High-dose statin therapy in AMI patients reduced clot lysis time from 126 to 114 min (P=0.022) at 6 months, with the reduction independently predicted by baseline OCT lesion volume (P<0.001).
Cohort (n=100)
Does high-dose statin therapy reduce clot lysis time and is this reduction associated with OCT lipid plaque parameters in statin-naive patients with acute myocardial infarction?
In statin-naive patients with acute myocardial infarction, the reduction in clot lysis time following 6 months of high-dose statin therapy is independently associated with baseline OCT lipid plaque parameters.
Absolute Event Rate: 114% vs 126%
p-value: p=0.022
Abstract Background Statins are the most important lipid-lowering drugs in acute myocardial infarction (AMI). The additional effects of statins traditionally defined as independent of cholesterol-lowering actions, encompass suppression of blood coagulation and enhancement of fibrinolysis. As has been shown high-dose statins contribute to the favorable modification of the atherosclerotic plaque in ST-segment elevation myocardial infarction (STEMI) patients. Purpose We aim to assess the relationship between the change of fibrin clot properties on statins treatment in AMI and lipid plaque parameters in optical coherence tomography (OCT). Methods 100 patients (median age 63 years, 76% males) with STEMI or high-risk non-ST-segment elevation myocardial infarction (NSTEMI) not previously treated with statins undergoing primary PCI with OCT were included in the study. In all patients high-dose statin therapy (rosuvastatin 20-40 mg/day or atorvastatin 40-80 mg/day) was initiated within 24 hours from admission. OCT imaging was performed according to current standards (Terumo systems). Lipid profile (Cobas 6000 biochemistry analyzer) along with thrombin generation, plasma clot permeability, clot lysis time, and fibrinolysis inhibitors were determined in the entire group during hospitalization and additionally after 6 months. Results After 6 months the significant reductions of clot lysis time (126 vs 114 min, P=0.022), endogenous thrombin potential (1863 vs 1660 nM×min, P=0.001), total cholesterol (5.4 vs 3.4 mmol/L, P0.001) and low-density lipoprotein cholesterol (3.6 vs 1.5 mmol/L, P0.001), but not clot permeability (P=0.41) were observed. At baseline clot lysis time was associated with total cholesterol (R=0.286, P=0.040), lesion length (R=0.352, P=0.010) and lesion volume (R=0.476, P0.001). In turn, endogenous thrombin potential was correlated with lesion volume (R=0.406, P=0.003). 6 months reduction of clot lysis time was associated with the reduction of total cholesterol (R=0.300, P=0.036) and low-density lipoprotein cholesterol (R=0.326, P=0.022) as well as lesion length (R=0.383, P=0.007) and lesion volume (R=0.459, P=0.001). In the multivariable analysis lesion volume assessed in the acute AMI phase in OCT was the independent predictor of 6 months reduction of clot lysis time (P0.001). Conclusions As has been shown for the first time the statin-induced reduction of clot lysis time was independently associated with lipid plaque parameters assessed in the acute AMI phase in OCT. The detailed OCT analysis may serve for prediction of lipid-lowering and fibrinolytic response on high-dose statins in AMI.
Stępień et al. (2025) conducted a cohort in Acute myocardial infarction (STEMI or high-risk NSTEMI) (n=100). High-dose statin therapy (rosuvastatin or atorvastatin) vs. Baseline was evaluated on Clot lysis time (p=0.022). High-dose statin therapy in AMI patients reduced clot lysis time from 126 to 114 min (P=0.022) at 6 months, with the reduction independently predicted by baseline OCT lesion volume (P<0.001).