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Clinical Investigations: CARDIOLOGY |

Percutaneous Transluminal Mitral Valvuloplasty Reduces Circulating Vascular Cell Adhesion Molecule-1 in Rheumatic Mitral Stenosis*

Mien-Cheng Chen; Hsueh-Wen Chang; Shyh-Shiann Juang; Hon-Kan Yip; Chiung-Jen Wu; Teng-Hung Yu; Cheng-I Cheng
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*From the Division of Cardiology (Drs. Chen, Yip, Wu, Yu, and Cheng), Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung; Department of Biological Sciences (Dr. Chang), National Sun Yat-Sen University, Kaohsiung; and Chia Nan University of Pharmacy and Science (Mr. Juang), Tainan, Taiwan, ROC.

Correspondence to: Mien-Cheng Chen, MD, Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, 123, Ta Pei Rd, Niao Sung Hsiang, Kaohsiung Hsien 83301, Taiwan, ROC; e-mail: chenmien@ms76.hinet.net



Chest. 2004;125(4):1213-1217. doi:10.1378/chest.125.4.1213
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Background: The circulating levels of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), have been demonstrated to be elevated in patients with rheumatic mitral stenosis (MS). However, the impact of percutaneous transluminal mitral valvuloplasty (PTMV) on the elevated circulating levels of VCAM-1 and ICAM-1 in patients with MS has never been investigated.

Methods and results: A total of 19 patients with symptomatic MS undergoing PTMV were studied (group 1) [15 patients in chronic atrial fibrillation, and 4 patients in sinus rhythm]. The plasma levels of soluble VCAM-1 and ICAM-1 in the femoral vein and artery, and right and left atria before PTMV, and those in the peripheral venous blood at the 1-week and 4-week follow-ups after PTMV were determined by solid-phase sandwich enzyme-linked immunosorbent assay. The mitral valve area was calculated by means of the Doppler pressure half-time method. In addition, we measured plasma concentrations of soluble VCAM-1 and ICAM-1 in the peripheral venous blood samples obtained from 22 control patients (including 14 healthy volunteers in sinus rhythm [group 2] and 8 patients in chronic lone atrial fibrillation [group 3]). The plasma level of soluble VCAM-1 was significantly elevated in group 1 patients (1,205.4 ± 462.4 ng/mL [mean ± SD]) compared with group 2 (580.9 ± 208.0 ng/mL) and group 3 patients (716.4 ± 221.6 ng/mL) [p < 0.0001]. In group 1 patients, the plasma levels of soluble VCAM-1 and ICAM-1 in the left atrium did not differ from those in the right atrium, femoral vein, or femoral artery (p = 0.668 for VCAM-1, and p = 0.232 for ICAM-1). The area of mitral valve increased significantly after PTMV (1.08 ± 0.14 cm2 vs 1.48 ± 0.33 cm2, p < 0.0001). The mean left atrial pressure fell significantly after PTMV (22.9 ± 5.2 mm Hg vs 17.7 ± 6.0 mm Hg, p < 0.0001). The peripheral venous plasma level of soluble VCAM-1 obtained before PTMV fell significantly after PTMV (before, 1,205.4 ± 462.4 ng/mL; 1 week after PTMV, 915.7 ± 280.2 ng/mL; 4 weeks after PTMV, 859.0 ± 298.7 ng/mL; p < 0.0001).

Conclusions: In patients with moderate-to-severe MS, the venous plasma level of soluble VCAM-1 fell significantly after PTMV, and the elevated plasma soluble VCAM-1 concentration was associated with hemodynamic abnormality rather than with rheumatic activity.

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