Aims: To estimate if chronic anticoagulant (CAC) treatment is associated with morbidity and mortality outcomes of patients hospitalized for SARS-CoV-2 infection. Methods: In this European multicentric cohort study, we included 1186 patients of whom 144 were on CAC (12.1%) with positive coronavirus disease 2019 testing between 1 February and 30 July 2020. The average treatment effect (ATE) analysis with a propensity score-matching (PSM) algorithm was used to estimate the impact of CAC on the primary outcomes defined as in-hospital death, major and minor bleeding events, cardiovascular complications (CCI), and acute kidney injury (AKI). We also investigated if different dosages of in-hospital heparin were associated with in-hospital survival. Results: In unadjusted populations, primary outcomes were significantly higher among CAC patients compared with non-CAC patients: all-cause death (35% vs. 18% P < 0.001), major and minor bleeding (14% vs. 8% P = 0.026; 25% vs. 17% P = 0.014), CCI (27% vs. 14% P < 0.001), and AKI (42% vs. 19% P < 0.001). In ATE analysis with PSM, there was no significant association between CAC and primary outcomes except for an increased incidence of AKI (ATE +10.2%, 95% confidence interval 0.3–20.1%, P = 0.044). Conversely, in-hospital heparin, regardless of dose, was associated with a significantly higher survival compared with no anticoagulation. Conclusions: The use of CAC was not associated with the primary outcomes except for the increase in AKI. However, in the adjusted survival analysis, any dose of in-hospital anticoagulation was associated with significantly higher survival compared with no anticoagulation.

Objectives: Dapagliflozin has shown efficacy in clinical trials in patients with heart failure and reduced ejection fraction (HFrEF). However, real-world data on its use and outcomes in routine clinical practice are limited. We aimed to evaluate the utilisation and safety profile of dapagliflozin in a real-world population of HFrEF patients within the Marche region. Methods: Nine cardiology departments within the Marche region retrospectively included HFrEF patients who were initiated on dapagliflozin therapy in an outpatient setting. Data on medical history, comorbidities, echocardiographic parameters, and laboratory tests were collected at baseline and after 6 months. Telephone follow-up interviews were conducted at 1 and 3 months to assess adverse events. We defined the composite endpoint score as meeting at least 50% of four objective measures of improvement among: weight loss, NYHA decrease, ≥50% Natriuretic peptides (NP) decrease, and guideline/directed medical therapy (GDMT) up titration. Results: We included 95 HFrEF patients aged 66 ± 12 years, 82% were men, 48% had ischemic heart disease, and 20% had diabetes. At six months, glomerular filtration rate declined (p = 0.03) and natriuretic peptides levels decreased, on average, by 23% (p < 0.001). Echocardiographic measurements revealed a decrease in pulmonary artery pressure (p < 0.001) and E/e’ (p < 0.001). In terms of drug therapy, furosemide dosage decreased (p = 0.001), and the percentage of the target dose achieved for angiotensin receptor–neprilysin inhibitors increased (p = 0.003). By multivariable Cox regression, after adjustment for age, sex, the presence of diabetes/prediabetes, and HF duration, higher baseline Hb concentrations (HR 1.347, 95% CI 1.038–1.746, p = 0.025), and eGFR levels (HR 1.016, 95% CI 1.000–1.033, p = 0.46). Conclusions: In a real-life HFrEF population, dapagliflozin therapy is safe and well-tolerated, improves echocardiographic parameters and biomarkers of congestion, and can also facilitate the titration of drugs with a prognostic impact.

Cardiogenic shock (CS) after acute myocardial infarction (AMI) represents the most severe form of acute heart failure (AHF) syndromes with an high rate of in–hospital mortality. Purpose describe predictors of in–hospital mortality; evaluate ten years mortality temporal trend in our CICU; assess the feasibility of CARDSHOCK risk score; elaborate a simpler version of CARDSHOCK risk score. All consecutive patients with CS after AMI admitted at our CICU from March 2012 to July 2021 were included in this single–centre retrospective study. We included 167 patients [males 67%; age 71 years] with ischemic CS. Patients had severe LV dysfunction in 66%. Baseline serum lactate was 5,2 mmol/L. All patients required inotropes: 71% required dopamine, 65% noradrenaline, 32% dobutamine; 32% adrenalina,17,4% received levosimendan alone. Mechanical cardiac support (MCS) was pursued in 91,1% [65% IABP, 23% Impella CP, 4% VA–ECMO]. From March 2012 to July 2021 we observed a significative temporal trend mortality reduction (p=0.0015) from 57% of first time–quartile to 29% of the fourth quartile (fig1). In addition we noted a significant increase in Impella catheter use (p=0,0005) with a consequent reduction of IABP (p=0,01), a reduction in dopamine administration (p=0,007) and a greater use of inotropic drugs with vasodilatory action (p=0,015 and p=0,001). In our population of AMI–CS patients CARDSHOCK risk score was a reliable in–hospital mortality predictor tool (p=0.00011). After the multivariate analysis only EF at baseline (p=0,009), lactate level at presentation (p=0,015) and presence of three–vessels CAD (p=0,0038) resulted to be in–hospital mortality predictors. A new prediction model composed by those three variables was created and it exhibited better predictive performance for in–hospital mortality than Cardshock risk score (AUC 0,94 vs 0,72 respectively, p=0,015) (fig2).

