Circulating Soluble Tumor Necrosis Factor-α and Cell Adhesion Molecules in Patients with Acute Cardiogenic Pulmonary Edema

附分子濃度與發生急性心因性肺水腫之相關性研究

殷偉賢(Wei-Hsian Yin) ； 任勗龍(Hsu-Lung Jen) ； 江孟橙(Meng-Cheng Chiang) ； 黃文彬(Wen-Pin Huang) ； 馮安寧(An-Ning Feng) ； 楊茂勳(Mason Shing Young)

《中華民國急救加護醫學會雜誌》 15卷1期 (2004/03) Pp. 9-19

https://doi.org/10.30018/JECCM.200403.0002

摘要

Background: Circulating soluble tumor necrosis factor-alpha (TNF-α) and cell adhesion molecules (CAMs) are elevated in patients with heart failure. Whether this elevation plays a role in heart failure or is merely a marker of inflammatory response remains to be determined. We hypothesized that TNF-α activated the vascular endothelium, resulting in endothelial dysfunction and permeability changes that may play a role in the development of acute cardiogenic pulmonary edema.
Materials and Methods: We measured plasma levels of TNF-α and three CAMs [vascular cell adhesion molecule-1, (VCAM-1) intercellular adhesion molecule-1, (ICAM-1) and P-selectin] in 35 patients (mean age, 64±14 years) with acute myocardial infarction. Patients who had acute pulmonary edema (APE) were placed in the APE group, and those with no pulmonary edema were placed in the non-APE group. Univariate and multivariate comparisons of the clinical and hemodynamic characteristics and levels of TNF-α and CAMs between these two groups were performed.
Results: The left ventricular ejection fraction was significantly lower (p=0.00l), the left ventricular end-diastolic pressure was significantly higher (p=0.005), and the levels of the TNF-ct and VCAM-1 were also significantly higher (p＜0.0001 and p=0.003, respectively) in the APE group than in the non-APE group. After adjustment for possible adverse baseline variables, circulating levels of TNF-α and VCAM-1 remain significant predictors of the development of APE [hazard ratio (HR) 32.7, p=0.015 and HR 27.6, p=0.048, respectively].
Conclusions: These findings indicated that inflammation and immune activation were associated with the development of acute cardiogenic pulmonary edema.

關鍵字

急性心肌梗塞 ； 急性肺水腫 ； 細胞黏除分子 ； 甲型腫瘤壞死因子

並列摘要

Background: Circulating soluble tumor necrosis factor-alpha (TNF-α) and cell adhesion molecules (CAMs) are elevated in patients with heart failure. Whether this elevation plays a role in heart failure or is merely a marker of inflammatory response remains to be determined. We hypothesized that TNF-α activated the vascular endothelium, resulting in endothelial dysfunction and permeability changes that may play a role in the development of acute cardiogenic pulmonary edema.
Materials and Methods: We measured plasma levels of TNF-α and three CAMs [vascular cell adhesion molecule-1, (VCAM-1) intercellular adhesion molecule-1, (ICAM-1) and P-selectin] in 35 patients (mean age, 64±14 years) with acute myocardial infarction. Patients who had acute pulmonary edema (APE) were placed in the APE group, and those with no pulmonary edema were placed in the non-APE group. Univariate and multivariate comparisons of the clinical and hemodynamic characteristics and levels of TNF-α and CAMs between these two groups were performed.
Results: The left ventricular ejection fraction was significantly lower (p=0.00l), the left ventricular end-diastolic pressure was significantly higher (p=0.005), and the levels of the TNF-ct and VCAM-1 were also significantly higher (p＜0.0001 and p=0.003, respectively) in the APE group than in the non-APE group. After adjustment for possible adverse baseline variables, circulating levels of TNF-α and VCAM-1 remain significant predictors of the development of APE [hazard ratio (HR) 32.7, p=0.015 and HR 27.6, p=0.048, respectively].
Conclusions: These findings indicated that inflammation and immune activation were associated with the development of acute cardiogenic pulmonary edema.

並列關鍵字

acute pulmonary edema ； acute myocardial infarction ； cell adhesion molecules ； tumor necrosis factor-alpha