The infection with the SARS-CoV-2 virus is associated with numerous systemic involvements. Besides the severe respiratory injuries and cardiovascular complications, it became obvious early on that this disease carries an increased risk of thromboembolic events, but a higher propensity for bleedings as well. We researched the medical literature over significant PubMed published articles debating on the prevalence, category of patients, the moment of occurrence, and evolution of venous thromboembolism (VTE), but also of venous and arterial “in situ” thrombosis (AT), and hemorrhagic events as well. Most researchers agree on an increased prevalence of thromboembolic events, ranging between 25 and 31% for VTE, depending on the analyzed population. For AT and hemorrhagic complications lower rates were reported, namely, about 2–3%, respectively, between 4.8 and 8%, occurring mostly in older patients, suffering from moderate/severe forms of COVID-19, with associated comorbidities. It is important to mention that patients suffering from hemorrhages frequently received thromboprophylaxis with anticoagulant drugs. As a consequence of thromboembolic and hemorrhagic complications which are both important negative prognostic factors, the evolution of patients infected with the SARS-CoV-2 virus is aggravated, determining an augmented morbidity and mortality of this population.

Background: Heart failure with preserved ejection fraction (HFpEF) represents a significant portion of heart failure cases, but diagnosis is challenging due to its diverse presentation and the limitations of traditional echocardiographic parameters. Left atrial (LA) strain provides valuable insights into LA function and is increasingly used to evaluate cardiac function, including left ventricular (LV) diastolic function. LA strain, particularly reservoir strain, is considered a reliable indicator of LV diastolic function and can be used to grade diastolic function and estimate LV filling pressure. Unlike traditional LA measurements, LA strain offers detailed insights into LA function, conduit, and booster-pump phases, making it crucial for evaluating both structural and functional cardiac performance, especially in HFpEF. HFpEF diagnosis currently relies on a combination of echocardiographic parameters, clinical symptoms, and natriuretic peptide levels, encompassing various pathophysiological entities and complicating standardized management. Precise characterization of cardiac pathologies in HFpEF patients is essential. This review assesses global longitudinal strain (GLS) and left atrial strain (LAS) as echocardiographic biomarkers for diagnosing and characterizing HFpEF. Strain imaging, particularly speckle tracking echocardiography, offers a refined assessment of myocardial deformation, providing detailed insights into left heart function beyond traditional measures. Normal ranges for GLS and LAS are discussed, acknowledging demographic and technical influences. Clinical studies confirm the prognostic value of GLS and LAS in HFpEF, especially for predicting cardiovascular outcomes and distinguishing HFpEF from other dyspnea causes. However, variability in strain measurements and false-negative risks necessitate cautious clinical interpretation. The HFA-PEFF scoring system includes these biomarkers but does not fully cover the HFpEF pathology spectrum. Combining GLS and LAS shows promise in defining HFpEF phenogroups, potentially guiding individualized treatments. Global longitudinal strain (GLS) and left atrial strain (LAS) are central to non-invasive HFpEF diagnosis and stratification, with potential for more tailored therapies. Integration of these biomarkers into standard diagnostic practice requires an organized approach, and future guidelines should recommend their combined use for comprehensive HFpEF assessment.

Background: SGLT2 inhibitors are key therapies in heart failure (HF), but their combined multidomain effects have not been analyzed together. Methods: We conducted a PROSPERO-registered (CRD420251235850) systematic review and meta-analysis of all randomized controlled trials (RCTs) comparing SGLT2i (dapagliflozin, empagliflozin, canagliflozin, sotagliflozin) with placebo in adults with HF, regardless of ejection fraction or diabetes status. We searched PubMed/MEDLINE, Embase, Cochrane CENTRAL, and Web of Science through 1 February 2025. Outcomes were grouped into four domains: (1) clinical events, (2) symptoms/health status (Kansas City Cardiomyopathy Questionnaire, KCCQ), (3) functional capacity (6 min walk distance, peak VO₂), and (4) cardiac remodeling/energetics (cardiac MRI, 31P-MRS). We used random-effects models with Hartung–Knapp adjustment and assessed heterogeneity by I² and prediction intervals. Results: Eleven RCTs with 23,812 patients (HFrEF, HFmrEF, HFpEF, and acute or recently decompensated HF) were included. SGLT2i lowered the risk of cardiovascular death or first HF hospitalization by 23% (HR 0.77, 95% CI 0.72–0.82; p < 0.0001; I² = 28%; prediction interval 0.68–0.87), with similar effects across ejection fraction, diabetes status, and presentation type. All-cause and cardiovascular mortality dropped by 12% (HR 0.88, 95% CI 0.81–0.96) and 14% (HR 0.86, 95% CI 0.78–0.95), respectively. SGLT2i improved KCCQ—Clinical Summary Score by 4.6 points (95% CI 3.4–5.8; p < 0.0001) and increased the odds of a ≥5-point improvement (OR 1.49, 95% CI 1.32–1.68; NNT = 12). Six-minute walk distance increased by 21.8 m (95% CI 9.4–34.2; p = 0.001), and mechanistic trials showed significant reverse remodeling (ΔLVEDV −19.8 mL, ΔLVEF +6.1%; both p < 0.001). No improvement was observed in myocardial PCr/ATP ratio. Safety was favorable, with no excess ketoacidosis or severe hypoglycemia. Conclusions: This multidomain synthesis demonstrates that SGLT2 inhibitors provide consistent, robust reductions in mortality and hospitalizations, while also delivering early, clinically meaningful improvements across multiple patient-centered domains. These results establish SGLT2i as a foundational component of contemporary HF management.

