<0.001) from 6.1±2.2 to 8.6±2.9 mm2 at follow-up (P=0.001 compared with the medical treatment group at 12 months). There were no cases of restenosis or stent thrombosis. No significant atherosclerosis progression occurred at the nonstented SVG segments. At 12-month follow-up, the cumulative incidence of major adverse cardiac events related to the target SVG was 19% in the medical treatment group versus 3% in the PES group (P=0.091).

Conclusions— Stenting moderate nonsignificant lesions in old SVGs with PES was associated with a lower rate of SVG disease progression and a trend toward a lower incidence of major adverse cardiac events at 1-year follow-up compared with medical treatment alone, despite very low low-density lipoprotein cholesterol values. This pilot study supports further investigation into the role of plaque sealing in SVGs.

Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT002289835.

  E Larose , D Behrendt , S Kinlay , A. P Selwyn , P Ganz and J. C. Fang
 

Background— Transplant coronary arteriosclerosis (TCA) is the principal long-term complication in cardiac transplant recipients. The mediators responsible for vascular proliferation and vasoconstriction typical of TCA remain largely unknown. We tested whether endothelin-1 (ET-1), a potent vasoconstrictor and mitogen, contributes to the pathogenesis and manifestations of TCA.

Methods and Results— BQ-123, an ET-1 receptor-A antagonist, was infused into a coronary artery (40 nmol/min for 60 minutes) of 18 subjects, 6±4 years after transplantation. Vasomotor responses were measured in the infused artery and in a noninfused control artery in patients with (n=10) and without (n=8) advanced TCA (108 total coronary segments). Changes in diameters were compared at 15-minute intervals up to 60 minutes. Contribution of ET-1 to coronary constrictor tone was assessed by comparing vasodilation from BQ-123 with that of the maximal vasodilator nitroglycerin (200-µg intracoronary bolus).

BQ-123 dilated coronary arteries of transplanted patients (8.4% at 60 minutes versus –0.4% in noninfused arteries, P<0.001). Dilation was greater for arteries with advanced TCA defined as diameter stenosis ≥15% (dilation 15.2% with versus 0.6% without advanced TCA, P=0.004). Judged against the response to nitroglycerin, ET-1 accounted for 53.2% of coronary tone in advanced TCA but only 12.9% without advanced TCA.

Conclusions— This study shows for the first time in humans that ET-1 is an important mediator of coronary vasoconstriction in TCA and accounts for >50% of the increased vasomotor tone. Therapeutic targeting of ET-1 may retard the development of TCA.

 
 
 
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