We decided to assess the prognostic value of NLRP3 inflammasome level in acute coronary syndrome (ACS) patients and whether it was related to coronary atherosclerotic severity. Study population included one-hundred and twenty-three (123) subjects. Peripheral blood monocyte NLRP3 protein level was correlated with clinical presentation, angiographic characteristics and its scoring systems as well as GRACE and TIMI risk scores. Follow-up for major adverse cardiac events (MACE) was carried out at 180 days. Peripheral blood monocyte NLRP3 was found to be elevated in ACS patients (P < 0.05) and showed positive correlation with GRACE score (r = 0.619), TIMI score (r = 0.580), SYNTAX score (r = 0.550), Clinical SYNTAX score (r = 0.564) and Gensini score (r = 0.516). NLRP3 was also increased with increasing number of vessels, the number of lesions present and the presence bifurcation lesions (P < 0.05). Multivariate Cox regression analysis showed NLRP3 to be an independent predictor of MACE (P = 0.043). Kaplan-Meier analysis and receiver operating characteristic curves for NLRP3 showed good predictive value for MACE. There is a positive correlation of NLRP3 level with severity of coronary atherosclerosis. NLRP3 level is a promising prognostic utility and is efficient in event prediction for MACE.
Introduction: β-blockers and angiotensin receptor blocker (ARB)/angiotensin-converting enzyme inhibitors (ACEI) are well known as critical therapies for improving the prognosis in patients with acute myocardial infarction, however, their use in some case may be limited. We believe that in such cases as when β-blockers and ARB/ACEI use is limited, ivabradine plays a potential role in the improvement of individual prognoses. Case Presentation: A 49-year-old man from Dalian, China. He was diagnosed with acute inferior myocardial infarction in Feb, 2016. And he still experienced palpitations and heart failure after drug treatment and percutaneous coronary intervention (PCI). We used metoprolol at a low dose, although the symptoms were not relieved, β-blockers could not be used or increase dose because of his hypotension. Finally, we chose ivabradine to alleviate the symptoms of the patient related to heart rate and palpitations without affecting blood pressure so as to promote the recovery of heart function. We witnessed a gradual reduction in heart rate (HR) and a gradual increase in blood pressure. Finally, we administered an ARB and increased via titration the dose of ARB and β-blocker. Conclusions: When there are limitations to the use of ARB/ACEI and β-blockers, we can use ivabradine, which reduces HR without affecting blood pressure. Ivabradine can help with the titration of the dose of ARB/ACEI or β-blockers.
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