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• De Ritis ratio predicts 3-year all-cause mortality after acute myocardial infarction. • De Ritis ratio predicts 3-year cardiac mortality after acute myocardial infarction. • De Ritis ratio predicts 30-day risk of bleeding after percutaneous coronary intervention. • De Ritis ratio has a moderate sensitivity regarding prediction of mortality. The association between aspartate aminotransferase to alanine aminotransferase ratio (De Ritis ratio) and prognosis of patients with acute myocardial infarction (AMI) remains poorly investigated. This study included 3000 patients with AMI undergoing percutaneous coronary intervention. Patients were categorized in groups according to tertiles of the De Ritis ratio: tertile 1 (De Ritis ratio < 1.11; 905 patients), tertile 2 (De Ritis ratio 1.11 to 1.95; 1003 patients) and tertile 3 (De Ritis ratio > 1.95; 1002 patients). The primary endpoint was 3-year all-cause mortality. At 3 years, all-cause deaths occurred in 487 patients: 119 deaths (13.2%) in patients of 1st tertile, 164 deaths (17.8%) in patients of 2nd tertile and 204 deaths (21.9%) in patients of 3rd tertile of the De Ritis ratio (adjusted hazard ratio [HR] = 1.16, 95% confidence interval [CI] 1.02 to 1.31], P = 0.023 per unit increment in the logarithmic scale of the De Ritis ratio); cardiac deaths occurred in 328 patients: 76 deaths (8.2%) in patients of 1st tertile, 110 deaths (12.0%) in patients of 2nd tertile and 142 deaths (15.4%) in patients of 3rd tertile of the De Ritis ratio (adjusted HR = 1.20 [1.04–1.40], P = 0.014 per unit increment in the logarithmic scale of De Ritis ratio). The C-statistic of the multivariable model(s) with baseline data without and with De Ritis ratio was 0.822 [0.805–0.839] and 0.823 [0.805–0.840], (P = 0.419) for all-cause mortality and 0.831[0.811–0.852] and 0.832 [0.811–0.853], P = 0.621) for cardiac mortality. In patients with AMI, elevated De Ritis ratio was associated with increased risk of 3-year mortality. [ABSTRACT FROM AUTHOR]

• Tenascin-C is expressed in diseased hearts, not in normal hearts. • Clinical utility of Tenascin-C in diseased heart is unclear. • Tenascin-C was independently associated with acute myocardial infarction, cardiomyopathy, diabetic retinopathy. • Tenascin could predict cardiovascular outcomes in patient with stable coronary heart disease. We investigated the prognostic value of tenascin-C in patients with stable coronary heart disease. A total of 666 patients were enrolled and followed for 72 months. The primary outcome was a composite of cardiac events. The secondary outcomes were all-cause death, cardiovascular death, acute myocardial infarction (AMI), and heart failure hospitalization. Results: The area under the curve of tenascin-C to discriminate the occurrence of composite cardiac events was 70 % (95 % CI: 64.2 % to 75.8 %), and the corresponding optimal cutoff value was 19.91 ng/ml. A higher concentration of tenascin-C was associated with a greater risk of composite cardiac events (P trend < 0.001). Similar results were observed in all-cause death, AMI, and heart failure hospitalization. Tenascin-C was found to be an independent predictor of total cardiovascular events in patients with stable coronary heart disease at 72 months, and also for all-cause death, AMI, and heart failure hospitalization. [ABSTRACT FROM AUTHOR]

• MAp19 did not demonstrate diagnostic ability in distinguishing between patients with and without functional coronary artery disease. • A·MAp19 concentrations were associated with the risk of non-fatal myocardial infarction. • The concentration of MAp19 increased at peak exercise and subsequently decreased within two hours, demonstrating that physical activity may influence the blood concentration of MAp19. • The concentration of MAp19 was found to be weakly associated with age, cholesterol and eGFR levels. This study aimed to evaluate the diagnostic and prognostic potential of MAp19, a regulating component of the lectin pathway of the complement system, in patients with suspected functionally relevant coronary artery disease (fCAD) as well as the determinants of MAp19 levels. The presence of fCAD was adjudicated using myocardial perfusion imaging with single-photon emission tomography and, where available, coronary angiography. MAp19 levels were measured in participants at rest, at peak stress tests, and two hours after the stress. The study also tracked major cardiovascular events, including non-fatal myocardial infarction and cardiovascular death, over a five-year follow-up period. Among the 1,571 patients analyzed (32.3 % women), fCAD was identified in 462 individuals (29.4 %). MAp19 demonstrated no diagnostic significance, yielding an area under the curve (AUC) of 0.51 (0.47–0.55). Throughout the five-year follow-up, 107 patients (6.8 %) experienced non-fatal myocardial infarctions, 99 (6.3 %) had cardiovascular death, 194 (12.3 %) experienced all cause death and 50 (3.1 %) suffered a stroke. Cox and Kaplan-Meier analysis confirmed prognostic value of MAp19 for myocardial infarction, but not for cardiovascular death. Significant increases in the concentration of MAp19 were observed during bicycle (p = 0.001) and combined stress tests (p = 0.001). MAp19 demonstrated an association with the risk of myocardial infarction. Increases in MAp19 concentration were observed during bicycle and combined stress-tests. [ABSTRACT FROM AUTHOR]

