Matteo Francioni

Infective endocarditis (IE) is a life-threatening condition with a rising incidence, demanding rapid and precise diagnosis. While echocardiography remains the cornerstone of initial evaluation, its limitations in complex cases—such as those involving prosthetic valves or cardiac devices—are well-known. This review synthesizes current evidence and guidelines to outline a practical, multimodality imaging approach for IE. We emphasize that integrating advanced techniques like cardiac computed tomography (CT) and [18F]-fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) early in the diagnostic pathway, particularly in high-risk scenarios, significantly enhances diagnostic certainty, guides therapeutic decisions, and improves patient outcomes. A tailored imaging strategy, driven by clinical presentation and integrated within a multidisciplinary endocarditis team, is paramount for modern IE management.

Background: The management of cardiogenic shock (CS) after ACS has evolved over time, and the development of a multidisciplinary team-based approach has been shown to improve outcomes, although mortality remains high. Methods: All consecutive patients with ACS-CS admitted at our CICU from March 2012 to July 2021 were included in this single-center retrospective study. In 2019, we established a “shock team” consisting of a cardiac intensivist, an interventional cardiologist, an anesthetist, and a cardiac surgeon. The primary outcome was in-hospital mortality. Results: We included 167 patients [males 67%; age 71 (61–80) years] with ischemic CS. The proportion of SCAI shock stages from A to E were 3.6%, 6.6%, 69.4%, 9.6%, and 10.8%, respectively, with a mean baseline serum lactate of 5.2 (3.1–8.8) mmol/L. Sixty-six percent of patients had severe LV dysfunction, and 76.1% needed ≥ 1 inotropic drug. 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 in mortality reduction from 57% to 29% (OR = 0.90, p = 0.0015). Over time, CS management has changed, with a significant increase in Impella catheter use (p = 0.0005) and a greater use of dobutamine and levosimendan (p = 0.015 and p = 0.0001) as inotropic support. In-hospital mortality varied across SCAI shock stages, and the SCAI E profile was associated with a poor prognosis regardless of patient age (OR 28.50, p = 0.039). Conclusions: The temporal trend mortality reduction in CS patients is multifactorial, and it could be explained by the multidisciplinary care developed over the years.

Levosimendan is a Ca²⁺–sensitizer with inodilator action able to improve cardiac contractility without increse oxygen demand. In AHF setting clinical trial and registries showed an improvement in systemic haemodynamics without a decrease in in–hospital mortality. Purpose: evaluate safety and efficacy of Levosimendan 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. 39 patients received Levosimendan alone or in combination with other inotropic drugs. All patients had an invasive monitoring of arterial pressure and continuous ECG–monitoring. Patients with severe renal failure were excluded. An echocardiogram was performed before drug infusion and 3 days after. We collected data from haemodynamics and from ECG monitoring looking for arrhythmic events. We enrolled 167 patients with CS after AMI, 39 patients received Levosimendan and 10 of them required association with low–dosage noradrenaline. 32 received Levosimendan at dosage of 0,1 mcg/kg/min. The drug was started on average 4 days after hospitalization. Statistical analysis showed a significant change in left ventricular EF assessed by echocardiogram from 25% to 31% (P = 0.018, fig 1). We observed also an improvement of symptoms with an overall relief of dyspnea and fatigue clinically evaluated. The ECG monitoring showed ventricular arrhythmias (VA) in 11 patients (NSVT, SVT, VF) but the most frequent arrhythmia after Levosimendan was atrial fibrillation (AF) which was significantly associated with in–hospital mortality (OR = 1,82, p = 0,002), whereas VA did not. Moreover patients with new onset AF after Levosimendan showed a lower clinical and instrumental response to the drug. No significant changes in electrolytes (sodium and potassium) have been documented during arrhythmic events.

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).

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.