C-reactive protein elevation independently influences the procedural success of percutaneous balloon mitral valve commissurotomy Richard A. Krasuski, MD, a Anneke Bush, PhD, a Joseph E. Kay, MD, b Charles E. Mayes, Jr, MD, b Andrew Wang, MD, b Judy Fleming, c Cynthia Pierce, RN, b Katherine B. Kisslo, RDCS, b J. Kevin Harrison, MD, b and Thomas M. Bashore, MD b Lackland AFB, Tex, and Durham, NC Background Markers of systemic inflammation including C-reactive protein (CRP) appear to predict morbidity and mortality in various clinical conditions. The presence of systemic inflammation and its impact on the procedural success of percutaneous balloon mitral valve commissurotomy (PBMC) in patients with rheumatic mitral stenosis has not been previ- ously demonstrated. Methods Measurements of CRP with a high-sensitivity assay were performed at the time of PBMC or during post- procedural follow-up in 119 patients with mitral stenosis of rheumatic morphology. Patients were questioned to exclude confounders of CRP elevation and categorized into undetectable (0.10 mg/L) and detectable (0.10 mg/L) CRP levels. Detectable levels were further classified into assay range (0.10 and 6.0 mg/L) and elevated (6.0 mg/L). Results CRP was detectable in 76% of patients and elevated (6.0 mg/L) in 36% of patients studied. Procedural suc- cess occurred in 89% of patients with undetectable CRP, as compared with only 67% in patients with detectable CRP (P = .028). This effect remained after controlling for age and valve score (previously described predictors of PBMC success). Conclusions Systemic inflammation is common in patients with rheumatic mitral valve stenosis, and the relationship between procedural success and CRP suggests persistent inflammation may affect the results of PBMC. (Am Heart J 2003; 146:1099-104.) Systemic inflammation plays an important role in the pathogenesis and outcomes of many diverse disease processes. Elevations in levels of C-reactive protein (CRP), a serologic marker of acute and chronic inflam- mation, correlate well with overall vascular disease burden 1 and appear to predict future adverse events in patients with coronary disease, end-stage renal disease, and cancer. 2–7 Recent studies have demonstrated evi- dence of active inflammation in pathologic specimens of excised, calcific aortic valves. 8 In addition, Galante and colleagues found elevated levels of CRP in patients with calcific aortic valves, 9 and statin therapy, which is known to decrease CRP levels, may slow the pro- gression of calcific aortic stenosis. 10 Rheumatic valvu- lar disease, however, differs from calcific lesions be- cause of a more obvious inciting event (rheumatic carditis). Previous epidemiological studies have defined a close relationship between streptococcal infection and rheumatic fever. Despite these accepted tenets, some uncertainties remain about the etiology of mitral stenosis. In particular, it is uncertain whether the in- flammation associated with the acute infection and the subsequent healing process is only short-lived, or whether it is persistent and an important factor in dis- ease progression. Prominent leukocyte infiltration and evidence of ac- tive inflammation has been previously noted in patho- logical specimens of excised rheumatic mitral valves. 11 This is similar to other systemic lesions including ath- erosclerosis, in which an active inflammatory process is presumed to be critical to disease progression and clinical complications. 12,13 Animal models of athero- genesis suggest a possible role for the cumulative ef- fects of multiple systemic infections, 14 and the extent to which they may contribute to mitral stenosis has yet to be defined. In addition, certain human leukocyte From the a Division of Cardiology, Wilford Hall Medical Center, United States Air Force, Lackland AFB, Tex, b Division of Cardiology, Department of Medicine, and the c Clinical Immunology Laboratory, Duke University Medical Center, Durham, NC. The opinions or assertions contained within this article are those of the individual au- thors and not of the US Department of the Air Force or the US Department of Defense. Guest Editor for this manuscript was Blase A. Carabello, MD, Baylor University, Hous- ton, Tex. Submitted December 2, 2002; accepted June 10, 2003. Reprint requests: Richard A. Krasuski, MD, Division of Cardiology, Wilford Hall Medi- cal Center, Lackland AFB, TX 78236-5300. E-mail: richard.krasuski@lackland.af.mil © 2003, Mosby, Inc. All rights reserved. 0002-8703/2003/$30.00 + 0 doi:10.1016/S0002-8703(03)00506-4