Bayan Abu al-rub1,*, Said Y Khatib1, Nosayba Z Alazzam1, Sana’a A Jaber2, Issam SM Mokhadder3, Anas Alshannag3, Osama Dweekat3
1Department of Physiology, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan
2Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan
3Medical Student, Jordan University of Science and Technology, Irbid, Jordan
*Corresponding author: Bayan Abu al-rub, Department of Physiology, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan, Tel: 00962780557521, E-mail: [email protected]
Received Date: August 08, 2024
Publication Date: November 09, 2024
Citation: Abu al-rub B, et al. (2024). Blood Level of Alpha-1 Antitrypsin in the Course of Acute Myocardial Infarction. Cardiac. 4(1):9.
Copyright: Abu al-rub B, et al. © (2024).
ABSTRACT
Even though cardiovascular disease is the leading cause of death in the Middle East, studies that evaluated the effect of acute phase reactants such as Alpha-1 Antitrypsin (A1AT) in the course of myocardial infarction (MI) are not enough. The current study aimed to examine the level of A1AT during the first 48 hours after MI. Additionally, to assess if its concentration is affected by some co-morbidities, namely, smoking, hypertension, and diabetes. Blood samples were collected from MI patients at specific time points after admission. Control blood samples were collected from 20 healthy individuals. A1AT was determined in plasma using Enzyme-Linked Immunosorbent Assay (ELISA) kits. All values are expressed as mean and Standard Error of the Mean (mean ± SEM) by unit g/L. There was a significant difference in A1AT concentration between the control group (1.012 g/L ± 0.155 g/L) and the 6-hour sample (1.505 g/L ± 0.11 g/L), (P value of 0.046). There was a significant difference in A1AT concentration in the first sample, between hypertensive MI patients (1.126 g/L ± 0.155 g/L) and non-hypertensive MI patients (1.740 g/L ± 0.124 g/L) P<0.05. There was a difference between smokers (1.321 g/L, 1.310 g/L) and non-smokers (1.726 g/L, 1.438 g/L) in 12-hour and 24-hour samples respectively, but this difference doesn’t reach a significant level. We concluded that A1AT concentration increases during acute MI, as it is one of the acute phase reactants. Moreover, A1AT levels differ between patients with different comorbidities. Our findings suggest that A1AT response during acute MI is affected by the presence or absence of smoking or hypertension (HTN).
NEW & NOTEWORTHY
A1AT concentration significantly increased during the first hours after acute Myocardial Infarction (MI) compared to the control group. During the first 6 hours after MI, A1AT concentration was significantly higher in non-hypertensives than hypertensives. Regarding the ratio of A1AT concentration in our MI patients to the control group, it is higher in non-smokers compared to smokers during the whole period of our study and higher in non-hypertensives compared to hypertensives during the first 12 hours of our study.
Keywords: Alpha-1 Antitrypsin, Cardiovascular Disease, Acute Myocardial Infarction, Smoking, Hypertension, Diabetes