An elevated heart rate is a marker of cardiovascular risk in patients with stable coronary artery disease. Ivabradine selectively inhibits the "f" current in the sinus node and reduces heart rate without any modifications of blood pressure, myocardial contractility and arteriolar resistance. However the addition of ivabradine to standard therapy to reduce heart rate did not improve outcomes in the recent SIGNIFY trial. Moreover, a significant interaction between the effect of ivabradine among subgroups with and without angina was detected, with a worse outcome in patients in CCS class >II at baseline. The explanation for this surprising finding despite a significant reduction in angina and myocardial revascularization procedures is uncertain. A J-curve for heart rate was not demonstrated. We speculate a significant interference on adverse events (mainly atrial fibrillation and consequently acute coronary syndromes) and on the outcome of unfavorable interactions between ivabradine and diltiazem, verapamil and strong inhibitors of CYP3A4 (4.6% of the total population). Indeed, when these patients are excluded from subgroup analysis, the harmful effect of Ivabradine among patients with severe angina disappears. In conclusion, heart rate is a marker of risk but is not a risk factor and/or a target of therapy in patients with stable coronary artery disease and preserved ventricular systolic function. Standard doses of ivabradine are indicated for treatment of angina as an alternative or in addition to beta-blockers, but should not be administered in association with CYP3A4 inhibitors or heart rate-lowering calcium-channel blockers.

Background: Cardiogenic shock (CS) after acute myocardial infarction (AMI) is a life-threatening condition with an high rate of in-hospital mortality. Purpose: This study aims to 1) describe predictors of in-hospital mortality; 2) evaluate ten years mortality temporal trend in our Cardiac Intensive Care Unit (CICU); 3) assess the feasibility of CARDSHOCK risk score in our population; 4) elaborate a simpler version of CARDSHOCK risk score. Methods: All consecutive patients with CS after AMI admitted at our CICU from March 2012 to July 2021 were included in this single-centre retrospective study. Results: We included 167 patients [males 67%; age 71 (61–80) years] with ischemic CS. Patients had severe LV dysfunction in 66%. Baseline serum lactate was 5.2 (3.1–8.8) mmol/L. All patients required inotropes: 71% required dopamine [mean dose 5.6 (2.4–11,3) mcg/kg/min], 65% required noradrenaline [mean dose 0.10 (0.05–0.18) mcg/kg/min], 32% required dobutamine [mean dose 4.5 (2.2–15.9) mcg/kg/min]; 17.4% received levosimendan alone [mean dose 0.1 mcg/kg/min]. Mechanical cardiac support (MCS) was pursued in 91.1% [65% IABP, 23% Impella CP, 4% VA-ECMO]. From March 2012 to July 2021 we observed a significative temporal trend mortality reduction (OR=0.90, 95% CI: 0.84–0.96, p=0.0015), in particular in-hospital mortality has reduced from 57% of first time-quartile to 29% of the fourth quartile (Figure 1). In addition we also noted a significant increase in Impella catheter use (p=0.0005) with a consequent reduction of IABP (p=0.01), a reduction in dopamine administration (p=0.0007) and a greater use of dobutamine and levosimendan (p=0.015 and p=0.0001). In our population of AMI-CS patients CARDSHOCK risk score was a reliable in-hospital mortality predictor tool (OR 1.11; 95% CI, 1.06–1.17; p=0.00011). After the multivariate analysis only ejection fraction (EF) at baseline (OR=0.99, 95% CI: 0.98–0.99, p=0.009), lactate level at presentation (OR=1.03, 95% CI: 1.01–1.06, p=0.015) and presence of three-vessels coronary artery disease (OR=0.73, 95% CI: 0.59–0.90, p=0.0038) resulted to be in-hospital mortality predictors. For this reason, a prediction model composed by those three variables was created which exhibited better predictive performance for in-hospital mortality than Cardshock risk score (AUC of 0.94 vs AUC of 0.72 respectively, p=0.015) (Figure 2). Conclusions: In our retrospective single-centre study a significant reduction of mortality through the years is observed, probably due to more extensive use of micro axial pumps and better manipulation of inotropic drug therapies. The use of Cardshock risk score has been proven to be a feasible tool in prediction on in-hospital mortality also in our sample composed only of AMI-CS patients. In addition, a more simplified risk score made up of only three clinical variables demonstrates at least the same predictive performance. Future validation in a larger population could be advisable to validate the simplified score. Funding Acknowledgement: Type of funding sources: None.

Plasmatic procalcitonin (PCT) is an acute–phase inflammatory marker, its value tends to increase during inflammatory conditions such as septic shock, cardiogenic shock (CS) and bacterial infections. Patients with CS complicating acute myocardial infarction (AMI) and signs of systemic inflammatory response syndrome (SIRS) can show increased PCT values but its prognostic role in this setting is still unknown. Purpose: evalute prognostic role of plasmatic PCT in an ischemic CS population. All consecutive patients with CS after AMI admitted at our CICU from March 2012 to July 2021 were included in this single–centre retrospective study. We evaluated PCT and C reactive protein (CRE) values in blood sample only in patients with clinical signs of SIRS or infection. Microbiological examination were also collected to exclude a bacterial infection. We included 167 patients [males 67%; mean age 71 years] with ischemic CS. Patients had severe LV dysfunction in 66%. Baseline serum lactate was 5,2 (3,1–8,8) mmol/L. All patients required inotropes while 91,1% required mechanical cardiac support (MCS). The overall in–hospital mortality rate was 46%. The PCT values resulted to be an in–hospital mortality predictor at multivariate analysis (p = 0,018) and we observed a generally lower PCT values in surviving CS patients (Fig 1). At the analysis the optimal maximum PCT cut–off value to predict in–hospital mortality was 5,77 ng/l (SE 0,82; SP 0,72, accuracy 0,78) with an area under the receiver operating characteristic curve of 0.80 (Fig 2). Moreover positivity to microbiological examination such as urine colture, blood colture, bronchoalveolar lavage and maximum CPR values were not associated with in–hospital death at univariable analysis.