Search

Growth differentiation factor-15 (GDF-15) is produced by cardiomyocytes and atherosclerotic lesions under stress conditions, but little is known about its relation with severity and complexity of coronary lesions. The aim of this study was to investigate the association between GDF-15 and the syntax score for risk prediction of major adverse cardiovascular events (MACE) at 2-year follow-up in patients with non-ST-segment elevation acute coronary syndrome (NSTEACS). This is a prospective cohort study of 502 patients with NSTEACS. The syntax score was calculated from baseline coronary angiography. Blood samples were obtained at study entry for the assessment of GDF-15 and high-sensitivity C reactive protein. One hundred and three patients (20.5%) showed MACE at 2-year follow-up. Patients who developed MACE had greater GDF-15 concentrations and syntax score (p <0.001) compared to patients who did not. There was a positive, but moderate, correlation between GDF-15 and syntax score (ρ = 0.45, p <0.0001). On Cox regression analysis, only GDF-15 levels (p <0.001), body mass index (p = 0.04), and syntax score (p <0.001) remained independent predictors of the MACE. The area under the curve of GDF-15 (0.912, 95% confidence interval 0.894 to 0.944) was significantly greater compared to high-sensitivity C reactive protein and syntax score. In conclusion, in patients with NSTEACS, levels of GDF-15 at admission were correlated with the syntax score and independently associated with an increased risk of MACE during 2-year follow-up. [ABSTRACT FROM AUTHOR]

Growth differentiation factor-15 (GDF-15) is a stress-responsive cytokine that increased in patients with established type 2 diabetes mellitus (DM). Diabetic cardiomyopathy (DC), defined as left ventricular diastolic dysfunction (LVDD) in patients with type 2 DM in the absence of arterial hypertension, heart disease, or other heart disease, was assessed by GDF-15 levels in type 2 DM patients with and without DC. A total of 213 DM outpatients had blood samples drawn and on the same day (basal) underwent echocardiography and treadmill exercise testing. Plasma GDF-15 concentrations were measured by an enzymelinked immunosorbent assay (ELISA) at baseline. DC was diagnosed in the presence of LVDD, defined when early mitral valve flow velocity (E) and early diastolic lengthening velocity (E') ratio was E/E' ⩾15. The prevalence of DC was 21.13%. GDF-15 levels were higher in patients with DC compared with those without DC (5,273 [8,708.4] vs 2,812.66 [7,662.1] pg/ml, respectively, p <0.001). We assessed predictors of DC using multivariate regression analysis. GDF-15 (odds ratio 9.9; 95% confidence interval [3.9 to 24.5], p <0.001) was the unique independent predictor of DC. The results of receiver operating characteristic curve show that the cut-off point of 3,812 pg/ml of GDF-15 was indicative for DC (AUC = 0.83, sensitivity = 82.2% and specificity = 70.2%, p <0.0001). In conclusion, GDF-15 represents a useful and novel tool to screen DC in patients with type 2 DM. [ABSTRACT FROM AUTHOR]

The development of left ventricular remodeling (LVR) after myocardial infarction is associated with a high risk of heart failure and death. LVR is difficult to predict, and limited information is available on the association of cardiac biomarkers and LVR. Growth-differentiation factor-15 (GDF-15) is induced during heart failure development and, in animals models, might influence the different processes involved in cardiac remodeling. The aim of the present investigation was to assess the association between the serum levels of GDF-15 within the first 24 hours of ST-segment elevation myocardial infarction and the development of subsequent LVR at 12 months of follow-up. This prospective study included 97 patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Echocardiography was performed in all patients within the first 96 hours of admission and at 12 months of follow-up. LVR was defined as a >20% increase in the left ventricular end-diastolic volume at 12 months of follow-up compared to baseline. Blood samples for the determination of GDF-15 and brain natriuretic peptide were obtained within the first 24 hours after symptom onset. According to the pre-established criteria, 21 patients (22%) had LVR. Patients with LVR had greater levels of GDF-15 at study entry (median 3,439 pg/ml, interquartile range 2,391 to 6,168 vs median 1998 pg/ml, interquartile range 1,204 to 3,067, respectively; p <0.001). Multivariate analysis showed that GDF-15 (odds ratio 10.1, 95% confidence interval 2.5 to 40.1, p <0.001) and treatment with angiotensin-converting enzyme inhibitors (odds ratio 3.9, 95% confidence interval 1.2 to 12.3, p <0.01) were independents predictors of LVR. Receiving operating characteristics analysis showed an area under the curve of 0.77 for GDF-15 (95% confidence interval 0.67 to 0.84, p <0.001). In conclusion, the results of the present study have identified GDF-15 as an independent marker of LVR in patients with ST-segment elevation myocardial infarction. [Copyright &y& Elsevier]

