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Background Cardiac resynchronization therapy (CRT) is an effective treatment for left ventricular reverse remodeling (LVRR) in patients with congestive heart failure (HF) and ventricular dyssynchrony. Melatonin is a secretory product of the pineal gland with highly beneficial effects from any tissues including the heart. Herein, we investigated whether the response to CRT is associated with levels of melatonin before CRT implantation in patients with HF and ventricular dyssynchrony. Methods Diurnal melatonin levels were performed in serum from 93 patients with HF and ventricular dyssynchrony before CRT implantation. Moreover, we calculated the MADIT-CRT score. Evaluation of patients at 1-year follow-up included an echocardiographic study since the patients were categorized as responders if they presented both a reduction in left ventricular end-systolic volume index > 10% and an increase in left ventricular ejection fraction > 10%. Results At 1-year, 34 patients (36.5%) were considered responders to CRT according to the predefined criteria. The diurnal melatonin levels were significantly lower in the non-responder group (9.9 ± 2.84 vs 14.7 ± 2.32 pg/mL). After adjustment by multivariate analysis, diurnal serum melatonin levels ( P < 0.001) and diabetes mellitus ( P = 0.03) were predictors of LVRR. On Cox regression analysis, diurnal serum melatonin levels ( P < 0.001) and left atrial volume < 40 mL/m 2 ( P = 0.04) remained independent predictors of the adverse clinical events. The area under of curve for the prediction LVRR of melatonin (0.91, 95%CI 0.85–0.97; P < 0.001) was significantly higher compared to MADIT-CRT score (0.69, 95%CI 0.58–0.80; P = 0.002). Conclusion Diurnal levels of melatonin before CRT implantation are associated with LVRR at 12 month follow-up. [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]

Abstract: Background: Ischemia-modified albumin (IMA) has been shown to be elevated in patients after percutaneous coronary intervention (PCI). Our goal was to investigate the association between IMA levels and left ventricular ejection fraction in patients with ST-segment elevation myocardial infarction (STEMI) treated with PCI and who developed heart failure during their Coronary Care Unit (CCU) stay. Methods: We assessed 75 patients with a first STEMI. Presence of heart failure was assessed during CCU admission, and patients were subdivided into 2 groups: group A (n =45) comprised patients in Killip class I, and group B (n =30) Killip classes>I. Serum IMA concentration was measured within the first 15 min post-PCI. The IMA measured was performed using an indirect method based in the Albumin Cobalt Binding (ACB) colorimetric assay. The ideal cutoff value of IMA was calculated by the receiver operating characteristic (ROC) curve analysis. Results: Serum IMA concentrations were significantly higher in group B than in group A (0.37±0.09 vs 0.30±0.06 (A.U.); p <0.0001). The sensitivity and specificity of IMA for heart failure were 93.3% and 37.7%, respectively, at 0.31 A.U. Multivariable adjustment IMA showed a significant inverse correlation with left ventricular ejection function (r =−0.32; p =0.004). On multivariable analysis both IMA (OR=2.1, 95%CI: 1.2 to 3.9, p <0.001) and left ventricular ejection function (OR=1.7, 95%CI: 1.1 to 2.1, p <0.01) correlated with the occurrence of heart failure. Conclusion: In patients with STEMI undergoing PCI, serum IMA concentrations are significantly related to LVEF and represent an early marker of left ventricular dysfunction. [Copyright &y& Elsevier]

Abstract: Introduction: The balance between pro-inflammatory and anti-inflammatory molecules is likely to modulate the processes that lead to atherogenesis and rapid coronary artery disease progression. We sought to compare the positive predictive values of serum soluble CD40 ligand (sCD40L)/interleukin-10 (IL-10) ratio, versus individual sCD40L, and IL-10 measurements regarding in-hospital events in patients admitted into the hospital with ST-segment elevation myocardial infarction (STEMI). Methods: We recruited 96 patients with STEMI. sCD40L and IL-10 were measured at hospital admission in every patient. The composite of in-hospital death and heart failure represented the study end-point. Heart failure was defined as Killip class>1. Multivariable logistic regression analysis was performed to identify independent variables related to in-hospital events. Results: Thirty two patients (33%) achieved the study end-point and 64 (67%) had no adverse events during hospital admission. IL-10 levels (pg/ml) were lower (28.2±9.8 versus 33.24±11.3, p =0.03) and sCD40L levels (pg/ml) higher (156.8±54.2 versus 135.4±38.70, p =0.02) in patients with events compared to those without events. Significantly higher odd ratios were found for sCD40L/IL-10 ratio (OR=2.10, 95% CI: 1.90 to 2.80, p =0.01) compared to individual sCD40L (OR=1.40, 95% CI: 0.90 to 2.20, p =0.08) and IL-10 (OR=0.70, 95% CI: 0.50 to 0.93, p =0.02) measurements. Conclusion: Our study showed that serum ratio of sCD40L/IL-10 is a better independent predictor of in-hospital adverse events than individual sCD40L and IL-10 measurements in patients with STEMI. [Copyright &y& Elsevier]

