Background: Mitsugumin 53 or Tripartite motif 72 (MG53/TRIM72), a myokine/cardiokine belonging to the tripartite motif family, can protect the heart from ischemic injury and regulate lipid metabolism in rodents. However, its biological function in humans remains unclear. This study sought to investigate the relationship between circulating MG53 levels and coronary artery disease (CAD).Methods: The concentration of MG53 was measured by enzyme-linked immunosorbent assay (ELISA) in serum samples from 639 patients who underwent angiography, including 205 controls, 222 patients with stable CAD, and 212 patients with acute myocardial infarction (AMI). Logistic and linear regression analyses were used to analyze the relationship between MG53 and CAD.Results: MG53 levels were increased in patients with stable CAD and were highest in patients with AMI. Additionally, patients with comorbidities, such as chronic kidney disease (CKD) and diabetes also had a higher concentration of MG53. We found that MG53 is a significant diagnostic marker of CAD and AMI, as analyzed by logistic regression models. Multivariate linear regression models revealed that serum MG53 was significantly corelated positively with SYNTAX scores. Global Registry of Acute Coronary Events (GRACE) scores also correlated with serum MG53 levels, indicating that MG53 levels were associated with the severity of CAD and AMI after adjusting for multiple risk factors and clinical biomarkers.Conclusion: MG53 is a valuable diagnostic marker whose serum levels correlate with the presence and severity of stable CAD and AMI, and may represent a novel biomarker for diagnosing CAD and indicating the severity of CAD.

Background: Mitsugumin 53 (MG53), a muscle-specific protein belonging to the TRIM family, has been demonstrated to protect the heart against oxidative injury. Although previous studies indicated that ischemic hearts released MG53 into circulation in mice, its effects in humans remains unknown. We aimed to evaluate the prognostic value of MG53 in patients with ST-segment elevation myocardial infarction (STEMI). Methods: Serum levels of MG53 were measured in 300 patients with STEMI, all patients were followed for 3 years. The primary endpoint was major adverse cardiovascular events (MACE), defined as a composite of cardiovascular (CV) death, heart failure causing-rehospitalization, recurrent myocardial infarction (MI), and stroke. Results: Patients with a higher concentration of serum MG53 tended to be older, with a history of diabetes. MG53 levels were also highly associated with indicators reflecting heart function, such as left ventricular ejection fraction (LVEF), N terminal pro B type natriuretic peptide (NT-pro-BNP), and cardiac troponin I (cTnI) at baseline. Kaplan-Meier survival curves demonstrated that patients with MG53 levels above the cutoff value (132.17 pg/ml) were more likely to have MACEs. Moreover, it was found to be a significant predictor of CV death (HR: 6.12; 95% CI: 2.10–17.86; p = 0.001). Furthermore, the C-statistic and Integrated Discrimination Improvement (IDI) values for MACEs were improved with MG53 as an independent risk factor or when combined with cTnI. Conclusions: MG53 is a valuable prognostic marker of MACE in patients with AMI, independent of established conventional risk factors, highlighting the significance of MG53 in risk stratification post-MI.

The progression of NTLs after PCI accounts for a significant portion of future adverse cardiac events. The reduction in LDL-C reduces cardiovascular events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes with progression in NTLs. A total of 847 patients with successful PCI were enrolled. Patients with follow-up LDL-C ≥ 1.4 mmol/L or percent reduction <50% compared to baseline were Non-optimal group (n = 793); patients with follow-up LDL-C < 1.4 mmol/L and percent reduction ≥50% compared to baseline were Optimal group (n = 54). Compared to Non-optimal group, Optimal group presented a lower rate of NTL plaque progression (11.11% vs. 23.96%; p = 0.007) and a lower follow-up TC (2.77 ± 0.59 vs. 3.66 ± 0.97; p < 0.001) and LDL-C (1.09 ± 0.26 vs. 2.03 ± 0.71; p < 0.001). The univariate logistic regression analysis revealed that follow-up LDL-C < 1.4 mmol/L and a percent reduction ≥50% from baseline was a protective factor for NTL plaque progression (OR: 0.397; 95%CI: 0.167–0.941; p = 0.036). The multivariate logistic regression model revealed that follow-up LDL-C < 1.4 mmol/L and percent reduction ≥50% was indeed an independent factor associated with a lower rate of plaque progression of NTLs (OR: 0.398; 95% CI: 0.167–0.945; p = 0.037). Therefore, achieving guideline-recommended LDL-C level was associated with a significantly reduced risk of NTL plaque progression.

Objectives: The B cell activating factor (BAFF) is a B cell survival factor involved in atherosclerosis and ischemia-reperfusion (IR) injury. This study sought to investigate whether BAFF is a potential predictor of poor outcomes in patients with ST-segment elevation myocardial infarction (STEMI). Methods: We prospectively enrolled 299 patients with STEMI, and serum levels of BAFF were measured. All subjects were followed for three years. The primary endpoint was major adverse cardiovascular events (MACEs), including cardiovascular death, nonfatal reinfarction, hospitalization for heart failure (HF), and stroke. Multivariable Cox proportional hazards models were constructed to analyze the predictive value of BAFF for MACEs. Results: In multivariate analysis, BAFF was independently associated with risk of MACEs (adjusted HR 1.525, 95% CI 1.085–2.145; p = 0.015) and cardiovascular death (adjusted hazard ratio [HR] 3.632, 95% confidence interval [CI] 1.132–11.650, p = 0.030) after adjustment for traditional risk factors. Kaplan-Meier survival curves demonstrated that patients with BAFF levels above the cut-off value (1.46 ng/mL) were more likely to have MACEs (log-rank p < 0.0001) and cardiovascular death (log-rank p < 0.0001). In subgroup analysis, the impact of high BAFF on MACEs development was stronger in patients without dyslipidemia. Furthermore, the C-statistic and Integrated Discrimination Improvement (IDI) values for MACEs were improved with BAFF as an independent risk factor or when combined with cardiac troponin I. Conclusions: This study suggests that higher BAFF levels in the acute phase are an independent predictor of the incidence of MACEs in patients with STEMI.

