ABC | Volume 113, Nº1, July 2019

Original Article Kızıltunç et al. Sirtuins in acute myocardial infarction patients Arq Bras Cardiol. 2019; 113(1):33-39 Breitenstein et al. 29 found that peripheral monocyte sirtuin 1 expression was lower in coronary artery disease patients compared to healthy subjects. 29 Judging by our results, this study may arise a debate about the protective functions of circulating sirtuin 1, 3 and 6 in cardiovascular disorders. The first issue is about the association between atherosclerosis and sirtuins. In our study population, median serum sirtuin 1, 3 and 6 levels did not significantly differ between the groups. According to our knowledge, this study is the first one comparing ‘serum’ sirtuin levels between normal coronary artery patients and AMI patients. There exist several studies evaluating sirtuin 1 levels in human atherosclerosis using different methodological manners. Breitenstein et al. 29 measured sirtuin 1 mRNA levels in peripheral monocytes and Gorenne et al. 28 measured sirtuin 1 mRNA and protein expression amount in human carotid endarterectomy materials. 28 While both of these studies found a negative association between atherosclerosis and sirtuin expression, Kilic et al. 30 found that serum sirtuin 1 levels were higher in stable CAD patients than in the control patients. 30 By taking all these data together, the causality between sirtuins and human atherosclerosis needs more investigation. Additionally, we firstly investigated the temporal change of serum sirtuin 1, 3 and 6 levels in the AMI course and did not found any significant change between admission, first and secondday of AMI. Another issue needs to be addressed is the association between inflammation and sirtuin levels. In our study, serum sirtuin 1 and 3 levelswere not correlated and serumsirtuin6 levelswere positively correlatedwith serumCRP levels, awidely accepted inflammatory marker. As we mentioned above, experimental studies suggested that sirtuins have anti-inflammatory effects and this is hypothesized as one of the mechanisms for atheroprotection. 31 We expected to find a negative association between sirtuins and CRP, but the results were not concordant with our hypothesis. Although sirtuin 6 has an anti-inflammatory feature, a possible positive regulatory role for SIRT6 in the induction of pro-inflammatory cytokine expression is evident both in innate and adaptive immune cells. Thus our positive correlation finding between sirtuin 6 and CRP can be interpreted in this context. 32 Figure 1 – Baseline, first day and second day median serum sirtuin levels of the acute myocardial infarction patients. Temporal changes of serum sirtuin 1,3 and 6 were statistically insignificant in acute myocardial infarction course. 3 2 1 2.5 1.5 0.5 0 Sirtuin Levels (ng/ml) Baseline First Day Second Day Sirtuin 1 p = 0.083 Sirtuin 3 p = 0.671 Sirtuin 6 p = 0.465 Sirtuin 1 Sirtuin 3 Sirtuin 6 Table 2 – Clinical and laboratory features of AMI patients (n = 40) Presence of Pre-infarction Angina, n(%) 15(37.5) Time to Perfusion (minutes) 225(120-300) GRACE Score In hospital mortality 126(104-149) 6. month mortality 101(77-124) In hospital MI/mortality 188(151-209) 6. month MI/mortality 148(121-167) Killip Class 1 38(95) 2 1(2.5) 3 1(2.5) TIMI Risk Score 2(1-4) Troponin T Levels(ng/L) Baseline 4.67(1.00-34.27) First day 28.50(7.08-58.70) Second day 14.11(6.46-39.95) Peak 30.18(10.53-63.40) MI Location n(%) Anterior 17(42.5) Inferior 22(55) Lateral 1(2.5) Infarct Related Artery n(%) LAD 18(45) Cx 3(7.5) RCA 19(47.5) Contrast Induced Nephropathy n(%) 4(10) AMI: acute myocardial infarction; Cx: left circumflex artery; LAD: left anterior descending artery; MI: myocardial infarction; RCA: right coronary artery; TIMI: thrombolysis in myocardial infarction. 36