Elevated levels of TNF-alpha and IL-6 in the coronary sinus compared to systemic and peripheral veins suggest that the failing myocardium is a major source of proinflammatory cytokines in idiopathic dilated cardiomyopathy.
Myocardial TNF-alpha production may drive inflammation in dilated cardiomyopathy; hypothesis-generating and should not yet change practice.
Proinflammatory cytokines and their receptors are increased in the peripheral blood of patients with heart failure. We measured cytokines and their receptors in systemic artery (SA), coronary sinus (CS) and infra-renal inferior vena cava (IVC), in order to investigate their origin and influential factors. Thirty patients with idiopathic dilated cardiomyopathy were performed echocardiography at admission, and right heart catheterization after stabilization. Blood was drawn from 3 sites for measurement of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and soluble tumor necrosis factor-alpha receptor (sTNFR) I, II. TNF-alpha at CS (3.25 +/- 0.34 pg/mL) was higher than those of SA (1.81 +/- 0.39 pg/mL) and IVC (1.88 +/- 0.38 pg/mL, p<0.05). IL-6 at CS (18.3 +/- 3.8 pg/mL) was higher than that of SA (5.8 +/- 1.2 pg/mL, p<0.01). The levels of sTNFR I, II showed increasing tendency in sequence of SA, IVC and CS. TNF-alpha and sTNFR I, II from all sites were proportional to worsening of functional classes at admission (p<0.05). E/Ea by Doppler study at admission, which reflects left ventricular end-diastolic pressure (LVEDP) was positively correlated with TNF-alpha from SA (R=0.71, p<0.01), CS (R=0.52, p<0.05) and IVC (R=0.46, p<0.05). Thus, elevated LVEDP during decompensation might cause cytokine release from myocardium in patients with idiopathic dilated cardiomyopathy.
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Chang et al. (2003) studied this question.
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