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 < 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 < 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.

Funding Acknowledgements Type of funding sources: None. Background. Hereditary hemochromatosis (HH) is a genetic condition associated with a systemic iron overload caused by a reduction in the concentration of the iron regulatory hormone hepcidin or the hepcidin-ferroportin complex activity.  Heart failure is the leading cause of death.  It has been demonstrated early stages of systolic and diastolic left ventricular dysfunction in previous studies. The main function of the left atrium (LA) is to modulate the left ventricular filling through the reservoir, conduct and bump phases. Purpose. To compare the LA function between asymptomatic and recently diagnosed HH patients and a control group using two-dimensional speckle tracking. Methods. In this prospective study, 30 patients with HH (90% males, 47 ± 18 years old)  and 30 healthy controls with a normal echo stress test (85% males, 45 ± 13 years old) were included. A conventional echocardiogram was performed. LA strain, LA strain rate and LA volumetric parameters during the reservoir, conduit and bump phases were studied according to the current recommendations. The LA stiffness index was calculated by using the ratio between E/e´ ratio and LA strain during the reservoir phase. Results. LA volume was similar in both groups (36,5 ± 10 ml vs 32,3 ± 6,5 ml; p = 0.09). No differences were observed in LA ejection fraction (EF) (57.5 ± 10% vs 60 ± 5%; p = 0.32), LA passive EF (35 ± 12% vs 36 ± 9%; p = 0.82) or LA bump function (34 ± 11% vs 36 ± 9.9%; p = 0.41) between both groups. On the contrary, the HH group had lower LA reservoir strain (31.5 ± 6.5% vs 38.3 ± 7.9%; p = 0.002) and during the conduct phase (18 ± 7% vs 23.3 ± 6.4%; p = 0.01) than the control group. The LA stiffness index was significantly higher in the HH group (25.5 ± 9.1 vs 19.5 ± 6.4; p = 0.01). Conclusion. Early abnormalities in the LA function could be detected by using two-dimensional speckle tracking study despite no evidence of changes in atrial size or volumetric parameters. Abstract Figure.

Introduction Sick euthyroid syndrome (SES) constitutes an acute response to stress, and patients who develop it usually show more severe illness than those who do not. It could be related to disease severity in acute coronary syndrome (ACS), as assessed with Killip-Kimball class (KK), since cardiomyocytes are specifically sensitive to T3 levels. Objective To determine the prevalence of SES and low T3 in patients with ACS, and to assess its association with disease severity. Methods Prospective, observational and single center study in consecutive patients admitted to the CCU with a diagnosis of ACS. Clinical variables were collected from medical records; blood samples were obtained at admission to measure TSH, T3 and free T4 levels. SES was defined as low T3 with normal TSH and free T4. Maximum KK was determined by treating physicians. Categorical variables were compared with the chi-squared test, and categorical variables with Kruskal-Wallis and Wilcoxon tests. Statistical significance was set at p<0.05. Results There were 149 patients with complete data available for analysis. Their age was 67.8±12.4 years, and 64% were male. A total of 16.3% had SES. There were 7.5% patients with SES and KK-A, 34.8% KK-B, 14.3% KK-C and 70% KK-D (p<0.001). Thus, SES was more frequent in patients with some grade of heart failure, particularly cardiogenic shock. Figure 1 shows the difference in T3 values according to Killip-Kimball class. Conclusion Cardiomyocytes lack deiodinase and only possess T3 receptors, which makes them dependent on circulating T3 levels. T3 directly stimulates calcium channel and contractile protein synthesis in cardiomyocytes, and its deficit could affect cardiac contractility. Future studies should determine if thyroid hormone administration in cardiogenic shock can improve contractility and contribute to hemodynamic stability. T3 values according to Killip-Kimball Funding Acknowledgement Type of funding source: None

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