Abstract

It has been established that renin angiotensin system gene polymorphism, such as angiotensin converting enzyme (ACE), could contribute to a higher occurrence of acute myocardial infarction (AMI). Thus, the objective of this study was to evaluate the effects of the variation of the number of copies of the ACE gene in the AMI. Adult mice, genetically modified to express different concentrations of the ACE were used (one, two and three copies – ACE 1, ACE 2 and ACE 3). The animals were divided into 9 groups (n = 10): 3 without AMI ‐ ACE 1, ACE 2 and ACE 3; 3 infarcted groups assessed 7 days after AMI ‐ ACE 1‐MI7, ACE 2‐MI7 and ACE 3‐MI7; 3 infarcted groups assessed 28 days after AMI ‐ ACE 1‐MI28, ACE 2‐MI28 and ACE 3‐MI28. Infarcted animals were submitted to AMI by ligature of the left coronary artery. Cardiac function by echocardiography, heart rate variability (HRV) and baroreflex sensitivity were evaluated. Regarding the echocardiographic data, the E/A ratio was higher in the ACE group 3‐MI7 than in the non‐infarcted groups with one and two copies of ACE and higher than in the infarcted group with two copies of the ACE gene (ACE 3‐MI7: 3.47 ± 0.50 vs. ACE 1: 1.08 ± 0.14, ACE 2: 1.24 ± 0.16 and ACE 2‐MI7: 1.74 ± 0.25); the fractional area change was lower in the infarcted groups ACE 1‐MI7, ACE 2‐MI7 and ACE 3‐MI7 compared to non‐infarcted and was lower in the ACE group 3‐MI7 than in the ACE groups 2‐MI7 and ACE 1‐MI7 (ACE 3‐MI7: 21,30 ± 1,47 vs. ACE 1‐MI7: 30,10 ± 1,80 and ACE 2‐MI7: 31,12 ± 1,47%). Regarding the autonomic parameters sympathetic modulation was higher in the ACE group 3‐MI7 than in the ACE 1, ACE 2 and ACE 1‐MI7 groups (ACE 3‐MI7: 14.85 ± 2.36 vs. ACE 1: 4.76 ± 2.00, ACE 2: 4.34 ± 1.40 and ACE 1‐MI7: 5.13 ± 1.88 ms2); and the sympatovagal balance was higher in the ACE group 3‐MI7 than in the ACE group 1‐MI7 (ACE 3‐MI7: 2.22 ± 0.17 vs. ACE 1‐MI7: 0.81 ± 0.25). When comparing infarcted groups 7 and 28 days after AMI, it was observed that the baroreflex efficiency index was higher in the ACE group 1‐MI28 than in the infarcted groups assessed 7 days after the infarction (ACE 1‐MI28: 0.28 ± 0.03 vs. ACE 1‐MI7: 0.15 ± 0.02, ACE 2‐MI7: 0.17 ± 0.01 and ACE 3‐MI7: 0.17 ± 0.01). Infarcted animals with 3 copies of the ACE gene had lower survival (41%) and animals with 1 copy of the ACE gene had greater survival (71%) at the end of the study.CONCLUSIONOur results of cardiac function, cardiovascular autonomic function and survival curve indicate that animals with three copies of the ACE gene presented a worse evolution after myocardial infarction in relation to the animals with one copy of the ACE gene.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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