Cardiogenic shock (CS) is a complex multifactorial clinical syndrome, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large phenotypic variability in CS, as a result of the diverse aetiologies, pathogenetic mechanisms, haemodynamics, and stages of severity. Although early revascularization remains the most important intervention for CS in settings of acute myocardial infarction, the administration of timely and effective antithrombotic therapy is critical to improving outcomes in these patients. In addition, other clinical settings or non-acute myocardial infarction aetiologies, associated with high thrombotic risk, may require specific regimens of short-term or long-term antithrombotic therapy. In CS, altered tissue perfusion, inflammation, and multi-organ dysfunction induce unpredictable alterations to antithrombotic drugs' pharmacokinetics and pharmacodynamics. Other interventions used in the management of CS, such as mechanical circulatory support, renal replacement therapies, or targeted temperature management, influence both thrombotic and bleeding risks and may require specific antithrombotic strategies. In order to optimize safety and efficacy of these therapies in CS, antithrombotic management should be more adapted to CS clinical scenario or specific device, with individualized antithrombotic regimens in terms of type of treatment, dose, and duration. In addition, patients with CS require a close and appropriate monitoring of antithrombotic therapies to safely balance the increased risk of bleeding and thrombosis.

(1) Introduction and Aims: Right ventricular (RV) remodeling significantly impacts the prognosis of dilated cardiomyopathy (DCM) patients, and right atrial (RA) size and function are still often neglected in DCM patients. Accordingly, our aims were to (i) evaluate right heart subclinical changes and (ii) the prognostic value of RA compared to left atrial (LA) size and function in patients with DCM by advanced echocardiography. (2) Materials and Methods: Sixty-eight patients with DCM (with a mean age of 60 years; 35 men) were evaluated by comprehensive transthoracic echocardiography, compared to 62 age- and sex-matched healthy controls (with a mean age of 61 years; 32 men), and followed up for 12.4 ± 5 months. (3) Results: DCM patients have RV and RA global longitudinal dysfunction by 2DSTE, higher RA minimum volumes and tricuspid annulus areas despite having normal RV volumes, ejection fractions, and RA maximum volumes by 3DE compared to the controls. The RA strain and RV strain are correlated with each other. The RA reservoir strain (with an AUC = 0.769) has an increased value for outcome prediction compared to that of the LA strain. (4) Conclusion: Patients with DCM have RV longitudinal dysfunction and decreased RA function, in the absence of clinical RV involvement or atrial arrhythmias, and the RA strain is associated with an increased risk of hospitalization and cardiac death.

Coronary endarterectomy (CE) emerged as a necessity to achieve complete surgical myocardial revascularization in patients with diffusely diseased coronary arteries and it also serves as aid to coronary bypass grafting (CABG). The safety and postoperative prognosis of this procedure are still matters of debate. There are no clear preoperative indications, a standard technique has not yet been established as gold standard and the postoperative management differs depending on each institution. CE of the left anterior descending artery (LAD) is technically challenging and potentially hazardous with high risk of postoperative myocardial infarction. In this article, we describe the open technique for CE of the LAD with its specific details, which we believe could be the safest and the best reproductible option. To better understand the profile of a patient requiring such a procedure we present the case of a 73-years old male with diffused coronary artery disease (CAD) and a short review of literature.

Acute heart failure with preserved ejection fraction (acute heart failure–heart failure with preserved ejection fraction) is increasingly prevalent, resulting from the interaction between a dysfunctional ventricle, the patient’s comorbidity burden and acute triggers. Patients are typically older, commonly female and have cardiometabolic, renal, arrhythmic, ischaemic and inflammatory comorbidities that produce vulnerability to decompensation. Acute episodes manifest with pulmonary and/or systemic congestion, from abrupt rises in left-sided filling pressures due to cardiac and arterial stiffness driven by neurohormonal activation and inflammation. Congestion and elevated blood pressure are common, but clinical presentation is more heterogeneous, reflecting the haemodynamic abnormalities, severity of triggers and comorbidity load. Diagnosis relies on integrating clinical context, echocardiography, adjusted thresholds of natriuretic peptides, and invasive and/or stress haemodynamics when diagnosis is uncertain. Management requires individualised decongestion, alongside treatment of precipitants. Early initiation of disease-modifying therapies after haemodynamic stability, including sodium–glucose cotransporter 2 inhibitors, mineralocorticoid receptor antagonists and glucagon-like peptide-1 receptor agonists, improves outcomes. Acute heart failure–heart failure with preserved ejection fraction follows a relapsing–remitting trajectory, underscoring the importance of comorbidity management, structured follow-up and preventive strategies.

There is a large spectrum of acute decompensated heart failure presentations resulting from the interaction between an acute precipitant and the patient’s underlying cardiac and non-cardiac conditions. A robust classification scheme at admission is crucial for appropriate triage and targeted treatment of high-risk populations. Such a scheme should incorporate timely actionable items to generate immediate management decisions, including characteristics that suggest life-threatening clinical presentations, the factors that could be favourably modified by in-hospital interventions, such as correctable aetiologies and congestion/hypoperfusion status, and in-hospital trajectories determined by patient responses to inpatient treatment. In-hospital trajectories determine the intensity of escalation therapies and timing for initiation/up-titration of guideline-directed medical treatment. In the long term, some patients experience a progressive downsloping course culminating in advanced heart failure, while others maintain a relatively stable remitting-relapsing trajectory. For future clinical trials, a comprehensive classification scheme integrating in-hospital and long-term trajectories could profoundly affect study design by ensuring interventions are tested in more homogeneous patient populations and facilitating nuanced patient stratification.