Relationship between minor myocardial damage and inflammatory acute-phase reaction in acute coronary syndromes.

Abstract

In severe acute coronary syndromes (ACS) elevation of markers of inflammation and acute phase reaction (APR) like C-reactive protein (CRP) as well as a release of troponin have been reported. Using a high sensitivity troponin T (TnT) test we investigated whether an APR occurs in ACS only in the presence of ischemic myocardial damage. In 85 patients with ACS C-reactive protein (CRP), serum amyloid A (SAA), fibrinogen, thrombin antithrombin III complexes (TAT) and kallikrein were determined vs. high sensitive TnT (> or =0.02 ng/ml) initially and 2 d later vs. 45 patients with stable angina pectoris and 42 controls. In stable angina pectoris, markers of inflammation and coagulation were slightly elevated (p < 0.05). Initially in ACS elevations of CRP to 1.2 +/- 0.3 mg/dl, SAA to 4.8 +/- 2.6 mg/dl and fibrinogen to 448 +/- 21 mg/dl (all p < 0.01 vs. controls) were found followed by a significant APR (p < 0.01). In the subgroup of TnT positive ACS patients, an APR with increased CRP (4.1 +/- 1.3 mg/dl), SAA (20.4 +/- 8.3 mg/dl), and fibrinogen (641 +/- 45 mg/dl) was detectable (all p < 0.05 vs. TnT negative patients). In contrast, patients without TnT release showed APR markers comparable to patients with stable angina pectoris. Our findings demonstrate an association between myocardial injury in ACS and acute phase reaction as evidenced by several molecular markers. A highly sensitive TnT-test identified myocardial injury in about all patients with APR while a standard TnT cut-off (0.1 ng/ml) missed 32% of these patients. Thus, the APR in patients with ACS is strongly associated with at least minor ischemic myocardial damage and prior findings of an APR independent from myocardial injury are probably based on less sensitive troponin tests.