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Aims: Frailty status impacts the prognosis in older patients with heart disease. However, frailty status impact is unknown in patients with non-ischaemic cardiomyopathy after cardiac resynchronization therapy (CRT)., Methods and Results: Functional measures of baseline frailty and clinical data were collected for all patients with non-ischaemic cardiomyopathy before CRT defibrillator (CRT-D) implantation. The level of frailty was assessed using the Fried and Walston definition. Cox proportional hazard regression models were used to examine the association between baseline frailty and decompensated heart failure (HF) at the 12 months follow-up. The cohort study consisted of 102 patients with a mean age of 73 ± 4 years, 53% of which were male patients. Twenty-nine patients (28%) were classified as frail before CRT-D implantation. Twenty-seven patients experienced decompensated HF after CRT-D implantation at the 12-month follow-up. In the non-frail group, 12 of 73 patients (16.4%) experienced episodes of decompensated HF. In contrast, 15 of 29 (55.6%) frail patients experienced higher proportions of decompensated HF (P < 0.001). Patients who were frail (hazard ratio 4.55, 95% confidence interval 1.726-12.013) were at increased risk for the decompensated HF (P for trend = 0.002) compared with those who were not frail., Conclusion: Frailty is a strong predictor of adverse post-implantation outcome in patients with non-ischaemic cardiomyopathy undergoing CRT-D., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.)

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]

Aims: Frailty status impacts the prognosis in older patients with heart disease. However, frailty status impact is unknown in patients with non-ischaemic cardiomyopathy after cardiac resynchronization therapy (CRT). Methods and resulits: Functional measures of baseline frailty and clinical datawere collected for all patients with non-ischaemic cardiomyopathy before CRT defibrillator (CRT-D) implantation. The level of frailty was assessed using the Fried and Walston definition. Cox proportional hazard regression models were used to examine the association between baseline frailty and decompensated heart failure (HF) at the 12 months follow-up. The cohort study consisted of 102 patients with a mean age of 73 ± 4 years,53%of whichwere male patients. Twenty-nine patients (28%) were classified as frail before CRT-Dimplantation. Twenty-seven patients experienced decompensated HF after CRT-D implantation at the 12-month follow-up. In the non-frail group, 12 of 73 patients (16.4%) experienced episodes of decompensated HF. In contrast, 15 of 29 (55.6%) frail patients experienced higher proportions of decompensated HF (P < 0.001). Patients who were frail (hazard ratio 4.55, 95% confidence interval 1.726-12.013) were at increased risk for the decompensated HF (P for trend = 0.002) compared with those who were not frail. Conclusion: Frailty is a strong predictor of adverse post-implantation outcome in patients with non-ischaemic cardiomyopathy undergoing CRT-D. [ABSTRACT FROM AUTHOR]

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]