Recent studies have found increases in the cardiovascular mortality rates during poor air quality events due to outbreaks of desert dust. In Tenerife, we collected (2014–2017) data in 829 patients admitted with a heart failure diagnosis in the Emergency Department of the University Hospital of the Canaries. In this region, concentrations of PM10 and PM2.5 are usually low (~20 and 10 µg/m3), but they increase to 360 and 115 μg/m3, respectively, during Saharan dust events. By using statistical tools (including multivariable logistic regressions), we compared in-hospital mortality of patients with heart failure and exposure to PM10 and PM2.5 during dust and no-dust events. We found that 86% of in-hospital heart failure mortality cases occurred during Saharan dust episodes that resulted in PM10 > 50 µg/m3 (interquartile range: 71–96 µg/m3). A multivariate analysis showed that, after adjusting for other covariates, exposure to Saharan dust events associated with PM10 > 50 µg/m3 was an independent predictor of heart failure in-hospital mortality (OR = 2.79, 95% CI (1.066–7.332), p = 0.03). In conclusion, this study demonstrates that exposure to high Saharan dust concentrations is independently associated with in-hospital mortality in patients with heart failure. [ABSTRACT FROM AUTHOR]

Abstract: Background: Recent studies have shown that pro-inflammatory cytokines play a significant contributory role in the pathogenesis of the acute heart failure. The purpose of this study was to determine whether the serum IL-8 concentration in patients with acute myocardial infarction (AMI), who were undergoing percutaneous coronary intervention (PCI) was related to the subsequent presence or absence of heart failure. Methods: The study included 50 patients who underwent successful PCI. During their subsequent stay in the coronary care unit, their maximum degree of heart failure was recorded. Patients were then divided into two groups: group A (Killip I) and group B (Killip class >I). The serum IL-8 concentration was measured during the 24 h following admission to the coronary care unit. Results: Serum levels of IL-8 in the group B were significantly higher than those of group A (P <0.001). By multivariante analysis a higher level of IL-8 was a significant predictor of heart failure after PCI. Conclusions: Serum levels of IL-8 after PCI appear to be a predictor for the development of heart failure in patients with AMI. [Copyright &y& Elsevier]

Cardiovascular disease is the cause of physical infirmity and thousands of deaths annually. Typically, during heart failure, cardiomyocyte mitochondria falter in terms of energy production and metabolic processing. Additionally, inflammation and the accumulation of non-contractile fibrous tissue contribute to cardiac malfunction. Melatonin, an endogenously produced molecule, experimentally reduces the initiation and progression of atherosclerotic lesions, which are often the basis of coronary artery disease. The current review critically analyzes published data related to the experimental use of melatonin to forestall coronary artery pathologies. Collectively, these studies document melatonin's anti-atherosclerotic actions in reducing LDL oxidation and triglyceride levels, lowering endothelial malfunction, limiting adhesion molecule formation, preventing macrophage polarization to the M1 pro-inflammatory phenotype, changing cellular metabolism, scavenging destructive reactive oxygen species, preventing the proliferation and invasion of arterial smooth muscle cells into the lesioned area, restricting the ingrowth of blood vessels from the vasa vasorum, and solidifying the plaque cap to reduce the chance of its rupture. Diabetic hyperglycemia, which aggravates atherosclerotic plaque formation, is also inhibited by melatonin supplementation in experimental animals. The potential value of non-toxic melatonin as a possible inhibitor of cardiac pathology in humans should be seriously considered by performing clinical trials using this multifunctional molecule. [ABSTRACT FROM AUTHOR]