Document Type : Original Article


1 Pediatric Pulmonology Department, Mofid Children's Hospital, Shahid Beheshti University of medical Sciences, Tehran, Iran.

2 Department of Cardiology, Jahrom University of Medical Sciences, Jahrom, Fars, Iran

3 Student Research Committee, Jahrom University of Medical Sciences, Jahrom

4 Department of Pediatric Cardiology, Mofid Children's Hospital, Shahid Beheshti University of medical Sciences, Tehran, Iran.

5 Department of Cardiology, Shiraz University of Medical Sciences, Shiraz, Fars, Iran

6 Cardiology Department, Jahrom University of Medical Sciences. Jahrom, Fars, Iran



Background: Coronary artery disease (CAD) is a leading cause of myocardial infarction(MI). The etiology is a combination of genetics and environmental factors. The extracellular matrix proteins have a crucial regulatory role in vascular pathologies such as atherogenesis and, therefore, recently appreciated as a target for pharmacotherapy. Thrombospondins (TSP) are extracellular proteins that regulate cell-matrix interactions, and functional responses depend on these interactions. A missense mutation in Thrombospondin-4 (TSP-4) gene is believed to be related to an increased risk of CAD and MI. This study aims to evaluate the effect of rs1866389 guanosine to cytosine (G/C) single nucleotide polymorphism of the thrombospondin-4 gene on the incidence of premature MI in the Iranian population.


This case-control study was done on 100 patients with premature MI, and 100 healthy individuals under 50 years old. DNA was extracted from nucleated blood cells, and Polymerase Chain Reaction (PCR) was performed. The sequence of the TSP-4 gene was investigated. Then the frequency of alleles C (mutated allele) and G (Normal) of the TSP-4 gene were compared between case and control groups.


The results of this study demonstrated that the TSP4 rs1866389 G/C polymorphism was associated with an increased risk of premature myocardial infarction (OR = 1.80; 95% CI = 1.01 to 3.19, P-value=0.043).


The TSP4 rs1866389 G/C SNP increased the risk of premature MI in Iranian population. This finding might be helpful as a target for pharmacotherapy and a genetic marker for early diagnosis of high-risk populations.