NSTEMI, diabetes, and baseline creatinine independently predicted 5-year MACE, with NSTEMI patients having more plaques and higher non-fatal recurrent coronary events.
Do residual risk determinants (NSTEMI, diabetes, chronic kidney disease, female gender) impact coronary atherosclerosis extent and long-term outcomes in ACS patients on high-intensity lipid-lowering therapy?
In ACS patients on high-intensity lipid-lowering therapy, NSTEMI, diabetes, and baseline creatinine are independent predictors of long-term MACE, with NSTEMI patients exhibiting a greater extent of coronary atherosclerosis.
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Abstract Background The term "residual risk" after acute coronary syndromes (ACS) refers to the occurrence of cardiovascular events in individuals on lipid-lowering medications. Several factors affect residual risk, as consistent literature has shown. A greater burden of cardiovascular risk factors increases the residual risk and exposes patients to a higher risk of subsequent cardiovascular events. However, less is known about the distinctive pathophysiological mechanism that characterizes each residual risk determinant and the specific clinical, angiographic, and bio-humoral consequences. Purpose We investigated how female gender, non-ST-segment elevation myocardial infarction (NSTEMI) as a type of ACS, diabetes mellitus (DM), and chronic kidney disease (CKD) differently impacted coronary atherosclerosis extent, culprit plaque location, and bio-humoral data. The rate of both major adverse cardiovascular events (MACE) and non-fatal recurrent coronary events (RCE) was also assessed. Methods We enrolled 1,404 ACS patients and followed them for up to 5 years. Coronary culprit and non-culprit plaques were analyzed using angiography. Patients were discharged on high-intensity statin and ezetimibe treatments. Bio-humoral results were assessed at admission as well as at 1 month and 12 months after discharge. Patients were compared based on gender, type of ACS, DM, and CKD presence. Results NSTEMI patients had a higher number of total coronary plaques (3.5 vs. 3.3, p=0.013) and non-culprit plaques (2.3 vs. 1.6, p=0.0001). Non-culprit plaque stenosis was significantly greater in NSTEMI patients as compared to STEMI patients (57.9% vs. 47.1%, p=0.0001). DM patients had a higher frequency of bifurcation lesions (41% vs. 25%, p=0.0001). CKD patients more frequently presented with left main coronary artery disease (3.4% vs. 1.5%, p= 0.038). Female patients had higher LDL cholesterol values at 1 month and 12 months (Figure). The mean follow-up duration was 61.3 months ±13.6 for the entire studied population. NSTEMI, DM, and baseline creatinine values were independent predictors of MACE. Female gender was not an independent predictor of MACE (Table). NSTEMI patients showed a significantly higher risk of non-fatal RCE as compared to STEMI patients (17.3% vs 6.1%, 0=0.0001), and a non-significant trend toward a higher risk was also observed for DM patients as compared to non-DM patients (13.4% vs 10.0%, p=0.089). Conclusions NSTEMI patients had a greater extent of coronary atherosclerosis. Culprit lesions more commonly involved bifurcation sites in DM subjects, while CKD patients showed a greater prevalence of left main coronary artery disease. NSTEMI, DM, and creatinine levels at admission were independent predictors of MACE at the 5-year follow-up time. Female gender was not an independent predictor after correcting for comorbidities. Female patients had higher LDL cholesterol values despite receiving high-intensity lipid-lowering therapy.Figure.LDL changes on treatment Table.MACE predictors
Vito et al. (Sat,) reported a other. NSTEMI, diabetes, and baseline creatinine independently predicted 5-year MACE, with NSTEMI patients having more plaques and higher non-fatal recurrent coronary events.