Heart failure is a complex medical syndrome that is attributed to a number of risk factors; nevertheless, its clinical presentation is quite similar among the different etiologies. Heart failure displays a rapidly increasing prevalence due to the aging of the population and the success of medical treatment and devices. The pathophysiology of heart failure comprises several mechanisms, such as activation of neurohormonal systems, oxidative stress, dysfunctional calcium handling, impaired energy utilization, mitochondrial dysfunction, and inflammation, which are also implicated in the development of endothelial dysfunction. Heart failure with reduced ejection fraction is usually the result of myocardial loss, which progressively ends in myocardial remodeling. On the other hand, heart failure with preserved ejection fraction is common in patients with comorbidities such as diabetes mellitus, obesity, and hypertension, which trigger the creation of a micro-environment of chronic, ongoing inflammation. Interestingly, endothelial dysfunction of both peripheral vessels and coronary epicardial vessels and microcirculation is a common characteristic of both categories of heart failure and has been associated with worse cardiovascular outcomes. Indeed, exercise training and several heart failure drug categories display favorable effects against endothelial dysfunction apart from their established direct myocardial benefit.

Sepsis is a systemic inflammatory response syndrome of suspected or confirmed infectious origin, which frequently culminates in multiorgan failure, including cardiac involvement. Septic cardiomyopathy (SCM) remains a poorly defined clinical entity, lacking a formal or consensus definition and representing a significant knowledge gap in critical care medicine. It is an often-underdiagnosed complication of sepsis. The only widely accepted aspect of its definition is that SCM is a transient myocardial dysfunction occurring in patients with sepsis, which cannot be attributed to ischemia or pre-existing cardiac disease. The pathogenesis of SCM appears to be multifactorial, involving inflammatory cytokines, overproduction of nitric oxide, mitochondrial dysfunction, calcium homeostasis dysregulation, autonomic imbalance, and myocardial edema. Diagnosis primarily relies on echocardiography, with advanced tools such as tissue Doppler imaging (TDI) and global longitudinal strain (GLS) providing greater sensitivity for detecting subclinical dysfunction and guiding therapeutic decisions. Traditional echocardiographic findings, such as left ventricular ejection fraction measured by 2D echocardiography, often reflect systemic vasoplegia rather than intrinsic myocardial dysfunction, complicating accurate diagnosis. Right ventricular (RV) dysfunction, identified as a critical component of SCM in many studies, has multifactorial pathophysiology. Factors including septic cardiomyopathy itself, mechanical ventilation, hypoxemia, and hypercapnia—particularly in cases complicated by acute respiratory distress syndrome (ARDS)—increase RV afterload and exacerbate RV dysfunction. The prognostic value of cardiac biomarkers, such as troponins and natriuretic peptides, remains uncertain, as these markers primarily reflect illness severity rather than being specific to SCM. Treatment focuses on the early recognition of sepsis, hemodynamic optimization, and etiological interventions, as no targeted therapies currently exist. Emerging therapies, such as levosimendan and VA-ECMO, show potential in severe SCM cases, though further validation is needed. The lack of standardized diagnostic criteria, combined with the heterogeneity of sepsis presentations, poses significant challenges to the effective management of SCM. Future research should focus on developing cluster-based classification systems for septic shock patients by integrating biomarkers, echocardiographic findings, and clinical parameters. These advancements could clarify the underlying pathophysiology and enable tailored therapeutic strategies to improve outcomes for SCM patients.

Obesity, hypertension, insulin resistance, and dyslipidemia are all clusters of an entity called “Metabolic Syndrome”. The global trends of this syndrome’s incidence/prevalence continue to increase reciprocally, converting it into a massive epidemic problem in the medical community. Observing the risk factors of atrial fibrillation, a medical condition that is also converted to a scourge, almost all parts of the metabolic syndrome are encountered. In addition, several studies demonstrated a robust correlation between metabolic syndrome and the occurrence of atrial fibrillation. For atrial fibrillation to develop, a combination of the appropriate substrate and a trigger point is necessary. The metabolic syndrome affects the left atrium in a multifactorial way, leading to atrial remodeling, thus providing both the substrate and provoking the trigger needed, which possibly plays a substantial role in the progression of atrial fibrillation. Due to the remodeling, treatment of atrial fibrillation may culminate in pernicious sequelae, such as repeated catheter ablation procedures. A holistic approach of the patient, with simultaneous treatment of both entities, is suggested in order to ensure better outcomes for the patients.

