Background The pathogenesis of unstable angina is poorly understood,and predicting the prognosis is problematic. Evidence suggeststhat there may be active inflammation, possibly in the coronaryarteries, in this syndrome. We therefore studied the prognosticvalue of measurements of the circulating acute-phase reactantsC-reactive protein and serum amyloid A protein, which are sensitiveindicators of inflammation.
Methods We measured C-reactive protein, serum amyloid A protein,creatine kinase, and cardiac troponin T in 32 patients withchronic stable angina, 31 with severe unstable angina, and 29with acute myocardial infarction.
Results At the time of hospital admission, creatine kinase andcardiac troponin T levels were normal in all the patients, butthe levels of C-reactive protein and serum amyloid A proteinwere 0.3 mg per deciliter (exceeding the 90th percentile ofthe normal distribution) in 4 of the patients with stable angina(13 percent), 20 of the patients with unstable angina (65 percent),and 22 of the patients with acute myocardial infarction (76percent). The 20 patients with unstable angina who had levelsof acute-phase reactants 0.3 mg per deciliter had more ischemicepisodes in the hospital than those with levels <0.3 mg perdeciliter (mean [±SD] number of episodes per patient,4.8 ±2.5 vs. 1.8 ±2.4; P = 0.004); 5 patientssubsequently had a myocardial infarction, 2 died, and 12 requiredimmediate coronary revascularization. In contrast, no deathsor myocardial infarction occurred among the 11 patients withlevels of acute-phase reactants <0.3 mg per deciliter, andonly 2 of them required coronary revascularization. Among thepatients admitted with a diagnosis of acute myocardial infarction,unstable angina preceded infarction in 14 of the 22 patients(64 percent) with levels of acute-phase reactants 0.3 mg perdeciliter but in none of the 7 patients with levels <0.3mg per deciliter.
Conclusions Elevation of C-reactive protein and serum amyloidA protein at the time of hospital admission predicts a pooroutcome in patients with unstable angina and may reflect animportant inflammatory component in the pathogenesis of thiscondition. .
Source Information
From the Istituto di Cardiologia (G.L., L.M.B., A.G.R., A.M.) and Istituto di Microbiologia (R.L.G.), Universita Cattolica del Sacro Cuore, Rome; and the Immunological Medicine Unit, Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London (J.R.G., M.B.P.).
Address reprint requests to Dr. Liuzzo at the Istituto di Cardiologia, Universita Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168, Rome, Italy.
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0.3 mg per deciliter (exceeding the 90th percentile of the normal distribution) in 4 of the patients with stable angina (13 percent), 20 of the patients with unstable angina (65 percent), and 22 of the patients with acute myocardial infarction (76 percent). The 20 patients with unstable angina who had levels of acute-phase reactants 
