Why the study?
Adenosine shows contrasting results in preventing periprocedural myocardial infarction (PMI), and the ADORA2A 1976 C>T polymorphism may condition individual response to adenosine and its potential benefits on PMI.
Does the ADORA2A 1976 C>T polymorphism influence the occurrence of periprocedural myocardial infarction in patients undergoing PCI?
Does the ADORA2A 1976 C>T polymorphism influence the occurrence of periprocedural myocardial infarction in patients undergoing PCI?
The ADORA2A 1976 C>T polymorphism is associated with more complex coronary lesions but does not significantly influence the risk of periprocedural myocardial infarction during PCI.
Answers are grounded in this paper and cite their sources.
ADORA2A variant may modulate adenosine response in PCI; hypothesis-generating, needs prospective validation before any clinical use.
AIM: Periprocedural myocardial infarction (PMI), a severe complication of Percutaneous Coronary Intervention (PCI) procedures, has a negative prognostic effect, both at short and long-term follow-up. So far, adenosine's role in preventing PMI has shown contrasting results. A genetic variant of ADORA2A receptor, 1976 C>T, has been suggested as a potential determinant of the interindividual response to adenosine, thus conditioning its potential benefits on PMI. In our study, we investigated whether the ADORA2A 1976 C>T polymorphism is associated with PMI occurrence in patients undergoing coronary stenting. METHODS: The study included consecutive patients undergoing PCI at the Azienda Ospedaliera-Universitaria "Maggiore della Carità," Novara, Italy, between January 2010 and January 2016. Their genetic status was assessed using polymerase chain reaction (PCR) and restriction-fragment-length-polymorphism technique. Myonecrosis biomarkers were measured at intervals from 6 to 48 hours. PMI was defined as CKMB increased 3 times over the Upper Limit of Normal (ULN), or 50% of pre-PCI value; periprocedural myonecrosis was defined as troponin I increased 3 times over the ULN or by 50% of the baseline value. RESULTS: We included 1,104 patients undergoing PCI, 863 (78.2%) of whom carried the ADORA2A T-allele. No difference was found for the main demographic, clinical features, or biochemistry parameters. However, C-carriers had lower statin therapy use (p=0.008) and lower HDL-cholesterol levels (p=0.01). Homozygous C/C patients had more frequent multivessel disease (p=0.03), longer lesions (p=0.01) and Type C lesions (p=0.01), thus requiring more complex procedures. After correction for baseline confounding factors at multivariate analysis, there was no difference in myocardial necrosis according to the ADORA2A genotype (p=0.40). In contrast, PMI tended to increase in the homozygous C/C population (p=0.06), but this trend was attenuated at multivariate analysis after correction for baseline confounding factors (C/C: OR[95%CI]=1.52 [0.88-2.6], p=0.14). CONCLUSIONS: Our study showed that the polymorphism rs5751876 of the ADORA2A receptor is associated with a higher prevalence of complex coronary lesions and multivessel disease. However, it does not significantly influence the occurrence of periprocedural MI or myonecrosis.
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Negro et al. (2020) studied this question.
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