IL‐6 and IL‐1 receptor antagonist in stable angina pectoris and relation of IL‐6 to clinical findings in acute myocardial infarction

Abstract

Abstract. Gabriel AS, Ahnve S, Wretlind B, Martinsson A (Karolinska Institute and Huddinge University Hospital, Stockholm, Sweden). J Intern Med 2000; 248: 61±66.Objectives. To determine if increased inflammatory activity, as reflected by interleukin-6 (IL-6) and interleukin-1 receptor antagonist (IL-1ra) levels, is present in patients with stable angina pectoris and if IL-6 levels on admission to the coronary care unit in patients with acute myocardial infarction (AMI) are related to heart failure and fever response. Subjects and methods. We studied 28 patients with stable angina pectoris enrolled for coronary angiography, and compared them with sex-and agematched controls. Thirty-four patients with AMI were studied and samples for determination of IL-6 levels were taken on admission within 36 h of onset of symptoms. IL-6 and IL-1ra were determined in serum by enzyme immunoassay. Results. Levels of IL-6 and IL-1ra were higher in patients with stable angina pectoris than in controls (mean 4.6 6 3.6 vs. 3.0 6 2.9 ng L 21 , P , 0.03, and 774 6 509 vs. 490 6 511 ng L 21 , P , 0.01, respectively). IL-6 and IL-1ra levels were not related to angiographic findings. IL-6 levels were high in patients with AMI (38.9 6 75.6 ng L 21 ). Patients with prolonged fever (duration . 4 days) had higher IL-6 levels (94.7 6 138.2 vs. 21.7 6 29.7 ng L 21 , P , 0.05). IL-6 levels were not related to heart failure. Conclusions. Our results indicate that increased inflammatory activity is present not only in acute coronary syndromes, but also in a chronic form of ischaemic heart disease, giving further evidence for a central role of inflammatory processes in coronary artery disease. With regard to AMI, we found increased inflammatory activity in patients with prolonged fever.

Human CRP Gene Polymorphism Influences CRP Levels

“…[2][3][4][5][6][7][8][9][10] In healthy subjects in the steady state, CRP concentrations are 100-to 1000-fold lower than those found during acute infection and inflammation and lie in the range of 0.1 to 10 mg/L. Steady-state CRP concentrations are approximately 2-fold higher in patients with stable coronary heart disease (CHD), 11,12 but when an acute coronary syndrome supervenes, CRP concentrations rise acutely, with the level attained predicting the probability of an additional CHD event in the short to intermediate term. [13][14][15][16][17] CRP is present in atherosclerotic plaques, 18 where it might exert several potential proinflammatory and atherogenic actions that include the binding of oxidized LDL cholesterol, 19 induction of adhesion molecule expression, 20 activation of complement, 18 and stimulation of tissue factor production by monocytes.…”

Altered Atrial Electrical Restitution and Heterogeneous Sympathetic Hyperinnervation in Hearts With Chronic Left Ventricular Myocardial Infarction

“…22 Alternatively, atrial nerve sprouting might result from circulating cytokines and growth factors that become elevated during chronic MI. 25,26 This alternative mechanism is suggested by our demonstration of lack effect of left stellectomy on atrial nerve density.…”

Prevention of Inflammation-Induced Endothelial Dysfunction

“…Furthermore, IL-1ra levels are increased in patients with angina, and specific polymorphisms in the IL-1ra gene are associated with coronary artery disease. 13,14 Studies with IL-1 antagonists would be required to test the causality of these associations. This study does not rule out contribution by other important proinflammatory and anti-inflammatory cytokines, and it is possible that the IL-1ra simply acts as a surrogate marker for some other cytokine or mediator that causes endothelial dysfunction.…”