CVD are still the leading cause of death worldwide. Inflammation plays a substantial role in the initiation and propagation of the atherosclerotic process . Coronary artery luminal obstructions and plaque cracks due to atherosclerosis are the most frequent causes of CAD . Apoptosis and necrosis of cardiomyocytes, endothelial cells, and monocytes with severe inflammation are the major causes of vessel damage under CAD. Thus, strategies that repress cell death and manage unsuitable proinflammatory responses are potential therapeutic strategies for improving the clinical prognosis of patients with CAD .
SIRTs are NAD+-dependent histone deacetylases that are implicated in a variety of cellular functions, including cell cycle regulation and cellular metabolism. Among the seven known human sirtuins, SIRT1 is implicated in a wide range of cellular functions .
Baur et al.  proposed a role of SIRT1 in aging and diseases that involve ischemia/reperfusion and neurodegeneration . Hsu et al.  showed that cardiac-specific knockout SIRT1 mice exhibit a significant increment in the size of the risky myocardial infarction area . The authors concluded that SIRT1 has a cardioprotective effect. SIRT1 induces the upregulation of cardioprotective molecules and downregulation of proapoptotic molecules, thereby attenuating oxidative stress, and inhibiting apoptosis. Consequently, the activation of SIRT1 could be a novel method of cardioprotection.
In addition, SIRT1 inhibition causes oxidative stress and inflammation in patients with CAD, whereas the activation of SIRT1 function reverses these atherosclerotic events which may provide new knowledge that is relevant for the management of CAD patients .
Stein and Matter  demonstrated that SIRT1 delays the progression of atherosclerosis by preventing macrophage foam cell formation .
Breitenstein et al.  also found that the SIRT1 expression in monocytes was lower in ACS patients. SIRT1 exerts atheroprotective effects on the vascularity by downregulating the expression of various proinflammatory cytokines and mediating vasodilatation via the actions of eNOS-derived nitric oxide and scavenging reactive oxygen species .
To our knowledge, few studies have assessed the serum level of SIRT1 in patients with CAD [11, 12].
The present study aimed to measure the plasma levels of SIRT1 in CAD patients and to explore its relationship with cardiovascular risk factors.
Our results showed that plasma SIRT1 levels were significantly lower in the UA and AMI groups than in the CCS and control groups. However, the difference between the AMI and CCS groups was not statistically significant, while the plasma SIRT1 level was significantly lower in the CCS group than in the control group. Similar to our results, Doulamis et al.  reported a significantly low level of serum SIRT1 in patients with advanced CAD. Moreover, they noticed an increased prevalence of AMI in patients with low SIRT1 levels .
Another study by Mariani et al.  found that circulating SIRT1 is inversely correlated with epicardial fat thickness, which is a candidate marker of cardiac ischemia. The authors suggested that plasma SIRT1 measurement might provide additional information for risk assessment of CAD, especially in obese people . Low plasma SIRT1 levels in CAD patients may be due to its consumption in preventing the hazards of cardiac ischemia.
Another study reported that the cardiomyocyte-specific deletion of the SIRT1 gene sensitizes the myocardium to ischemia and reperfusion injury , which indicates that changes in SIRT1 may be a cause of cardiac ischemia.
Fry et al.  assessed the SIRT1 level in media other than plasma or serum in CAD patients. The authors found that vascular smooth muscle SIRT1 protects against aortic stiffness, which is a major risk factor for IHD .
Several studies have also reported that SIRT1 expression is reduced in the monocytes of patients with CAD, that the SIRT1 gene plays a protective role against ACS and that the activation of SIRT1 function reverses atherosclerotic events [9, 23, 25].
Interestingly, Li et al.  reported that SIRT1 expression significantly correlates with inflammatory cytokine levels in patients with CAD but not with the severity of coronary lesions .
Yamac and Kilic  noticed a significant increase in SIRT1 levels and expression in CAD patients who received statin therapy and concluded that SIRT1 might have a cardioprotective role after AMI. However, Kilic et al.  previously reported (in 2015) that the protective effect of statin treatment on CVD is through the inhibition of SIRT1 expression.
The present study showed no significant correlation between SIRT1 with age. This can be explained by the limited age range of the participants selected. However, few studies have assessed the negative correlation between SIRT1 and age [30, 31]. Engelfriet et al.  found that the SIRT1 level in blood lymphocytes might be a promising biochemical marker associated with aging .
In our study, there was a significant difference between serum urea and BUN levels between the study groups as they were significantly higher in the AMI group than in the other groups. In agreement with our findings, a prospective study carried out by Horiuchi et al. in 2018 found that BUN and serum urea levels were significantly higher in ACS patients and can be useful predictors of ACS .
We did not notice, however, a significant correlation between plasma SIRT1 levels and blood urea levels. This result is contrary to that obtained by Doulamis et al. , who reported a significant negative correlation .
In our study, serum total cholesterol, TG, and LDL were significantly lower, and HDL was significantly higher in the control group than in the CAD groups. In agreement with our results, Dobiasova and Frohlich  observed an inverse correlation between baseline HDL levels and both cardiovascular and all‐cause death in the general population. Moreover, they found a significant inverse correlation of HDL with LDL particles, which are strongly correlated with the initiation and progression of atherosclerosis . Moreover, Mendivil et al.  associated the risk contributed by LDL to the presence of apolipoprotein C-III .
In our study, there was a significant difference in CK-MB levels between the study groups. These levels were higher in the CAD group. Our results agree with those of Chan et al. , who found that creatine kinase, total cholesterol, and LDL concentrations were higher in CAD patients than in control subjects .
In our study, a significant positive correlation was found between plasma SIRT1 levels and platelet counts. This is similar to the results of Moscardó et al. . The authors demonstrated that the inhibition of SIRT1 was associated with a concentration‐dependent inhibition of the platelet responses, including platelet aggregation, dense granule secretion, and increase in cytosolic calcium levels, suggesting a regulatory role for SIRT1 in platelet responses.
In the present study, the plasma SIRT1 level was also found to be significantly negatively correlated with both cholesterol and TG. These results are congruent with those of Li et al. , who demonstrated that SIRT1 activates liver X receptors (LXRs), which in turn regulate the transfer of cholesterol from peripheral tissues to the liver (reverse cholesterol transport), thereby regulating cholesterol homeostasis .
Differences between our results and those of other studies may be explained by differences in ethnicity, lifestyle, and characteristics of the patients included.