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Clinical Investigations: CARDIOLOGY |

Increased Circulating Endothelin-1 in Rheumatic Mitral Stenosis*: Irrelevance to Left Atrial and Pulmonary Artery Pressures

Mien-Cheng Chen; Chiung-Jen Wu; Hon-Kan Yip; Hsueh-Wen Chang; Chien-Jen Chen; Teng-Hung Yu; Wei Chin Hung
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*From the Division of Cardiology (Drs. M-C Chen, Wu, Yip, C-J Chen, Yu, and Hung), Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung; and Department of Biological Sciences (Dr. Chang), National Sun Yat-Sen University, Kaohsiung, Taiwan, Republic of China.

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, Republic of China; e-mail: chenmien@ms76.hinet.net



Chest. 2004;125(2):390-396. doi:10.1378/chest.125.2.390
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Background: Increased plasma endothelin (ET)-1 concentrations have been observed in patients with rheumatic mitral stenosis (MS). However, the mechanisms of increased circulating ET-1 in patients with MS remain unclear.

Methods: We measured plasma concentrations of ET-1 in blood samples from the femoral vein and artery, and right and left atria obtained from 20 patients with moderate-to-severe rheumatic MS before and after percutaneous transluminal mitral valvuloplasty (PTMV) [group 1; 16 patients in chronic atrial fibrillation and 4 patients in sinus rhythm]. In addition, we measured plasma concentrations of ET-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]). Plasma ET-1 concentrations were measured by solid-phase, sandwich enzyme-linked immunosorbent assay.

Results: The peripheral venous plasma concentrations of ET-1 were significantly higher in group 1 patients (2.46 ± 0.90 pg/mL) than in group 2 and group 3 patients (0.74 ± 0.42 pg/mL and 0.99 ± 0.41 pg/mL, respectively [mean ± SD]; p < 0.0001). However, there was no significant difference in the peripheral venous concentrations of ET-1 between group 2 and group 3 patients. In group 1 patients, the plasma ET-1 concentration in the femoral vein (2.46 ± 0.90 pg/mL) was significantly higher than that in the right atrium (2.02 ± 0.69 pg/mL), left atrium (2.11 ± 0.99 pg/mL), and femoral artery (2.05 ± 0.75 pg/mL) [p = 0.0001]. The plasma ET-1 concentration in the femoral vein was not correlated with the mean left atrial pressure (r = 0.05; p = 0.838) and mean pulmonary artery pressure (r = 0.07; p = 0.757). The plasma ET-1 concentration in the left atrium was also not correlated with the mean left atrial pressure (r = 0.11; p = 0.656), mean pulmonary artery pressure (r = 0.06; p = 0.788), or mitral valve area (r = 0.02; p = 0.936). Although the area of mitral valve increased significantly (1.06 ± 0.17 cm2 vs 1.48 ± 0.32 cm2; p < 0.0001), and the mean left atrial pressure (23.0 ± 5.1 mm Hg vs 17.6 ± 5.9 mm Hg; p < 0.0001) and mean pulmonary arterial pressure (31.0 ± 7.9 mm Hg vs 25.5 ± 7.0 mm Hg; p < 0.001) fell significantly and immediately after PTMV, there were no significant changes in the plasma ET-1 concentrations in the femoral vein, right atrium, left atrium, and femoral artery immediately after PTMV.

Conclusion: Increased production of ET-1 in the pulmonary circulation in response to increased pulmonary artery pressure was not the mechanism of increased circulating ET-1 concentration in patients with MS. We proposed that one of the mechanisms of increased ET-1 concentration in the femoral vein was increased peripheral ET-1 release due to increased systemic venous pressure and mechanical damage of the endothelium.

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