سیتوکین ها و دستگاه ایمنی بدن در نارسایی سیستولیک قلبی: نقش شخصیت نوع D
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|37050||2003||6 صفحه PDF||سفارش دهید||4135 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Brain, Behavior, and Immunity, Volume 17, Issue 4, August 2003, Pages 304–309
The proinflammatory cytokine tumor necrosis factor-α (TNF-α) and its soluble receptors 1 (sTNFR1) and 2 (sTNFR2) are predictors of mortality in chronic heart failure (CHF) but the determinants of these increased levels of disease-promoting cytokines are largely unknown. Type D personality refers to the combination of the tendency to experience negative emotions (negative affectivity) and the tendency to inhibit the expression of emotions in social interaction (social inhibition). Type D is an independent predictor of cardiac events in coronary patients who are at risk for CHF. The present study examined the effect of Type D personality on TNF-α, sTNFR1, and sTNFR2 in 42 men with CHF (Full-size image (<1 K) years). There was a significant multivariate effect of Type D on TNF-α measures (p=.006); i.e., circulating levels of TNF-α (4.8±0.9 versus Full-size image (<1 K), p=.003), sTNFR1 (1814±314 versus Full-size image (<1 K), p=.014), and sTNFR2 (2465±243 versus Full-size image (<1 K), p=.019) were significantly higher in Type D patients as compared to non-Type D patients. The effect size (ES) of Type D personality ranged from rather large (sTNFR1, ES=0.77; sTNFR2, ES= 0.73) to large (TNF-α, ES=0.90). After controlling for ischemic etiology and severity of heart failure, Type D personality emerged as an independent predictor of increased circulating levels of both TNF-α (OR=9.5, 95% CI 2.1–43.8, p=.004) and TNF-α receptors (OR= 6.1, 95% CI 1.4–25.8, p=.014). These findings are consistent with the prognostic power of Type D personality regarding long-term morbidity and mortality in patients with established coronary heart disease. This study suggests that individual differences in personality contribute to the psychoneuroimmunological aspects of heart failure.
This opening quotation is in fact the very last sentence of the closing chapter of Dr. Willem Kop’s innovative work published in 1994. His conclusion was the harbinger for the integration of psychoneuroimmunology with psychosomatic cardiology. A number of reviews in primary journals (Kop, 1999; Rozanski et al., 1999; Ziegelstein, 2001) have provided abundant evidence suggesting that psychological factors may impact on the development and course of acute coronary syndromes. The underlying mechanisms explaining this association include indirect mechanisms such as poor adherence to treatment (Ziegelstein et al., 1998), and more direct physiological mechanisms such as impaired platelet function, decreased heart rate variability, and triggering of myocardial ischemia (Krantz et al., 1996). Lately, immune activation has been proposed as a novel mechanism that may explain the link between emotional distress and acute coronary events (Appels et al., 2000; Ishihara et al., 1999; Kop and Cohen, 2001).