Background: Nasogastric tube (NGT) placement is a daily routine in the Intensive Care Unit (ICU), and misplacement of the NGT can cause serious complications. In COVID-19 ARDS patients, proning has emerged the need for frequent NGT re-evaluations. The gold standard technique, chest X-ray, is not always feasible. In the present study we report our experience with the use of ultrasonographic confirmation of NGT position. Methods: A prospective study in 276 COVID-19 ARDS patients admitted after intubation in the ICU. Ultrasonographic evaluation was performed using longitudinal or sagittal epigastric views. Examinations were performed during the initial NGT placement and every time the patients returned to the supine position after they had been proned or whenever critical care physicians or nurses considered that reconfirmation was necessary. Results: Ultrasonographic confirmation of correct NGT placement was feasible in 246/276 (89.13%) patients upon ICU admission. In 189/246 (76.8%) the tube could be visualized in the stomach (two parallel lines), in 172/246 (69.9%) the ultrasonographic whoosh test (“flash” due to air instillation through the tube, seen with ultrasonography) was evident, while in 164/246 (66.7%) both tests confirmed correct NGT placement. During ICU stay 590 ultrasonographic NGT evaluations were performed, and in 462 (78.14%) cases correct NGT placement were confirmed. In 392 cases, a chest X-ray was also ordered. The sensitivity of ultrasonographic NGT confirmation in these cases was 98.9%, specificity 57.9%, PPV 96.2%, and NPV 3.8%. The time for the full evaluation was 3.8 ± 3.4 min. Conclusion: Ultrasonographic confirmation of correct NGT placement is feasible in the initial placement, but also whenever needed thereafter, especially in the COVID-19 era, when changes in posture have become a daily practice in ARDS patients.

The cardiovascular implications of non-alcoholic fatty liver disease (NAFLD) have been associated with heart failure with preserved ejection fraction (HFpEF). The purpose of this review was to conduct a bibliographic search regarding the correlation between NAFLD and the echocardiographic parameters of left ventricular diastolic function. A systematic literature search was conducted in PubMed and Embase for original research data reporting on the association of NAFLD with diastolic function markers [E/e′, left atrial volume index (LAVi), left ventricular mass index (LVMi)]. Meta-analysis was performed using the meta and dmetar packages in R studio v.1.4.1106, with p < 0.05 values being considered significant. Results are expressed as the standardized mean difference (SMD) for continuous variables and as the odds ratio (OR) for categorical variables, with respective 95% confidence intervals (CI). Heterogeneity between studies was expressed with index Ι². From the preliminary search, 2619 articles were found from which 31 studies were included in the final statistical analysis. The meta-analysis of 8 studies which reported on the prevalence of diastolic dysfunction showed that it was increased in patients with NAFLD (OR: 2.07, 95% CI 1.24–3.44 with p = 0.01, I²: 80% with p < 0.01). The meta-analysis of 21 studies showed significantly higher E/e′ in NAFLD patients (SMD 1.02, 95% CI 0.43–1.61 with p < 0.001, I²: 97% with p < 0.001). Individuals with NAFLD had increased LAVi (SMD: 0.87, 95% CI 0.38–1.37 with p < 0.001, I²: 96% with p < 0.001) and LVMi (SMD: 0.89, 95% CI 0.31–1.48 with p = 0.003, I²: 100% with p < 0.001). To conclude, in the meta-analysis of 31 observational studies, NAFLD patients were found to have affected left ventricular diastolic function, supporting the hypothesis of NAFLD being associated with HFpEF.

Acute respiratory distress syndrome (ARDS) accounts for a quarter of mechanically ventilated patients, while during the pandemic, it overwhelmed the capacity of intensive care units (ICUs). Lung protective ventilation (low tidal volume, positive-end expiratory pressure titrated to lung mechanics and oxygenation, permissive hypercapnia) is a non-pharmacological approach that is the gold standard of management. Among the pharmacological treatments, the use of neuromuscular blocking agents (NMBAs), although extensively studied, has not yet been well clarified. The rationale is to minimize the risk for lung damage progression, in the already-injured pulmonary parenchyma. By abolishing rigorous spontaneous efforts, NMBAs may decrease the generation of high transpulmonary pressures that could aggravate patients’ self-inflicted lung injury. Moreover, NMBAs can harmonize the patient–ventilator interaction. Recent randomized controlled trials reported contradictory results and changed the clinical practice in a bidirectional way. NMBAs have not been documented to improve long-term survival; thus, the current guidance suggests their use only in patients in whom a lung protective ventilation protocol cannot be applied, due to asynchrony or increased respiratory efforts. In the present review, we discuss the published data and additionally the clinical practice in the “war” conditions of the COVID-19 pandemic, concerning NMBA use in the management of patients with ARDS.