Background. Hyperglycemia is frequently observed in acute myocardial infarction (AMI). Diabetes mellitus (DM) patients and non-DM patients have different culprit lesion phenotypes and few data are available on non-DM patients with admission hyperglycemia. Therefore, we aimed to investigate the association between admission hyperglycemia and culprit lesion characteristics using optical coherence tomography (OCT) in AMI patients. Methods and Results. We consecutively enrolled 434 patients with AMI, and 277 patients were included in analysis: 65.7% (n=182) non-DM patients and 34.3% (n=95) DM patients. We measured acute blood glucose (ABG) and hemoglobin A_1c to calculate the acute-to-chronic glycemic ratio (A/C). Then, we grouped non-DM patients into tertiles of A/C. OCT-based culprit lesion characteristics were compared across A/C tertiles in non-DM patients and between DM and non-DM patients. Non-DM patients had fewer lipid-rich plaques (52.7% versus 68.4%, p=0.012) and thin-cap fibroatheroma (TCFA) (19.8% versus 34.7%, p=0.006) than DM patients but similar prevalence of plaque rupture (47.3% versus 56.8%, p=0.130). Non-DM patients with the highest A/C tertile had the highest prevalence of plaque rupture (pfortrend=0.002), lipid-rich plaque (pfortrend=0.001), and TCFA (pfortrend=0.003). A/C>1.22 but not ABG>140mg/dl predicted a high prevalence of plaque rupture, lipid-rich plaque, and TCFA in non-DM patients. Conclusions. In AMI patients without DM, admission hyperglycemia is associated with vulnerable culprit lesion characteristics, and A/C is a better predictor for vulnerable culprit plaque characteristics than ABG. These results call for a tailored evaluation and management of glucose metabolism in nondiabetic AMI patients. This trial is registered with NCT03593928.

Background. Inflammation poses dual effects after myocardial infarction, but robust evidence shows that high-sensitivity C-reactive protein (hsCRP), as an inflammatory marker, is constantly associated with worse outcomes. This study is aimed at investigating the probable nonlinear association between postprocedural hsCRP and mortality in patients with acute coronary syndromes (ACS) treated by percutaneous coronary intervention (PCI). Methods. A total of 3940 consecutive ACS patients treated by PCI with postprocedural hsCRP measurements were retrospectively recruited. Patients were stratified into 5 groups according to quintiles of hsCRP. Cox regression with adjustments for multiple covariates was used for outcome analysis. Restricted cubic spline (RCS) analysis was used to allow possible nonlinear associations. The primary outcome was all-cause death. Results. During a median follow-up of 727 days, mortality occurred in 207 (5.3%) patients. Adjusted hazard ratio (HR) was higher in the lowest (<2.26 mg/L, HR: 1.90, 95% confidence interval (CI): 1.08-3.33; P=0.025), second highest (10.16-12.56 mg/L, HR: 1.86, 95% CI: 1.09-3.16; P=0.023), and highest quintiles (≥12.56 mg/L, HR: 2.02, 95% CI: 1.21-3.36; P=0.007) of postprocedural hsCRP, compared to the second lowest quintile (2.26-4.85 mg/L). RCS analysis depicted a J-shaped association between postprocedural hsCRP and mortality (Pfornonlinearity=0.004). Similar association was observed between hsCRP and cardiac death (Pfornonlinearity=0.014), but not for noncardiac mortality (Pfornonlinearity=0.228). Conclusions. Both low and high postprocedural hsCRP were associated with higher risk of death in ACS patients treated by PCI.

Background and Aims: This study aimed to determine whether convertase subtilisin/kexin type 9 (PCSK9)-associated cardiovascular risk is modulated by triglyceride-glucose (TyG) in ST-segment elevation myocardial infarction (STEMI) patients with primary percutaneous coronary disease (PCI). Methods: A total of 1541 patients with STEMI (aged ≥ 18 years) undergoing primary PCI were consecutively enrolled between March 2017 and March 2019. Outcomes: When stratifying the overall population according to TyG indices less than or greater than the median (TyG median = 9.07) as well as according to quartiles of PCSK9 levels, higher TyG index levels were significantly associated with all-cause mortality only when TyG levels were 9.07 or higher (ie, relative to quartile 1 [Q1], the adjusted HR for all-cause mortality was 3.20 [95% CI, 0.54– 18.80] for Q2, p = 0.199; 7.89 [95% CI, 1.56– 40.89] for Q3, p = 0.013; and 5.61 [95% CI, 1.04– 30.30] for Q4, p = 0.045. During a median follow-up period of 1.96 years, the HR for all-cause mortality was higher in the subset of patients with TyG ≥median and PCSK9 ≥median (p for trend = 0.023) among those with type 2 diabetes mellitus (T2DM). However, there were no statistically significant differences among the subgroups. Among T2DM patients with a TyG index greater than the median, the Kaplan-Meier curve showed that patients with the highest PCSK9 levels had an increased risk of all-cause mortality (log-rank p = 0.017) and cardiac-cause mortality (log-rank p = 0.037) compared with lower PCSK9 quartile levels. Conclusion: Elevated PCSK9 levels are related to all-cause mortality and cardiac-related mortality when TyG levels are greater than the median, but not when levels are less than the median. This suggests a potential benefit of lowering circulating PCSK9 levels in STEMI patients with insulin resistance.

