Alpha 1-antitrypsin in acute myocardial infarction.

Abstract

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.

Rosuvastatin Alters the Proteome of High Density Lipoproteins: Generation of alpha-1-antitrypsin Enriched Particles with Anti-inflammatory Properties*

“…In fact, the magnitude of the increase of HDL bound A1AT in this study was much greater than changes found in previous studies that examined the effect of various diseases or therapy on lipoprotein proteome (5,15,16). Additionally, A1AT has been shown to be involved in cardiovascular disease by modulating various inflammatory processes (17,18).…”

High density lipoproteins are modulators of protease activity: Implications in inflammation, complement activation, and atherothrombosis

“…In addition, patients with A1AT deficiency are reported to have increased arterial stiffness, indicative of decreased vessel elasticity and an increased risk for CVD (47). Elevations in plasma A1AT were noted in patients following myocardial infarction and, in these patients, greater elevations were correlated with reduced mortality, further supporting a role for this SERPIN in protection against CVD (48). …”

COPD in individuals with the PiMZ alpha-1 antitrypsin genotype

“…During the acute phase response, AAT serum concentrations increase above the normal range [79]. In states of infection or inflammation, neutrophils are recruited into the lungs and the plasma concentration of AAT increases [80,81].…”