• Accurate etiological classification of stroke is the basis of treatment choice. • Studies have shown that plasma combined with cardiac markers is valuable for the diagnosis of cardioembolic stroke. • It is the first study to demonstrate that serum LRG1 might be a promising indicator to predict cardioembolic stroke. • Serum LRG1 was associated with the severity and prognosis of cardioembolic stroke patients. • The combined predictive model, including LRG1, BNP, and LAD, significantly improved the prediction effect. In recent years, LRG1 was found to be closely related to atrial fibrillation, heart failure, and myocardial remodeling after myocardial infarction. While its role in cerebral infarction was still controversial. We aimed to explore the value of LRG1 to identify the cardioembolic stroke. 283 acute ischemic stroke(AIS) patients and 169 controls were enrolled. The AIS patients were divided into a CE(cardiogenic embolism) group and a non-CE group. Serum LRG1 levels were quantified by ELISA. The serum LRG1 levels were decreased in the AIS patients. CE group had higher serum LRG1 levels than the non-CE group. LRG1 was an independent risk factor for cardioembolic stroke. The area under the curve (AUC) was 0.768 with a sensitivity of 72.5% and specificity of 69.5%, which was not second to BNP and LAD. The combined predictive model we designed, including LRG1, BNP, and LAD, greatly improved the prediction effect. A positive correlation was shown between LRG1 and stroke severity in the CE group. Those who experienced poor outcomes had higher serum LRG1 levels compared with good ones. Serum LRG1 was a promising indicator to predict cardioembolic stroke, as well as stroke severity and the 3-month prognosis of it. [ABSTRACT FROM AUTHOR]

• There is no review summarizing biomarkers in MINOCA. • We summarized the non-atherosclerotic biomarkers, including traditional markers, potential markers, and imaging markers. • Biomarkers of MINOCA are of great significance for diagnosis, treatment, prognosis and mechanism research. Myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) is an important subtype of myocardial infarction. Although comprising less than 50% stenosis in the main epicardial coronary arteries, it constitutes a severe health risk. A variety of approaches have been recommended, but definitive diagnosis remains elusive. In addition, the lack of a comprehensive understanding of underlying pathophysiology makes clinical management difficult and unpredictable. This review highlights ongoing efforts to identify relevant biomarkers in MINOCA to improve diagnosis, individualize treatment and better predict outcomes. [ABSTRACT FROM AUTHOR]

• H-ficolin at rest, at peak exercise, and 2 h after exercise did not demonstrate diagnostic ability in distinguishing between patients with fCAD versus patients without fCAD. • H-ficolin was not a predictor of cardiovascular death and non-fatal myocardial infarction in the overall cohort. • H-ficolin slightly increased during bicycle exercise stress, and decreased to baseline levels 2 h after bicycle stress. Similarly, H-ficolin slightly decreased during pharmacological (adenosine) or combined stress, and returned to baseline levels at 2 h. • H-ficolin was weakly correlated with systolic and diastolic blood pressure. We aimed to test the diagnostic and prognostic ability of H-ficolin, an initiator of the lectin pathway of the complement system, for functionally relevant coronary artery disease (fCAD), and explore its determinants. The presence of fCAD was adjudicated using myocardial perfusion imaging single-photon emission tomography and coronary angiography. H-ficolin levels were measured by a sandwich-type immunoassay at rest, peak stress-test, and 2 h after stress-test. Cardiovascular death and non-fatal myocardial infarction were assessed during 5-year follow-up. Among 1,571 patients (32.3 % women), fCAD was detected in 462 patients (29.4 %). H-ficolin concentration at rest was 18.6 (15.3–21.8) µg/ml in patients with fCAD versus 17.8 (15.4–21.5) µg/ml, p = 0.33, in patients without fCAD, resulting in an AUC of 0.53 (95 %CI 0.48–0.56). During follow-up, 107 patients (6.8 %) had non-fatal myocardial infarction and 99 patients (6.3 %) experienced cardiovascular death. In Cox regression analysis, H-ficolin was not a predictor of events in the overall cohort. Subgroup analysis suggested a potential link between H-ficolin and non-fatal myocardial infarction in patients without fCAD (adjusted HR 1.03, 95 % CI 1.02–1.15, p = 0.005). H-ficolin concentration showed a weak positive correlation with systolic (r = 0.069, p < 0.001) and diastolic blood pressure (r = 0.111, p < 0.001). H-ficolin concentration did not have diagnostic and/or prognostic value in patients referred for fCAD work-up. [ABSTRACT FROM AUTHOR]

