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Restenosis in intervened coronaries with hyperhomocysteinemia (RICH)

2003; Elsevier BV; Volume: 146; Issue: 6 Linguagem: Inglês

10.1016/s0002-8703(03)00518-0

1097-6744

Samuel A Kojoglanian, Michael B. Jorgensen, Girma Wolde-Tsadik, Raoul J. Burchette, Vicken Aharonian,

Esophageal and GI Pathology

Controversy exists regarding the contribution made by elevated serum homocysteine evels in raising the risk of restenosis after percutaneous coronary interventions. The objective of this study was to determine whether elevated homocysteine evels increase the risk of restenosis.Two hundred and two consecutive patients undergoing percutaneous coronary intervention with stents on previously nonintervened native coronary arteries were eligible for enrollment in the study. Before the percutaneous coronary intervention, a fasting serum homocysteine evel was drawn. Patients were followed-up by their primary cardiologists for recurrence of symptoms. Those patients who had a recurrence of anginal symptoms consistent with clinical restenosis were referred for a repeat angiogram. All other patients were followed-up medically. The homocysteine evels of the patients who had repeat angiography for recurrent symptoms were compared to those who were followed-up medically.Age, stent ength, stent diameter, and homocysteine evels were all associated with an increased risk of restenosis in the univariate analysis. In the multiple ogistic regression model, the only variable that remained significant in relation to an increased risk of restenosis was homocysteine. There was a significant difference in the mean homocysteine evels between the restenosis group (13.7 micromol/L) and those without restenosis (9.6 micromol/L; P <.0001). A homocysteine evel > or =11.1 micromol/L was identified as the best threshold for an increased risk of restenosis with a sensitivity of 75.0% and specificity of 76.9% (OR 6.5, CI 2.3-18.6; P =.0004).This study demonstrates that elevated homocysteine evels strongly correlate with an increased risk of restenosis.