Background: As a specialized pro-resolving lipid mediator, resolvin D1 (RvD1) inhibits atherosclerosis progression in vivo by reducing regional oxidative stress and chronic inflammation. However, it is unclear how RvD1 is involved in human coronary artery disease. This study aims to investigate the association between plasma levels of RvD1 and culprit-plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI). Methods: A total of 240 STEMI patients undergoing optical coherence tomography (OCT) examination were analyzed. RvD1 levels were measured in patient plasma samples using an enzyme-linked immunosorbent assay. Logistic regression was performed to assess the association between RvD1 levels and various culprit plaque morphologies, and the receiver operating curve was used to search for an optimal cutoff threshold to predict certain pathological features. Results: The median RvD1 level was 129.7 (56.6– 297.8) pg/mL. According to multivariable logistic regression, high RvD1 was associated with plaque rupture (≥ 111.5 pg/mL, odds ratio [OR]: 2.09, 95% confidence interval [CI]: 1.20– 3.66, P = 0.010), healed plaques (≥ 246.4 pg/mL, OR: 2.17, 95% CI: 1.11– 4.24, P = 0.023), and calcification (≥ 293.38 pg/mL, OR: 2.10, 95% CI: 1.21– 3.66, P = 0.008) at culprit lesions. Conclusion: Increased levels of RvD1 were associated with higher instability of coronary atherosclerotic plaques in STEMI patients.

Background and Aim: The aim of prospective study was to determine the prognostic value of combined measures of plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) and pentraxin 3 (PTX3) according to the culprit-plaque morphology (plaque rupture versus plaque erosion) in relation to the in patients with acute ST-elevated myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention. Methods: A total of 434 patients with STEMI aged ≥ 18 years who underwent pre-intervention OCT imaging of culprit lesions between March 2017 and March 2019 were enrolled. Finally, 235 patients who meet the inclusion criteria were enrolled and the cohort was divided into 3 groups according to PCSK9 and PTX3 levels: group A: PCSK9 < median and Pentraxin 3 (N = 72/30.6%); group B: PCSK9 ≥ median or Pentraxin 3≥ median (N = 91/38.7%); group C: PCSK9 ≥ median and Pentraxin 3≥ median (N = 72/30.6%). MACEs were defined as a composite of all-cause death, myocardial infarction (MI) recurrence, and ischemic stroke, revascularization and heart failure. Outcomes: During a median follow-up of 2.01 years, 50 patients has occurred MACE. Two-year MACE was higher in group C (23/31.9%) than in group B (16/17.6%) and group A (11/15.3%) (p = 0.028). There was a correlation between PCSK9 and PTX3 (r = 0.302, p < 0.003). In multivariable analysis adjusted for age, gender, risk factors, and serum indexes, being in group C remained independently associated with an increased risk of MACE (hazard ratio [HR]: 2.90; p = 0.010), and group B tended to have higher MACE (HR: 1.76; p = 0.172) compared with group A. Among patients with plaque erosion by OCT, group C was independently associated with an increased risk of MACE (HR: 9.04; p = 0.048) after fully adjustment. However, the significant association was absence among patients with plaque rupture. Conclusion and Relevance: This study demonstrated the usefulness of combined measures of PCSK9 and PTX3 to enhance risk stratification in patients with STEMI especially among patients with plaque erosion. Patients with elevation of both PCSK9 and PTX3 had a markedly increased risk of MACE.

Background. Circulating levels of cardiac troponin I (cTnI) after ST-segment elevation myocardial infarction (STEMI) were considered as prognostic factors for predicting the incidence of major adverse cardiovascular events (MACE). △cTnI is the difference between peak cTnI after primary percutaneous coronary intervention (PPCI) and cTnI on initial admission. Purpose. This study aimed to assess the relationship between △cTnI, the ratio of △cTnI to cTnI on initial admission, and the incidence of MACE during the follow-up period. Methods. A total of 2596 patients with cTnI measured upon admission and one-time measurement of cTnI during hospitalization were enrolled. Results. In the adjusted models of the survival receiver operating characteristic (ROC) curve, △cTnI and the ratio of △cTnI to cTnI on initial admission have stronger discrimination power of MACE (area under curve (AUC) 0.730 and 0.717) compared with peak cTnI after PPCI and cTnI at admission (AUC 0.590, 0.546). Multivariate Cox regression analysis identified △cTnI (hazard ratio (HR) 1.018, 95% confidence interval (CI) 1.001 to 1.035) as a relevant factor for MACE during follow-up. △cTnI was divided into quartiles, and maximum △ cTnI between 4.845 and 19.073 ng/ml comprised more patients with anterior wall myocardial infarction (p < 0.001), higher GRACE score (p = 0.038), CK-MB (p = 0.023), and Myoglobin (p < 0.001). On the K–M survival curves, the incidence of MACE, mortality, and angina pectoris were significantly higher in the group with maximum △cTnI (p = 0.035, 0.049, 0.026). Conclusion. The △cTnI level and the ratio of △cTnI have stronger discrimination power of predicting the incidence of MACE. The group with maximum △cTnI has higher incidence of MACE, mortality, and angina pectoris during the follow-up period.