Background Elevated triglyceride to high density lipoprotein cholesterol (TG/HDL-C) ratio has been identified as a surrogate marker of insulin resistance and an independent predictor for cardiovascular events in the general population. However, the prognostic value of TG/HDL-C ratio in revascularized ST-elevation myocardial infarction(STEMI) patients remains unclear. We examined the association between TG/HDL-C ratio and clinical outcome of revascularized STEMI patients in the Chinese population. Methods 464 STEMI patients who underwent successful revascularization were enrolled to determine the relationship between TG/HDL-C ratio and major adverse coronary events(MACEs) with a 30-month follow-up. The Kaplan-Meier analysis and Cox regression proportional hazard model were applied to assess the prognostic value of TG/HDL-C ratio. Results TG/HDL-C ratio was found to be significantly associated with age (p = 0.017), history of diabetes(p = 0.017), heart rate(p = 0.011), TG(p < 0.001), HDL-C(p < 0.001) and Gensini score(p = 0.034). The multivariate Cox regression analysis revealed that elevated TG/HDL-C ratio was an independent prognostic factor for MACE in female patients (HR = 2.624,95%CI = 1.211–5.687,p = 0.014) but not in male patients(HR = 0.756, 95%CI = 0.484–1.179,p = NS) after adjustment with other MACE-related prognostic factors. Conclusion The TG/HDL-C ratio may be independently associated with MACEs in female revascularized STEMI patients in the Chinese population. [ABSTRACT FROM AUTHOR]

Background IL-37 emerges as a natural suppressor of inflammatory responses. The potential role of IL-37 in the pathology of atherosclerosis is unclear. The purpose of this study was to assess IL-37 profile in acute coronary syndrome (ACS) and the prognostic role of this cytokine in patients with ST-segment elevation acute myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods In a case-control study, we prospectively enrolled 216 patients undergoing the first coronary angiography, which consisted of 5 groups: normal (n = 57), stable angina (SAP, n = 36), unstable angina (UAP, n = 42), non-STEMI (n = 36), STEMI (n = 45). Plasma IL-37, IL-6 and serum amyloid A (SAA) were measured using a commercially ELISA kit. Besides, in a prospective cohort study, 125 patients with STEMI of onset < 12 h undergoing PPCI were enrolled and divided into 2 groups according to the concentrations of IL-37 (< 341.1 pg/ml or ≥ 341.1 pg/ml). In-hospital major adverse cardiac event (MACE) including nonfatal myocardial infarction (MI), target lesion revascularization, acute heart failure, and cardiac death were estimated for prognosis. Results IL-37 was gradually increased in accordance with the severity of coronary artery disease. The circulating concentration of IL-37 was remarkably higher in the ACS patients than in either of the normal or SAP patients ( p < 0.05), and especially higher in the AMI patients including STEMI and non-STEMI than in the angina pectoris subjects no matter SAP or UAP ( p < 0.05). There was no statistical difference of IL-37 between normal and SAP patients, STEMI and non-STEMI patients ( p > 0.05). The trend of the change of IL-37 was consistent with that of SAA or IL-6. A higher circulating concentration of IL-37 before PPCI was accompanied with the decreased LVEF and the increased NT-proBNP concentrations, and independently predictive of in-hospital MACE rate in patients with STEMI undergoing PPCI (OR = 3.652, 95% CI = 1.113–11.983, p < 0.05). Conclusions We demonstrated the IL-37 profile in patients with acute coronary syndrome and the increased IL-37 concentration was associated with a worse clinical in-hospital outcome in STEMI patients undergoing PPCI. [ABSTRACT FROM AUTHOR]

Backgrounds The relation between serum total bilirubin (TBi) and mortality in patients with established coronary artery disease (CAD) remains undefined. We try to investigate the role of the subtypes of CAD in the association. Methods A total of 3013 patients with angiographically obstructive CAD were enrolled. A retrospective analysis was conducted. Patients were divided into 3 groups as follows: stable CAD (SCAD), unstable angina pectoris (UAP) and acute myocardial infarction (AMI). The predictive values of TBi for 30-day and long-term mortality were assessed using logistic and Cox regression, respectively. Results Higher initial serum TBi levels were significantly associated with increased risk of short-term mortality (OR 2.35, 95% CI 1.15–4.77) in AMI group. However, the association was absent among patients with SCAD and UAP. Serum TBi was able to independently predict the long-term mortality in SCAD (HR 0.34, 95% CI 0.16–0.70) and UAP (HR 0.49, 95% CI 0.31–0.78) groups. However, there was no significant relation between TBi and long-term mortality in AMI groups. Conclusion The different subtypes of CAD affected the relation between serum TBi and clinical prognosis. Initial serum TBi was positively correlated with short-term mortality of AMI patients, and negatively correlated with long-term mortality in SCAD or UAP patients. [ABSTRACT FROM AUTHOR]