Backgroud: Left ventricular remodeling (LVR) is a major predictor of adverse outcomes in patients with acute ST-elevation myocardial infarction (STEMI). This study aimed to prospectively evaluate LVR in patients with STEMI who were successfully treated with primary percutaneous coronary intervention (PCI) and examine the relationship between early left ventricular dilation and late LVR. Methods: Overall 301 consecutive patients with STEMI who underwent primary PCI were included. Serial echocardiography was performed on the first day after PCI, on the day of discharge, at 1 month, and 6 months after discharge. Results: Left ventricular remodeling occurred in 57 (18.9%) patients during follow-up. Left ventricular end-diastolic volume (LVEDV) reduced from day 1 postoperative to discharge in the LVR group compared with that in the non-LVR (n-LVR) group. The rates of change in LVEDV (ΔLVEDV%) were –5.24 ± 16.02% and 5.05 ± 16.92%, respectively (p < 0.001). LVEDV increased in patients with LVR compared with n-LVR at 1-month and 6-month follow-ups (ΔLVEDV% 13.05 ± 14.89% vs. –1.9 ± 12.03%; 26.46 ± 14.05% vs. –3.42 ± 10.77%, p < 0.001). Receiver operating characteristic analysis showed that early changes in LVEDV, including ΔLVEDV% at discharge and 1-month postoperative, predicted late LVR with an area under the curve value of 0.80 (95% confidence interval 0.74–0.87, p < 0.0001). Conclusions: Decreased LVEDV at discharge and increased LVEDV at 1-month follow-up were both associated with late LVR at 6-month. Comprehensive and early monitoring of LVEDV changes may help to predict LVR. Backgroud: Left ventricular remodeling (LVR) is a major predictor of adverse outcomes in patients with acute ST-elevation myocardial infarction (STEMI). This study aimed to prospectively evaluate LVR in patients with STEMI who were successfully treated with primary percutaneous coronary intervention (PCI) and examine the relationship between early left ventricular dilation and late LVR. Methods: Overall 301 consecutive patients with STEMI who underwent primary PCI were included. Serial echocardiography was performed on the first day after PCI, on the day of discharge, at 1 month, and 6 months after discharge. Results: Left ventricular remodeling occurred in 57 (18.9%) patients during follow-up. Left ventricular end-diastolic volume (LVEDV) reduced from day 1 postoperative to discharge in the LVR group compared with that in the non-LVR (n-LVR) group. The rates of change in LVEDV (ΔLVEDV%) were –5.24 ± 16.02% and 5.05 ± 16.92%, respectively (p < 0.001). LVEDV increased in patients with LVR compared with n-LVR at 1-month and 6-month follow-ups (ΔLVEDV% 13.05 ± 14.89% vs. –1.9 ± 12.03%; 26.46 ± 14.05% vs. –3.42 ± 10.77%, p < 0.001). Receiver operating characteristic analysis showed that early changes in LVEDV, including ΔLVEDV% at discharge and 1-month postoperative, predicted late LVR with an area under the curve value of 0.80 (95% confidence interval 0.74–0.87, p < 0.0001). Conclusions: Decreased LVEDV at discharge and increased LVEDV at 1-month follow-up were both associated with late LVR at 6-month. Comprehensive and early monitoring of LVEDV changes may help to predict LVR.

OBJECTIVE Obstructive sleep apnea (OSA) is a potential cardiovascular risk. We aimed to investigate the association of OSA with heart rhythm disorders and prognosis in elderly patients with new-onset acute myocardial infarction (AMI). METHODS We prospectively enrolled 252 AMI elderly patients (mean age, 68.5 +/- 6.9 years) who were undergoing revascularization and completed a sleep study during their hospitalization. All subjects were categorized into non-OSA (apnea-hypopnea index (AHI) < 15, n = 130) and OSA (AHI >= 15, n = 122) groups based on the AHI. The changes in the autonomic nervous system, incidence of arrhythmia during nocturnal sleep, and major adverse cardiovascular and cerebrovascular events (MACCEs) were compared between the groups. RESULTS The mean AHI value in all AMI patients was 22.8 +/- 10.9. OSA patients showed higher levels of body mass index and peak high-sensitivity C-reactive protein and lower levels of minimum nocturnal oxygen saturation (MinSaO(2)), as well as greater proportion of multivessel coronary artery disease (all P < 0.05). The OSA group also showed significant increases in heart rate variability and heart rate turbulence onset (both P < 0.05) and higher incidence of arrhythmia (including sinus, atrial, and ventricular in origin). At a median follow-up of 6 months (mean 0.8-1.6 years), OSA (AHI >= 15) combined with hypoxia (MinSaO(2) <= 80%) was independently associated with the incidence of MACCEs (hazard ratio [HR]: 4.536; 95% confidence interval [CI]: 1.461-14.084, P = 0.009) after adjusting for traditional risk factors. CONCLUSIONS OSA and OSA-induced hypoxia may correlate with the severity of myocardial infarction, increase the occurrence of heart rhythm disorders in elderly subacute MI patients, and worsen their short-term poor outcomes.