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Prepercutaneous Coronary Intervention Plasma Homocysteine Concentration Is a Useful Predictor of Angioplasty-Induced Myocardial Damage

¹ Department of Cardiology, Hôpital Robert Debré, Reims, France;² Department of Biochemistry, American Memorial Hospital, Hôpital Robert Debré, Reims, France;³ Department of Cardiology, HEGP, Paris, France;⁴ Unité d’Aide Méthodologique à la Recherche Clinique, Hôpital Maison Blanche, Reims, France;

^aaddress correspondence to this author at: Department of Cardiology, Hôpital Robert Debré, Centre Hospitalier Universitaire, 51092 Reims Cedex, France; fax 33-3-2678-4132, e-mail camille.brasselet@wanadoo.fr

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Plasma homocysteine is a modifiable cardiovascular risk factor related to the extent of both coronary and carotid atherosclerosis (1)(2)(3)(4). Plasma homocysteine has been shown to predict the occurrence of cardiac events and mortality in patients with coronary atherosclerosis (5)(6)(7). The predictive value of homocysteine on restenosis after percutaneous coronary intervention (PCI) has been debated (8)(9)(10). Recent evidence, however, indicated that the pre-PCI homocysteine plasma concentration was an independent predictor of death, nonfatal myocardial infarction (MI), and target lesion revascularization (11). Cardiac troponins provide prognostic information in patients with acute coronary syndrome (ACS) (12). Several studies have demonstrated that PCI induces MI as assessed by increases in cardiac troponins, particularly in the case of ACS (13)(14)(15). Furthermore, increased cardiac troponin concentrations after PCI are associated with poor clinical outcome (16)(17)(18)(19). We therefore hypothesized that the pre-PCI plasma homocysteine concentration could be related to the occurrence of MI after PCI, as assessed by changes in plasma cardiac troponin I (cTnI) concentration.

Consecutive admissions for nonemergency PCI were studied prospectively. All patients had a stenosis >70% in 1 or more coronary arteries. Two groups were examined: patients with stable angina (SA) pain and those with ACS. The SA pain group had myocardial ischemia during exercise stress testing (n = 29). The ACS group included patients admitted with unstable angina without a subsequent increase in troponin concentrations (n = 28) and those with a definite MI with a documented cTnI increase and electrocardiogram changes that had occurred 7–14 days previously (n = 39). Patients with inflammatory diseases, as well as those being treated with corticosteroids or . . . [Full Text of this Article]