Complex biological processes that enable optimal foetal growth throughout pregnancy are linked to notable haemodynamic and metabolic changes in the mother’s body. An inability to adapt to these changes can affect cardiovascular health. During pregnancy, women may experience mood swings, anxiety, and emotional ambivalence. These symptoms can lead to stress and harm the mental well-being of expectant mothers. It is crucial to know the aspects that can influence the development of cardiovascular problems among pregnant women. Effective management requires identifying risk factors. Applying the PRISMA ScR guidelines, we conducted a scoping review to explore and summarise the evidence regarding the impact of stress and anxiety on cardiovascular health in pregnant women. The following enquiries were looked into as research topics: What effects do anxiety and stress have on a pregnant woman’s cardiovascular health? How is it quantifiable? It is essential to comprehend the physiological changes that the body undergoes throughout pregnancy in order to inform and assist both patients and medical professionals. This makes it possible for them to identify any pathological disorders or risk factors that could worsen the health of expectant mothers. Psychological and cardiovascular risk factor screening, either before or during pregnancy, may be able to uncover circumstances that require specific medical and psychological therapies in order to lower maternal morbidity and death from cardiovascular disease. Our findings underscore the need for systematic psychological and cardiovascular screening during prenatal care to mitigate adverse outcomes and improve maternal–foetal health.

Background and Objectives: Patients with type 2 diabetes mellitus (T2DM) are at a heightened risk of adverse outcomes from Coronavirus Disease 2019 (COVID-19). However, the influence of glycemic control on systemic inflammation and clinical severity remains incompletely understood. This study aimed to compare inflammatory markers, composite severity scores, and clinical outcomes between T2DM patients with COVID-19 who had well-controlled diabetes (hemoglobin A1c < 7%) versus those with poorly controlled diabetes (hemoglobin A1c ≥ 7%). Methods: We retrospectively reviewed 181 adult patients with T2DM and severe COVID-19 admitted to a tertiary hospital between January 2022 and December 2023. Patients were divided into two groups: well-controlled (n = 117) and poorly controlled (n = 64) T2DM. Baseline demographics, comorbidities, and laboratory parameters (C-reactive protein, interleukin-6, ferritin, neutrophil and lymphocyte counts, platelets, and calculated indices such as the neutrophil-to-lymphocyte ratio [NLR] and systemic immune-inflammation index [SII]) were collected. Composite severity scores (APACHE II, CURB-65, and NEWS) and clinical outcomes (ICU admission, mechanical ventilation, mortality, and length of stay) were compared. Statistical tests used included Student’s t-test or the Mann–Whitney U for continuous variables and chi-square for categorical variables, with p < 0.05 deemed significant. Results: The two groups did not differ significantly in age or duration of diabetes (p = 0.40 and p = 0.75, respectively). Patients with poorly controlled T2DM exhibited higher inflammatory markers (mean CRP of 93.4 mg/L vs. 78.6 mg/L, p = 0.002; IL-6 of 64.2 pg/mL vs. 52.8 pg/mL, p = 0.004) and elevated severity scores (APACHE II of 16.8 vs. 14.1, p = 0.001). Poor glycemic control was associated with higher ICU admissions (39.1% vs. 22.2%, p = 0.02) and mortality (14.1% vs. 6.0%, p = 0.05). Conclusions: In T2DM patients hospitalized with COVID-19, poor glycemic control correlates with heightened inflammatory responses, worse composite severity scores, and increased rates of unfavorable outcomes. These findings underscore the necessity of stringent glucose management to mitigate inflammation and improve prognoses in this vulnerable patient population.

Most studies analyzing data from patients who experienced at least one episode of acute COVID-19 infection have attributed the cascade of immediate and late complications to disruption of the inflammatory system and neutrophil activity in particular. Among the various functions of neutrophils is the release of pro-inflammatory mediators, including interleukin-6 (IL-6). Oxidative stress induced by pro-inflammatory mediators secreted by neutrophils leads to vascular endothelial dysfunction. Neutrophil counts and the neutrophil-to-lymphocyte ratio (NLR) are directly associated with COVID-19 patient survival, with higher values correlating with increased mortality. To assess endothelial dysfunction secondary to COVID-19 infection, we conducted a retrospective study involving two patient cohorts, each comprising 99 participants: one group with a history of COVID-19 infection and another without. The study aimed to demonstrate the presence of endothelial dysfunction in patients with moderate COVID-19 infection using flow-mediated dilatation (FMD) of the brachial artery and to evaluate its correlation with key inflammatory markers (erythrocyte sedimentation rate—ESR, fibrinogen, NLR, IL-6). FMD values were significantly reduced (p < 0.0001) in post-COVID-19 patients compared to those without prior infection. ESR (p < 0.0001), fibrinogen (p < 0.0001), C-reactive protein (CRP) (p < 0.0001), leukocyte count (p < 0.0001), and granulocyte count (p < 0.0001) were inversely correlated with FMD values. Among post-COVID-19 patients, all analyzed parameters demonstrated a statistically significant impact on FMD, with ESR showing the strongest effect, accounting for nearly 63% of the dependency. ANOVA testing confirmed an inverse association between NLR quartiles and FMD, as well as between IL-6 levels and FMD. In conclusion, this study highlights the presence of endothelial dysfunction in post-COVID-19 patients, as assessed by FMD, and demonstrates statistically significant inverse correlations between FMD values, IL-6 levels, and the neutrophil-to-lymphocyte ratio.