Elevated levels of leukocyte- and blood-MPO are associated with the presence of CAD. These findings support a potential role for MPO as an inflammatory marker in CAD and may have implications for atherosclerosis diagnosis and risk assessment.

ITRIC OXIDE IS A VASODILAtor and inhibitor of platelet aggregation, leukocyte adhesion, and smooth muscle cell proliferation. 1-3 However, under pathological conditions, nitric oxide may be converted into potent nitrating oxidants that promote oxidative damage, cell injury, and conversion of low-density lipoprotein (LDL) into an atherogenic form. 1-5 One pathway for generating nitric oxide-derived oxidants involves interaction with superoxide anion, leading to formation of peroxynitrite. Peroxynitrite is a potent oxidant that promotes nitration of protein tyrosine residues producing a distinctive "molecular fingerprint" for nitric oxide-derived oxidants, nitrotyrosine. 6,7 An alternative mechanism for generating nitric oxide-derived oxidants involves myeloperoxidase, 7-11 a leukocyte-derived enzyme enriched in atherosclerotic lesions that serves as an

Background-Recent studies have supported the hypothesis that calcific aortic stenosis is the product of an active inflammatory process, with similarities to atherosclerosis. We sought to determine whether therapy with hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) might slow the progression of aortic stenosis. Methods and Results-A retrospective study of 174 patients (mean age 68Ϯ12 years) with mild to moderate calcific aortic stenosis was conducted. Patients required normal left ventricular function, Յ2ϩ aortic regurgitation, and Ն2 echocardiograms performed at least 12 months apart. Fifty-seven patients (33%) received treatment with a statin; the remaining 117 (67%) did not. The statin group was older and had a higher prevalence of hypertension, diabetes mellitus, and coronary disease. During a mean follow-up of 21 months, patients treated with statin had a smaller increase in peak and mean gradient and a smaller decrease in aortic valve area. When annualized, the decrease in aortic valve area for the nonstatin group was 0.11Ϯ0.18 cm 2 compared with 0.06Ϯ0.16 cm 2 for those treated with a statin (Pϭ0.03). In multivariate analysis, statin usage was a significant independent predictor of a smaller decrease in valve area (Pϭ0.01) and a lesser increase in peak gradient (Pϭ0.02). Conclusions-Statin-treated patients, despite a higher risk profile for progression, had reduced aortic stenosis progression compared with those not treated with a statin. These data provide justification for a prospective randomized trial to substantiate whether statin therapy slows the progression of aortic stenosis.

Organized left atrial appendage function returns in most patients immediately after cardioversion of atrial fibrillation. However, its function is impaired compared with that before cardioversion. Furthermore, spontaneous echo contrast increased in 7 (35%) of 20 patients after cardioversion. These observations suggest that stunned left atrial appendage function after cardioversion may predispose the chamber to thrombus formation, which may play a role in the mechanism involved in the occurrence of embolization after cardioversion.