Co-release of cytokines after drug-eluting stent implantation in acute myocardial infarction patients with PCI.

Acute Myocardial Infarction (AMI) after Percutaneous Coronary Intervention (PCI) often requires stent implantation leading to cardiovascular injury and cytokine release. Stent implantation induces cytokines production including TNFα, Hs-CRP, IL-1ß, IL2 receptor, IL6, IL8, and IL10, but their co-release is not extensively established. In 311 PCI patients with Drug-Eluting Stent (DES) implantation, we statistically evaluate the correlation of these cytokines release in various clinical conditions, stent numbers, and medications. We observed that TNFα is moderately correlated with IL-1ß (r2 = 0.59, p = 0.001) in diabetic PCI patients. Similarly, in NSTEMI (Non-ST Segment Elevation) patients, TNFα is strongly correlated with both IL-1ß (r2 = 0.97, p = 0.001) and IL8 (r2 = 0.82, p = 0.001). In CAD (Coronary Artery Disease)-diagnosed patients TNFα is highly correlated (r2 = 0.84, p = 0.0001) with IL8 release but not with IL-1ß. In patients with an increased number of stents, Hs-CRP is significantly coupled with IL8 > 5 pg/ml (t-statistic = 4.5, p < 0.0001). Inflammatory suppressor drugs are correlated as TNFα and IL8 are better suppressed by Metoprolol 23.75 (r2 = 0.58, p < 0.0001) than by Metoprolol 11.87 (r2 = 0.80, p = 0.5306). Increased TNFα and IL-1ß are better suppressed by the antiplatelet drug Brilinta (r2 = 0.30, p < 0.0001) but not with Clopidogrel (r2 = 0.87, p < 0.0001). ACI/ARB Valsartan 80 (r2 = 0.43, p = 0.0011) should be preferred over Benazepril 5.0 (r2 = 0.9291, p < 0.0001) or Olmesartan (r2 = 0.90, p = 0.0001). Thus, the co-release of IL-1ß, IL8 with TNFα, or only IL8 with TNFα could be a better predictor for the outcome of stent implantation in NSTEMI and CAD-diagnosed AMI patients respectively. Cytokine suppressive medications should be chosen carefully to inhibit further cardiovascular damage.

Elevated levels of sIL-2R, TNF-α and hs-CRP are independent risk factors for post percutaneous coronary intervention coronary slow flow in patients with non-ST segment elevation acute coronary syndrome.

To evaluate the association between circulating levels of inflammatory cytokines and the occurrence of post-percutaneous coronary intervention (PCI) coronary slow flow (CSF) in patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS). CSF after PCI commonly occurs and implies poor outcomes, while the determinants of post-PCI CSF in patients with NSTE-ACS remain controversial. In this multicenter case control study, 176 patients diagnosed with NSTE-ACS and with post-PCI CSF occurred composed of CSF group, while 352 matched NSTE-ACS patients composed control group. Corrected thrombolysis in myocardial infarction frame count (cTFC), circulating levels of inflammatory cytokines and PCI related parameters were analyzed using Logistic regression models. Among 528 patients with median age of 67 (59-76) and male proportion of 65.5%, 176 (35.0%) patients had occurrence of post-PCI CSF defined as cTFC ≥ 24. Patients with CSF presented more intense inflammatory activity revealed by higher levels of white blood cell, high-sensitivity C-reactive protein (hs-CRP), interleukin-1ß (IL-1ß), soluble IL-2 receptor (sIL-2R), IL-6, IL-8, IL-10 and tumor necrosis factor-α (TNF-α), while PCI related parameters were comparable. Correlation analysis showed cTFC was positively correlated with those inflammatory cytokines. Logistic regression model indicates that hs-CRP (odds ratio (OR) = 3.038, 95% confidence interval (CI) 1.545-5.975), sIL-2R (OR = 2.103, 95% CI 1.959-4.026) and TNF-α (OR = 3.708, 95% CI 1.426-9.641) were valuable predictors for CSF occurrence. Elevated circulating levels of inflammatory cytokine including hs-CRP, sIL-2R and TNF-α rather than PCI related parameters could predict post-PCI CSF in patients with NSTE-ACS.