Background Cancer therapy-related cardiac dysfunction (CTRCD) is a critical problem with an impact on both oncological and cardiovascular prognosis, especially when it prevents patients from receiving cancer treatment. Standard therapy for heart failure (HF) is recommended for CTRCD, but there is no well-established evidence on how sacubitril/valsartan may help cancer patients with cardiotoxicity. Objectives The aim of this trial was to study the effectiveness of sacubitril-valsartan in patients with CTRCD treated in cardio-oncology units. Methods We enrolled 635 patients with breast cancer and followed them with echocardiography and NT- proBNP. Patients who developed left ventricular dysfunction and heart failure were treated with angiotensin-converting enzyme inhibitors (ACEI) (enalapril) or angiotensin receptor blockers (ARB) (valsartan), aldosterone antagonists (eplerenone), digitalis and diuretics (furosemide), as needed. When patients remained symptomatic and met the PARADIGM-HF inclusion criteria, sacubitril/valsartan was started instead of enalapril or valsartan. We analyzed clinical, laboratory and echocardiographic variables to determine the beneficial effects of sacubitril/valsartan on left ventricular remodeling (improvement of left ventricular ejection fraction (LVEF), left ventricle internal diameter in diastole), diastolic dysfunction (E/e’ ratio), reduction in NT-proBNP levels, New York Heart Association (NHYA) class and improvement in the 6-min walk test. Also, we analyzed serum creatinine and potassium levels to determine treatmentsafety in this population. Median follow-up was 20 months. Results Twenty-eight patients developed cardiotoxicity and were treated with sacubitril/valsartan. The sacubitril/valsartan dose was 100 mg (sacubitril 49 mg/valsartan 51 mg) in 12 patients (42.85%) and 200 mg (sacubitril 97 mg/valsartan 103 mg) in 16 patients (57.15%). No deaths were reported, and one patient underwent heart transplantation. Baseline median NT-proBNP was 997.5 pg/ml (IQR 663.8 — 2380.8), which decreased to a median of 416.5 pg/ml (IQR 192.0–798.2) on follow-up with p < 0.001. Baseline NYHA functional class was III (78.6%) or IV (21.4%), and it improved to I (57.1%) or II (42.9%) on follow-up. LVEF increased with treatment from 26.7 ± 5.4% to 32.3 ± 5.5% (p < 0.001). There were also significant improvements in left ventricle internal diameter in diastole (LVIDD), diastolic function, 6-min walk test, and mitral valve regurgitation. There were no differences between basal and follow-up levels of serum creatinine or potassium. Conclusion Sacubitril/valsartan might be a promising treatment option in patients with refractory CTRCD.

IntroductionFrailty is a complex condition that results from the loss of physiological reserve across multiple systems. Its presence should be considered in the aging heart failure population, since it is an important predictor of death and institutionalization in the elderly.Methods and resultsIn a prospective, observational and analytical single-center study of 100 elderly patients hospitalized for acute heart failure, we assessed the characteristics associated with an increased hospital and 1-year mortality. Frailty was evaluated with the Clinical Frailty Scale, and there was a significant association between its presence and 1-year mortality (RR = 2.03; 95% CI = 1.18–3.48; p = 0.014), although not with in-hospital mortality. After adjusting for probable confounders, it remained independently associated with 1-year mortality.ConclusionFrailty can be assessed with a simple bed-side scale and provides significant prognostic information in acute heart failure patients.

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Plaque rupture triggers a prothrombotic response that is counterbalanced by a fibrinolytic response. D-dimer serves as a marker of both processes. Inflammatory mediators are also released, evidenced with the rise of high-sensitive C reactive protein (hsCRP). Current evidence with these biomarkers has shown conflicting results. Determine an association between D-dimer and hsCRP within hospital and 1-year mortality in patients with acute coronary syndromes. In total, 127 patients were included. In-hospital mortality was 5.7%, and 1-year all-cause and cardiovascular mortality were 14.6 and 9.7%, respectively. The median of admission D-dimer for patients who died during hospital stay was higher than those who survived [4.59 (interquartile ranges (IQR) 1.94-6.05 mg/ml fibrinogen equivalent units (FEU)) vs. 0.56 (IQR 0.31-1.12 mg/ml FEU), P U 0.001]. At 1-year follow-up, the median of admission D-dimer for patients who died was significantly higher than those who survived: 1.55 (IQR 0.91-5.08 mg/ml FEU) vs. 0.53 (IQR 0.29-0.90 mg/ml FEU), P < 0.001. Positive D-dimer vs. negative D-dimer at admission analysis evidenced that almost 25% of the positive patients were dead at 1-year follow-up (22.4 vs. 2.4% negative D-dimer, P U 0.011). Multivariate logistic regression analysis showed that D-dimer has an independent association with 1-year mortality [odds ratio 1.06 (95% confidence interval 1.02-1.10), P U 0.006]. Positive significative correlations between D-dimer and hsCRP levels (R U 0.56, P < 0.001) were found. High levels of admission D-dimer were strongly associated with inhospital and 1-year mortality. Significant correlations with hsCRP could explain the inflammatory nature that led to poorer outcomes. D-dimer could be useful in risk stratification in acute coronary syndromes; however, a specific threshold should be defined for this type of patient.

Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): University of Buenos Aires Background Cortisol is a stress marker in patients with acute coronary syndrome (ACS) and it has a permissive effect on the actions of hormones that increase glucose production. Its association with blood glucose levels in diabetic and non-diabetic patients could help to understand the relationship between stress, hyperglycaemia and mortality. Methods Prospective and observational single-centre study. All patients admitted with a diagnosis of ACS to the coronary care unit of a University Hospital were included. The age, sex and clinical characteristics were recorded, along with the clinical outcomes. On admission, blood samples were obtained to measure serum glucose (SG) and cortisol (SC). Results Over a total of 149 patients, 35.37% had a diagnosis of ST-segment elevation ACS. Median age was 69 (60.1 – 79) years, 61.1% were male, 59.5% were hypertense, 18.2% dyslipidemic, 23% smokers, and 28.4% diabetics. Total mortality during hospitalization was 6.8%, and cardiovascular mortality was 6.1%. We observed a significantly higher SC and SG on admission in patients who died (table 1), with a mild and positive correlation between them (Spearman’s rho = 0.24, p = 0.005). Diabetic patients had a higher SG on admission [191.1 mg/dl (157.5 – 250,8) vs. 116.0 mg/dl (99.0 – 141.0), &lt; 0.001]. Diabetes was not associated with mortality, although correlation between glucose and cortisol remained constant in diabetics and non-diabetics (figure 1). Conclusion Hypercortisolemia and hyperglycaemia were associated with an increased in-hospital mortality. Although hyperglycemia confers a worse prognosis, we found that its correlation with cortisol was constant in diabetics and non-diabetics. This suggests that hyperglycaemia could be a surrogate stress marker, not related to diabetes as a risk factor in an acute setting. Serum glucose and cortisol on admission LaboratorySurvivorsNon-survivorsp-valueGlucose (mg/dL)128 (101 - 163)156 (134.5 - 197.2)0.04Cortisol (ug/dL)13.7 (7,98 - 23.65)43.7 (34.6 - 50.0)0.0004Abstract Figure. Serum cortisol and glucose on admission.

Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Universidad de Buenos Aires. Introduction in acute coronary syndromes (ACS), plaque rupture elicits a prothrombotic response that is counter balanced by a fibrinolytic response. D-dimer (DD) serves as a marker of both processes, reflecting thrombin activity and through cross-linked fibrin degradation. Inflammatory mediators are also involved, evidenced with the rise of C-reactive protein (CPR) levels, enhancing the prothrombotic and proatherogenic endothelial vascular response. Current evidence with these biomarkers has shown conflicting results with no conclusive impact on cardiovascular outcomes, risk stratification nor potential treatments. Purpose our aim was to determine an association between DD and CRP with in-hospital and 1-year mortality in patients with ACS. Methods observational study of patients admitted to a coronary care unit with ACS and elevated troponin. Clinical characteristics, in-hospital and 1-year outcomes and serum levels at admission of DD and CRP were assessed. Results we included 127 patients with ACS. Mean age was 68.4 ± 12.8 years and 61% were male, 57.7% had hypertension, 17.1% had dyslipidemia, 25.2% had diabetes and 17.9% had previous myocardial infarction. Most patients received DAPT and 67.5% underwent PCI or CABG during the index hospitalization. In-hospital mortality was 5.7% and 1-year all-cause and cardiovascular mortality were 14.6% and 9.7% respectively. The median of admission DD for patients who died during hospital stay was higher than those who survived (4.59 [IQR 1.94-6.05 ug/ml FEU] vs 0.56 [IQR 0.31-1.12 ug/ml FEU], p = 0.001). At 1-year follow-up, the median of admission DD for patients who died was significantly higher than those who survived: 1.55 (IQR 0.91-5.08 ug/ml FEU) vs. 0.53 (IQR 0.29-0.90 ug/ml FEU), p &lt; 0.001 (figure A). We analyzed positive DD vs. negative DD at admission, with 0.5 ug/ml FEU cut-off value, almost a quarter of the positive patients were dead at 1-year follow up (22.4% vs. 2.4% negative DD, p= 0.011). We found a positive significative correlation between DD and CRP levels (R = 0.56, p &lt; 0.001) (figure B). Conclusion high levels of DD at admission were strongly associated with in-hospital and 1-year mortality. Significant correlations with CRP could explain the inflammatory nature that lead to poorer outcomes. DD could be useful in risk-stratification in ACS; however, a specific threshold should be defined for this type of patients. Abstract Figure A. Figure B.