Key result
MEF2A gene variants show no association with premature MI.
Why the study?
The association between MEF2A gene variants and premature myocardial infarction was uncertain and required investigation in a Turkish population.
Are MEF2A gene sequence variants associated with premature myocardial infarction in a Turkish population?
Case-Control (n=156)
Are MEF2A gene sequence variants associated with premature myocardial infarction in a Turkish population?
Absolute Event Rate: 0% vs 0%
This study supports previous evidence indicating no significant association between MEF2A gene variants and premature myocardial infarction.
MEF2A mutations absent in premature MI; leaves open its role and requires larger studies before any clinical consideration.
Myocyte enhancer factor 2 (MEF2) is present in skeletal, cardiac, and smooth muscles and in neurons. MEF2A gene encodes a transcription factor which was on 15q26. The objective was to study the MEF2A gene in patients with premature MI. The control group consisted of 87 subjects who were older than 45 years with no history of cardiovascular disease or MI and no family history of CAD. The premature MI group consisted of 69 patients with documented MI younger than 45 years. No abnormal bands with single strand conformation polymorphism were detected after screening exon 1 through exon 8. This is the first study that detected 145408: T>C polymorphism in intron 10. In both study groups, the rare polymorphism P279L in exon 7, T>C polymorphism in intron 10, and 21-bp deletion in exon 11 of the gene were not found. The data supported the previous studies indicating no association between MEF2A gene and premature MI.
No takes yet. Share an insight, caveat, or question.
Güleç et al. (2007) conducted a case-control in Premature Myocardial Infarction (n=156). MEF2A gene sequence variants vs. Controls without premature MI was evaluated on Presence of MEF2A gene sequence variants (P279L, T>C polymorphism, 21-bp deletion). MEF2A gene sequence variants were not found in either premature MI patients or controls, supporting no association between the MEF2A gene and premature myocardial infarction.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: