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SUMMARY Alpha,-antitrypsin serum levels were measured in 48 patients with acute myocardial infarction and in 19 control patients either with coronary heart disease without necrosis, or with neither coronary disease nor inflammation. Alpha,-antitrypsin was significantly raised in the group of patients with acute myocardial infarction. As some patients individually showed no change in alpha,-antitrypsin levels, however, they were divided into two groups according to the maximum serum levels attained. Patients with non-increasing levels of alpha,-antitrypsin showed increased mortality and a higher incidence of cardiogenic shock, whereas reinfarction occurred more frequently in the group with high alpha,-antitrypsin levels. Our findings may suggest that the course ofa myocardial infarction is determined not only by the severity of the ischaemic event, but also by the response of the "acute phase reaction" mechanism. We conclude that a failure of alpha,-antitrypsin levels to increase after myocardial infarction may be associated with a worse clinical course.At normal serum concentrations, alpha,-antitrypsin is a powerful inhibitor of proteolytic enzymes. 2 Since a rise in the plasma levels occurs during tissue injury,34 it is considered to be one of the "acute phase reactant" proteins. The mean plasma levels of alpha,-antitrypsin have been shown to increase after myocardial necrosis. Patients and methods Studies were carried out using sera from 48 patients who were admitted to the intensive cardiac care unit with acute myocardial infarction. The diagnosis of acute myocardial infarction was made when at least two of the following three criteria were present: (a) typical symptoms, (b) new Q waves developed on the electrocardiograph, and (c) increased levels of the serum enzymes, creatine kinase (CK) and aspartate aminotransferase. Patients were received in the intensive cardiac care unit about four hours after the onset of symptoms, and the duration of stay in the unit ranged from two to eight days. The coronary prognostic index of Norris et al.7 was constructed to every patient on admission. Attention was paid to the incidence of the complications of heart failure, hypotension, pericarditis, and cardiogenic shock, according to criteria previously reported.

SUMMARY Serum amyloid A concentrations were determined in serial serum samples of 41 patients with confirmed acute myocardial infarction (10 with acute ischaemia and two with myocarditis). A sharp increase in serum amyloid A concentration was observed early at onset of infarct; it peaked on the third day (up to 2200 fold of normal values) and declined towards normal during the following days, if no complications occurred. Different patterns were observed in patients with acute ischaemia or myocarditis.Although serum amyloid A is not a specific marker, it may, because of its high sensitivity and characteristic patterns of change, represent an additional useful biochemical variable in the diagnosis, follow up, and prognosis of acute ischaemic heart disease.Ischaemic necrosis of the myocardium is a powerful stimulus for activation of the acute phase reaction. This observation has been fully appreciated since the early days when fever, leucocytosis, and increased erythrocyte sedimentation rate were the usual indicators of acute reaction. The rise in fibrinogen after myocardial infarction is a well known phenomenon,1-3 as well as rises in C reactive protein4 s and al-antitrypsin.6 Serum amyloid A, an apolipoprotein of High density lipoproteins, is one of the most sensitive acute phase reactants.7 Its serum concentration increases greatly in response to tissue damage, malignancy, and bacterial or viral disease.8I-I It has been suggested that amyloid A, the main fibrillar protein deposit in secondary amyloidosis, is derived from serum amyloid A by proteolytic cleavage."2 4 The biological function of serum amyloid A is not known; in vitro studies, however, suggest that it may be responsible for the suppression of immune response.' 5 The aim of the present study was to evaluate the behaviour of serum amyloid A concentrations in early and late phases of acute myocardial infarction and acute ischaemia to find out if it can serve as a biochemical indicator in cases in which the known laboratory markers suit neither the clinical situation nor the patient's symptoms.Accepted for publication 23 January 1986 Material and methods Fifty three patients who were admitted to the coronary unit were included in the study. Fifty of these were men, and the mean (SD) age was 59-9 (11 2) years. Forty one patients developed acute myocardial infarction (diagnosed by the presence of at least two of the following three criteria: typical history; development of new Q waves in the electrocardiogram; and a typical rise in the enzyme creatine-P-kinase, glutamate oxaloacetate transaminase and lactic dehydrogenase. Creatine-P-kinase was tested in only 19 of the patients). Of the remaining 12 patients, acute myocardial ischaemia was diagnosed in 10 and myocarditis (probably of viral aetiology) in two. The ischaemic patients included those with chest pain, ST-P changes in electrocardiogram without development of Q waves, and those without an increase of serum enzyme activity.Blood samples were taken on admission and subsequently on the second, t...

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