Level of circulating phospholipase A2 in prediction of the prognosis of patients with suspected myocardial infarction

Citation
P. Porela et al., Level of circulating phospholipase A2 in prediction of the prognosis of patients with suspected myocardial infarction, BAS R CARD, 95(5), 2000, pp. 413-417
Citations number
17
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
BASIC RESEARCH IN CARDIOLOGY
ISSN journal
03008428 → ACNP
Volume
95
Issue
5
Year of publication
2000
Pages
413 - 417
Database
ISI
SICI code
0300-8428(200010)95:5<413:LOCPAI>2.0.ZU;2-G
Abstract
\Objectives. Atherosclerotic lesions result from inflammatory-proliferative responses of the endothelium and smooth muscle of the arterial wall. Poor prognosis of acute myocardial infarction (AMI) patients has been associated with elevated levels of acute phase proteins including C-reactive protein. We investigated the significance of circulating phospholipase A2 in the lo ng-term prognosis of suspected AMI patients. Methods. The concentration of phospholipase A2 was measured by an immunoassay in sera of 100 suspected AM I patients. Admission phospholipase A2 95 % fractile outliers were excluded to eliminate the effect of acute infectious diseases. The total and athero sclerotic mortalities were followed for a 4-year period. Results. The most powerful prognostic limit for both admission (p = 0.02, RR = 2.6 and 95 % C I = 1.2 to 5.6) and maximal (p = 0.06, RR = 2.4 and 95 % CI = 0.96 to 5.9) phospholipase A2 groups was greater than or equal to8 mug/l. The admission phospholipase A2 level had an independent prognostic significance for ather osclerotic mortality (p = 0.04, RR = 2.4 and CI = 1.02 to 5.8) in multivari ate analysis with CK-MB and age. Conclusions. The elevated serum phospholip ase A2 level at admission is an independent predictor of long-term atherosc lerotic mortality in patients with suspected AMI. The prognostic significan ce of phospholipase A2 weakens during hospitalisation concomitant to the on set of the acute inflammatory response to myocardial injury.