Objectives: The objectives of this study were to examine the time course of the inflammatory response in acute coronary syndromes(ACS) and to assess the markers of inflammation and their relation to disease severity. ...Objectives: The objectives of this study were to examine the time course of the inflammatory response in acute coronary syndromes(ACS) and to assess the markers of inflammation and their relation to disease severity. Methods: We prospectively studied 134 patients with ACS who survived for at least 30 months. The patients were divided into four groups: acute myocardial infarction(MI) with(n=54) or without(n=46) ST-segment elevation and unstable angina with(n=14) or without(n=20) increased risk. Plasma levels of C-reactive protein(CRP), interleukin-6(IL-6), secretory phospholipase A2 group IIA(sPLA2-IIA), and intercellular adhesion molecule-1(ICAM-1) were measured on days 1 and 4 and after 3 and 30 months. Results: The highest levels of CRP and sPLA2-IIA were seen on day 4 but for IL-6 on day 1. These three markers, but not ICAM-1, were significantly related to disease severity, CKMB, and ejection fraction. Patients in Killip class II-IV had higher levels than those in Killip class I. The individual acute-phase responses correlated with marker levels at 3 and 30 months. ICAM-1 correlated with the development of congestive heart failure. Conclusions: In ACS there seems to be an individual predisposition to inflammatory response. Plasma IL-6 is the first marker to rise, while sPLA2-IIA and CRP peak later. All three markers, especially CRP, may discriminate between MI and non-MI. ICAM-1 seems to reflect other aspects of the inflammatory processes than the other markers. The results emphasize the complexity of the inflammatory response in ACS and stress the need for further studies involving multiple markers.展开更多
文摘Objectives: The objectives of this study were to examine the time course of the inflammatory response in acute coronary syndromes(ACS) and to assess the markers of inflammation and their relation to disease severity. Methods: We prospectively studied 134 patients with ACS who survived for at least 30 months. The patients were divided into four groups: acute myocardial infarction(MI) with(n=54) or without(n=46) ST-segment elevation and unstable angina with(n=14) or without(n=20) increased risk. Plasma levels of C-reactive protein(CRP), interleukin-6(IL-6), secretory phospholipase A2 group IIA(sPLA2-IIA), and intercellular adhesion molecule-1(ICAM-1) were measured on days 1 and 4 and after 3 and 30 months. Results: The highest levels of CRP and sPLA2-IIA were seen on day 4 but for IL-6 on day 1. These three markers, but not ICAM-1, were significantly related to disease severity, CKMB, and ejection fraction. Patients in Killip class II-IV had higher levels than those in Killip class I. The individual acute-phase responses correlated with marker levels at 3 and 30 months. ICAM-1 correlated with the development of congestive heart failure. Conclusions: In ACS there seems to be an individual predisposition to inflammatory response. Plasma IL-6 is the first marker to rise, while sPLA2-IIA and CRP peak later. All three markers, especially CRP, may discriminate between MI and non-MI. ICAM-1 seems to reflect other aspects of the inflammatory processes than the other markers. The results emphasize the complexity of the inflammatory response in ACS and stress the need for further studies involving multiple markers.
