Temporal Expression of NLRP3 Inflammasome Components in Patients with Acute Coronary Syndrome

<b>Background:</b> Inflammation is a central driver of atherothrombosis, yet the temporal behavior of key inflammasome mediators following acute coronary syndrome (ACS) is not well characterized. The NLRP3 inflammasome, a major regulator of interleukin (IL)-1β activation, has been implicated in plaque destabilization and recurrent cardiovascular risk. This study aims to investigate the temporal expression of NLRP3 inflammasome components in peripheral blood mononuclear cells (PBMCs) of patients with ACS. <b>Methods:</b> In this prospective observational study, PBMCs were collected from 73 patients with ACS during the early in-hospital phase and at 8-12 weeks follow-up. Gene expression of NLRP3, caspase-1, and IL-1β was quantified by qRT-PCR, and fold-change was calculated using the 2^-ΔΔCT method. Associations with clinical and biochemical variables were evaluated using multivariable linear regression. <b>Results:</b> Expression of all measured inflammasome-related genes increased significantly at follow-up compared with baseline: caspase-1 (≈2-fold, <i>p</i> = 0.003), NLRP3 (>10-fold, <i>p</i> < 0.001), and IL-1β (≈4-fold, <i>p</i> < 0.001). Subgroup analyses showed that the post-ACS upregulation of NLRP3, caspase-1, and IL-1β was consistent across STEMI and NSTEMI presentations and was not significantly modified by diabetes status. Caspase-1 fold-change correlated positively with IL-1β, LDL-cholesterol, peak troponin I, and high sensitivity C reactive protein, whereas NLRP3 showed minimal correlations with clinical variables. In multivariable analysis, caspase-1 upregulation was independently associated with STEMI presentation and low-density lipoprotein-cholesterol, and IL-1β with type 2 diabetes. <b>Conclusions:</b> Patients with ACS exhibit significant and persistent upregulation of NLRP3 inflammasome components weeks after the acute event, indicating sustained immune cell priming during recovery. These findings highlight a potential molecular substrate for residual inflammatory risk and support further exploration of inflammasome-targeted therapies in the post-ACS period.