Platelet aggregates appear to have a pathogenic role in the no-reflow phenomenon, which is associated with impaired clinical outcome in patients with ST-segment elevation myocardial infarction (STEMI). Melatonin, a hormone that plays a major role in biological circadian rhythms, is present in human platelets. Lowered circulating melatonin levels predict poor outcome in patients with STEMI undergoing primary percutaneous coronary intervention (PPCI). We investigated whether intraplatelet melatonin levels correlate with angiographic no-reflow after PPCI in patients with STEMI. We studied 180 consecutive patients with a first STEMI who underwent PPCI within 6 hours from onset of symptoms. Intraplatelet melatonin levels were measured in platelet-rich plasma using an enzymatic immunoassay method. After PPCI, angiographic no-reflow (defined as Thrombolysis In Myocardial Infarction grade <2 flow) was observed in 63 patients (35%). Patients with angiographic no-reflow had lower intraplatelet melatonin levels compared to patients without no-reflow (12.32 ± 3.64 vs 18.62 ± 3.88 ng/100,000 platelets, p <0.0001). After adjusting by potential confounders, binary logistic regression analysis showed that intraplatelet melatonin levels were the only significant predictor of angiographic no-reflow (odds ratio 1.58, 95% confidence interval 1.37 to 1.82, p <0.0001). In conclusion, low intraplatelet melatonin concentration predicts angiographic no-reflow after PPCI in patients with STEMI. [ABSTRACT FROM AUTHOR]

Elevated cytokine levels have been reported after ischemia/reperfusion injury and might cause a systemic inflammatory response syndrome (SIRS) after primary percutaneous coronary intervention (PPCI). High myeloperoxidase (MPO) levels are reported to be a risk factor for early cardiac events in patients with acute coronary syndrome. Its role as a predictor of SIRS in patients with ST-segment elevation myocardial infarction treated with PPCI is unclear. Therefore, the aim of the present study was to investigate the role of MPO as a predictor of SIRS in patients with ST-segment elevation myocardial infarction treated with PPCI. A total of 250 patients with ST-segment elevation myocardial infarction treated with PPCI were admitted to our coronary care unit. The serum MPO levels were measured at admission using a commercially available enzyme-linked immunosorbent assay. Of the 250 patients, 47 developed SIRS within 48 hours after their admission to the coronary care unit; 10 of these patients were excluded from analysis because of the suspicion of sepsis. The remaining 203 patients had no SIRS during their coronary care unit stay. Compared to patients without SIRS, those with SIRS had greater serum MPO values (81.35 ± 18.07 vs 67.03 ± 16.98 ng/ml, p <0.0001) after PPCI. After controlling for different baseline clinical, laboratory, and angiographic variables, the baseline serum MPO levels were an independent predictor of SIRS (odds ratio 4.2, 95% confidence interval 1.9 to 8.4, p <0.001). In conclusion, our results have demonstrated that MPO is an independent predictor of SIRS after PPCI, suggesting a new clue for the interpretation of this phenomenon. [Copyright &y& Elsevier]

Inflammation plays a critical role in acute myocardial infarction. One inflammatory marker is myeloperoxidase (MPO). Its role as a predictor of in-hospital death in patients with ST-segment elevation myocardial infarction (STEMI) presenting with cardiogenic shock (CS) is unclear. Therefore, the aim of this study was to investigate the role of MPO as a predictor of in-hospital death in patients with STEMIs presenting with CS and treated with primary percutaneous coronary intervention. In 38 consecutive patients with CS complicating STEMIs who were treated with primary percutaneous coronary intervention, serum MPO levels were measured at coronary care unit admission using a commercially available enzyme-linked immunosorbent assay. The primary study end point was in-hospital cardiac death. Among the 38 patients included in the study, 20 died during their coronary care unit stays, whereas 18 survived. Compared with patients who survived, patients who died showed, at coronary care unit admission, higher serum MPO levels (81 ± 28 vs 56 ± 23 ng/ml, p <0.006). After controlling for different baseline clinical, laboratory, and angiographic variables, baseline serum MPO level was an independent predictor of in-hospital mortality on multivariate analysis (odds ratio 3.9, 95% confidence interval 1.8 to 7.5, p <0.001). In conclusion, admission MPO concentration is an independent predictor of in-hospital mortality in patients with STEMIs presenting with CS. [Copyright &y& Elsevier]

We evaluated the possible relation between circulating levels of nocturnal melatonin, C-reactive protein, and the development of adverse cardiovascular events in patients with ST-segment elevation myocardial infarction. Patients who had developed adverse events during follow-up had significantly lower nocturnal melatonin levels than patients without events. [Copyright &y& Elsevier]

C-reactive protein, a marker of inflammation, is increasingly measured to stratify risk for coronary artery disease and guide clinical management. Likewise, a relation has been suggested between decreased nocturnal melatonin levels and coronary artery disease. However, little is known about the association between melatonin and C-reactive protein in patients with ischemic heart disease. [Copyright &y& Elsevier]

A letter to the editor is presented in response to the article in previous issue related to prognostic usefulness of C-reactive protein (CRP) in patients with acute myocardial infarction.