Introduction: Alpha-1 antitrypsin (A1AT) is known to protect lung tissue from damage. Such protection is extended to myocardial tissues during myocardial ischemia/infarction.
Objective: The aim of the study was to determine the time course of A1AT levels in the plasma of myocardial infarction patients over 96 hours and compare it with healthy individuals.
Methods: Blood samples were collected from patients (n=40, age 58 ± 11 yrs, males 29 and females 11), at 1, 4, 24, 48 and 96 hrs after confirmed diagnosis and admission to King Salman Cardiac Center in King Fahad Medical City, Riyadh, Saudi Arabia. IRB approval and consent was signed by all patients. The patients were divided into diabetics (n=19) and nondiabetic (21). Blood samples were collected in purple top tubes containing EDTA to prevent blood coagulation and immediately centrifuged at 6000 rpm at 4 C for 20 min. Plasma was decanted and stored at - 20 C until analyzed. AlAT was determined in plasma using Eliza kits (abcam, USA). Control blood samples were collected from 20 healthy individuals (age 46±10 yrs.
Results: A1AT were significantly less in MI patients (1025±77 ug/ml at 96 hrs, P<001, n=40) compared to (1655±128 ug/ml, n=20) (mean ±SEM) in controls. Those patients in whom the decrease in A1AT was greater than 50 % of control values, they did not survive and deceased (673+71 ug/ml, approx 40%, n=3). The decrease was significantly greater in nondiabetic patients as compared to diabetics. A1AT after an MI attack was comparable in hypertensive and non-hypertensive and in STEMI and Non-STEMI patients.
Conclusion: A1AT seem to be important in providing some protection to myocardial cells during an MI attack. A1AT levels seem to drop following an MI attack. The drop is larger in nondiabetic as compared to diabetics. In those patients in whom the level of A1AT drops to more than 50 % of normal values they are less likely to survive the MI attack. More studies are needed to confirm the above findings.
S.Y. Khatib: None.
King Fahad Medical City Research Center (016-2018)