ABC | Volume 110, Nº4, April 2018

Original Article Wang et al Monocyte count and thrombus burden Arq Bras Cardiol. 2018; 110(4):333-338 Table 3 – Hematological parameters of the study population Variable Low thrombus burden (n = 178) High thrombus burden (n = 95) p value White blood cell count ×10 9 /L 9.6 ± 3.0 9.9 ± 3.2 0.326* Neutrophil count×10 9 /L 6.8 ± 2.8 6.9 ± 3.3 0.774* Hemoglobin g/dL 14.4 ± 1.9 14.4 ± 2.3 0.707* Platelet count×10 9 /L 214.3 ± 60.5 218.8 ± 53.8 0.551* Hematocrit % 42.3 ± 4.7 42.2 ± 4.9 0.835* Mean platelet volume fl 10.3 ± 0.8 10.2 ± 0.9 0.668* Lymphocyte count×10 9 /L 2.23 ± 1.94 2.32 ± 1.35 0.827* Monocyte count ×10 9 /L 0.53 ± 0.24 0.61 ± 0.29 0.021* *: Independent samples t-test. micro- and macro-vasculature embolization and is associated with poor outcomes in patients who underwent PPCI of culprit lesion. 6-8 However, management of thrombotic burden is still challenging during PPCI for STEMI. Early risk stratification to detect patients at high risk of high thrombus burden is very important for the individualized prevention and treatment of this condition. In the current study, elevated admission monocyte counts were found as an independent predictor of high thrombus burden of infarct-related artery (IRA) during PPCI in patients with STEMI. Inflammation and oxidative stress were found to play an important role in the pathogenesis of plaque rupture and subsequent thrombus formation. 9,10 Monocyte comprises 10% of human blood leukocytes and is one of the major players of systemic inflammatory response. They are associated with the inflammatory response at the vulnerable plaque in patients with STEMI. 11 Tissue factor (TF) is an essential component of the extrinsic coagulation cascade and is critical in arterial thrombosis. Recent data have suggested that monocytes appear to be the major source of blood TF. 12 Palmerini et al., 13 Table 4 – Independent predictors of high-thrombus burden in patients with ST-elevation myocardial infarction in logistic regression analyses Variable Univariate Multivariate Odds ratio (95%CI) p value Odds ratio (95%CI) p value Age 0.998(0.980–1.016) 0.829 Sex 1.033(0.549–1.943) 0.921 Diabetes mellitus 0.932(0.547–1.588) 0.797 Prior MI 1.869 (0.781–9.178) 0.092 1.745 (0.752–8.644) 0.495 LVEF 0.995 (0.968–1.022) 0.702 Time from symptom onset to PPCI 1.021 (1.008–1.208) 0.094 1.002 (0.979–1.195) 0.553 Creatinine 1 .007 (0.997–1.017) 0.194 Neutrophil count 1.016 (0.935–1.104) 0.704 Hemoglobin 0.998 (0.986–1.010) 0.780 Lymphocyte count 1.019 (0.886–1.173) 0.790 Monocyte count 2.429 (1.022–5.776) 0.045 3.107 (1.199–7.052) 0.020 MI: myocardial infarction; LVEF: left ventricular ejection fraction; PPCI: primary percutaneous coronary intervention. conducted a histological evaluation of thrombi aspirated from coronary arteries of patients with STEMI and found that monocytes consistently stained strongly for tissue factor, while neutrophils had a weakly and irregular tissue factor staining. Another explanation for the relationship between monocytes and high thrombus burden may be the increased formation of monocyte-platelet aggregates (MPA). MPA is a useful marker of platelet activation in ACS patients 14 and was found to be a significant predictor of no-reflow in patients with STEMI undergoing primary PCI. 15 Involvement of monocytes in the prothrombotic state is not restricted to the above-mentionedmechanisms. Aleman et al., 16 showed that microparticles (MPs) from monocytes are associated with prothrombinase activity and faster fibrin formation. Furthermore, monocytes may induce thrombus generation by promoting inflammation processes. Mach et al., 17 found that stimulation of human monocytes induced the expression of interstitial collagenase and stromelysin, which were associated with plaque destabilization and thrombotic events. Post-mortem investigation and histological studies of in 336