W observing cytokine changes after percutaneous transvenous mitral valvulotomy (PTMV), 2 potential causes of cytokine expression are found in patients with rheumatic mitral stenosis (MS) and congestive heart failure (CHF): the rheumatic process1–3 and hemodynamic abnormalities.4–9 This study examines the circulating levels of tumor necrosis factor(TNF) and interleukin-6 (IL-6) in these patients, and the response of cytokine levels to treatment with PTMV. • • • The initial sample group included 22 patients presenting at Chung Gung Memorial Hospital (TaoYuan, Taiwan) with an echocardiographic diagnosis of moderate or severe MS (mitral valve area 1.5 cm) and CHF (New York Heart Association functional class II to IV). To avoid left ventricular pressure or volume overload, which proved to be associated with elevated circulating cytokines, patients with coexisting significant valvular lesions (of moderate or greater severity as seen on echocardiography) were excluded. Additionally, patients with diseases associated with elevated serum cytokines, such as infection, malignancy, chronic inflammation, or renal failure, were also excluded. Accordingly, 16 patients were enrolled. All patients underwent PTMV using the Inoue balloon technique, guided by on-line transesophageal echocardioography as previously described.10 The end point of PTMV was attainment of a valve area 1.5 cm, or a significant increase in the severity of mitral regurgitation evaluated by on-line transesophageal echocardiography. All patients were optimally treated with drugs as clinically indicated. Control subjects consisted of 10 ageand gender-matched healthy volunteers who were screened for the absence of organic heart disease or diseases associated with elevated cytokines by history, physical examination, electrocardiography, and echocardiography. The study protocol was approved by our institutional review committee, and written informed consent was obtained from all patients. Echocardiographic parameters were measured in control subjects and in the patient group immediately before catheterization and 6 months after PTMV. The mitral valve area was measured by 2-dimensional planimetry or the pressure half-time method.11,12 The left atrial end-systolic diameter was measured with M-mode echocardiography. The severity of mitral regurgitation was assessed by color flow mapping,13 and left ventricular ejection fraction was measured by Simpson’s rule. Left atrial pressure was measured immediately after the puncture needle entered the left atrium and after the last inflation of the balloon. Blood samples in the patient group were collected from the femoral vein and right atrium during cardiac catheterization before PTMV. Left atrial blood was sampled during PTMV through a Brockenbrough puncture needle immediately after the needle entered the left atrium. Six months after PTMV, samples of peripheral blood were collected by puncturing the antecubital vein. Peripheral blood samples were collected in the control subjects using the same methods as used for the patient group. Blood samples were stored on ice immediately after collection and separated by centrifugation at 1,500 rpm for 15 minutes. Serum was collected, aliquoted, and stored at 70°C until the assay. Commercially available enzyme-linked immunosorbent assay kits (QuantiGlo; RD the Department of Public Health and the Graduate Institute of Clinical Medicine, Chang Gung University, Taipei; and the Division of Cardiology, Cathay General Hospital, Taipei, Taiwan. Dr. Chang’s address is: First Cardiovascular Division, Chang Gung Memorial Hospital, Fu-Shin Road no. 5, Kwei-Shan, Tao-Yuan, Taiwan 333. E-mail: cchijen@adm.cgmh.org.tw. Manuscript received September 17, 2002; revised manuscript received and accepted December 27, 2002.
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