Aims: While the prognosis of patients presenting with de novo atrial fibrillation (AF) during the acute phase of myocardial infarction has been controversially discussed, it seems intuitive that affected individuals have an increased risk for both thrombo-embolic events and mortality. However, profound data on long-term outcome of this highly vulnerable patient population are not available in current literature. Therefore, we aimed to investigate the impact of de novo AF and associated anti-thrombotic treatment strategies on the patient outcome from a long-term perspective. Methods and results: Patients presenting with acute myocardial infarction, treated at the Medical University of Vienna, were enrolled within a clinical registry and screened for the development of de novo AF. After discharge, participants were followed prospectively over a median time of 8.6 years. Primary study endpoint was defined as cardiovascular mortality. Out of 1372 enrolled individuals 149 (10.9%) developed de novo AF during the acute phase of acute myocardial infarction. After a median follow-up time of 8.6 years, a total of 418 (30.5%) died due to cardiovascular causes, including 93 (62.4%) in the de novo AF subgroup. We found that de novo AF was significantly associated with long-term cardiovascular mortality with an adjusted HR of 1.45 (95% CI 1.19–2.57; P < 0.001). While patients with de novo AF were less likely to receive a triple anti-thrombotic therapy as compared to patients with pre-existing AF at time of discharge, this therapeutic approach showed a strong and inverse association with mortality in de novo AF, with an adj. HR of 0.86 (95% CI 0.45–0.92; P = 0.012). Conclusion: De novo AF was independently associated with a poor prognosis with a 67% increased risk of long-term cardiovascular mortality. Intensified anti-thrombotic treatment in this high-risk patient population might be considered.

Background: Left ventricular thrombus (LVT) is a rare but dreaded complication during the acute phase of acute coronary syndrome (ACS). However, profound data on long‐term outcome and associated antithrombotic treatment strategies of this highly vulnerable patient population are scarce in current literature.Methods: Patients presenting with ACS were screened for presence of LVT and subsequently included within a prospective clinical registry. All‐cause mortality and the composite of major adverse cardiac events (MACE) and thromboembolic events were defined as primary and secondary endpoint.Results: Within 43 patients presenting with LVT, thrombus resolution during patient follow‐up was observed in 27 individuals (62.8%). Patients that reached a resolution of LVT experienced lower incidence rates of death (−23.9%; p = .022), MACE (−37.8%; p = .005), and thromboembolic events (−35.2%; p = .008). Even after adjustment for clinical variables, thrombus resolution showed an independent inverse association with all‐cause death with a hazard ratio (HR) of 0.14 (95% CI: 0.03–0.75; p = .021) and as well with MACE with a HR of 0.22 (95% CI: 0.07–0.68; p = .008) and thromboembolic events with a HR of 0.22 (95% CI: 0.06–0.75; p = .015). Triple antithrombotic therapy (TAT) with ticagrelor/prasugrel showed a strong and independent association with thrombus resolution with an adjusted HR of 3.25 (95% CI: 1.22–8.68; p = .019) compared to other strategies.Conclusion: The presented data indicate a poor outcome of ACS patients experiencing LVT. In terms of a personalized risk stratification, thrombus resolution has a strong protective impact on both all‐cause death and MACE with the potential to tailor treatment decisions—including an intensified antithrombotic treatment approach—in this patient population.

Background: The role of chronic inflammation in the pathogenesis of atherosclerosis has been unequivocally proven. However, the prognostic impact of C-reactive protein, a marker of inflammatory response in patients with acute myocardial infarction has not been fully clarified. Furthermore, there is no direct comparison of the diagnostic accuracy of C-reactive protein and high sensitivity C-reactive protein in the acute myocardial infarction population. Methods: In this prospective observational cohort study, 344 patients with acute myocardial infarction were enrolled. All-cause mortality was a primary endpoint. Patients were followed prospectively for a median of six years. Results: The correlation between high sensitivity C-reactive protein and C-reactive protein ( r = 0.99; P < 0.001) and the diagnostic accuracy (98.6%) was high. The ROC analysis revealed that C-reactive protein and high sensitivity C-reactive protein had a low AUC for prediction of mortality (C-reactive protein: 0.565, 95% CI [0.462–0.669], vs. high sensitivity C-reactive protein: 0.572, 95% CI [0.470–0.675]) or major adverse cardiac events (C-reactive protein: AUC 0.607, 95% CI [0.405–0.660], vs. high sensitivity C-reactive protein: AUC 0.526, 95% CI [0.398–0.653]) when assessed at time point of acute myocardial infarction. In contrast, longitudinal inflammatory risk assessment with serial C-reactive protein measurements in the stable phase of the disease revealed a 100% specificity, 100% negative predictive value, 32% sensitivity and 12% positive predictive value of C-reactive protein to predict long-term mortality. The Kaplan Meier analysis showed a significant survival benefit for patients at low residual inflammatory risk ( P = 0.014). Conclusion: C-reactive protein and high sensitivity C-reactive protein provide a similar diagnostic accuracy, highlighting that C-reactive protein might replace high sensitivity C-reactive protein in routine assessments. Furthermore, low inflammatory status during the stable phase after acute myocardial infarction predicts favourable six-year survival.

Background. Heart failure with reduced ejection fraction (HFrEF) constitutes a global health issue. While proinflammatory cytokines proved to have a pivotal role in the development and progression of HFrEF, less attention has been paid to the cellular immunity. Regulatory T lymphocytes (Tregs) seem to have an important role in the induction and maintenance of immune homeostasis. Therefore, we aimed to investigate the impact of Tregs on the outcome in HFrEF. Methods. We prospectively enrolled 112 patients with HFrEF and performed flow cytometry for cell phenotyping. Individuals were stratified in ischemic (iHFrEF, n=57) and nonischemic etiology (niHFrEF, n=55). Cox regression hazard analysis was used to assess the influence of Tregs on survival. Results. Comparing patients with iHFrEF to niHFrEF, we found a significantly lower fraction of Tregs within lymphocytes in the ischemic subgroup (0.42% vs. 0.56%; p=0.009). After a mean follow-up time of 4.5 years, 32 (28.6%) patients died due to cardiovascular causes. We found that Tregs were significantly associated with cardiovascular survival in the entire study cohort with an adjusted HR per one standard deviation (1-SD) of 0.60 (95% CI: 0.39-0.92; p=0.017). A significant inverse association of Tregs and cardiovascular mortality in patients with iHFrEF with an adj. HR per 1-SD of 0.59 (95% CI: 0.36-0.96; p=0.034) has been observed, while this association was not evident in the nonischemic subgroup (adj. HR per 1-SD of 0.62 (95% CI: 0.17-2.31); p=0.486). Conclusion. Our results indicate a potential influence of Tregs in the pathogenesis and progression of iHFrEF, fostering the implication of cellular immunity in iHFrEF pathophysiology and proving Tregs as a predictor for long-term survival among iHFrEF patients. A preview of this study has been presented at a meeting of the European Society of Cardiology earlier this year.