(1) Background: Although the infection with the SARS-CoV-2 virus affects primarily the lungs, it is well known that associated cardiovascular (CV) complications are important contributors to the increased morbidity and mortality of COVID-19. Thus, in some situations, their diagnosis is overlooked, and during recovery, some patients continue to have symptoms enclosed now in the post-acute COVID-19 syndrome. (2) Methods: In 102 patients, under 55 years old, and without a history of CV diseases, all diagnosed with post-acute COVID-19 syndrome, we assessed by transthoracic echocardiography (TTE) four patterns of abnormalities frequently overlapping each other. Their evolution was followed at 3 and 6 months. (3) Results: In 35 subjects, we assessed impaired left ventricular function (LVF), in 51 increased systolic pulmonary artery pressure, in 66 diastolic dysfunction (DD) with normal LVF, and in 23 pericardial effusion/thickening. All TTE alterations alleviated during the follow-up, the best evolution being observed in patients with pericarditis, and a considerably worse one in those with DD, thus with a reduction in severity (4) Conclusions: In patients with post-acute COVID-19 syndrome, several cardiac abnormalities may be assessed by TTE, most of them alleviating in time. Some of them, especially DD, may persist, raising the presumption of chronic alterations.

Data on bacterial or fungal pathogens and their impact on the mortality rates of Western Romanian COVID-19 patients are scarce. As a result, the purpose of this research was to determine the prevalence of bacterial and fungal co- and superinfections in Western Romanian adults with COVID-19, hospitalized in in-ward settings during the second half of the pandemic, and its distribution according to sociodemographic and clinical conditions. The unicentric retrospective observational study was conducted on 407 eligible patients. Expectorate sputum was selected as the sampling technique followed by routine microbiological investigations. A total of 31.5% of samples tested positive for Pseudomonas aeruginosa, followed by 26.2% having co-infections with Klebsiella pneumoniae among patients admitted with COVID-19. The third most common Pathogenic bacteria identified in the sputum samples was Escherichia coli, followed by Acinetobacter baumannii in 9.3% of samples. Commensal human pathogens caused respiratory infections in 67 patients, the most prevalent being Streptococcus penumoniae, followed by methicillin-sensitive and methicillin-resistant Staphylococcus aureus. A total of 53.4% of sputum samples tested positive for Candida spp., followed by 41.1% of samples with Aspergillus spp. growth. The three groups with positive microbial growth on sputum cultures had an equally proportional distribution of patients admitted to the ICU, with an average of 30%, compared with only 17.3% among hospitalized COVID-19 patients with negative sputum cultures (p = 0.003). More than 80% of all positive samples showed multidrug resistance. The high prevalence of bacterial and fungal co-infections and superinfections in COVID-19 patients mandates for strict and effective antimicrobial stewardship and infection control policies.

Background and Objectives: Coronavirus Disease 2019 (COVID-19) may cause extensive multi-organ pathology, particularly in the lungs, heart, kidneys, and liver. While hypercoagulability—often signaled by elevated D-dimer—has been thoroughly investigated, the concurrent pathological findings across organs and their interrelation with distinct D-dimer levels remain incompletely characterized. This study aimed to evaluate the pathological changes observed in autopsied or deceased COVID-19 patients, focusing on the prevalence of organ-specific lesions, and to perform subgroup analyses based on three D-dimer categories. Methods: We conducted a retrospective review of 69 COVID-19 patients from a Romanian-language dataset, translating all clinical and pathological descriptions into English. Pathological findings (pulmonary microthrombi, bronchopneumonia, myocardial fibrosis, hepatic steatosis, and renal tubular necrosis) were cataloged. Patients were grouped into three categories by admission D-dimer: <500 ng/mL, 500–2000 ng/mL, and ≥2000 ng/mL. Laboratory parameters (C-reactive protein, fibrinogen, and erythrocyte sedimentation rate) and clinical outcomes (intensive care unit [ICU] admission, mechanical ventilation, and mortality) were also recorded. Intergroup comparisons were performed with chi-square tests for categorical data and one-way ANOVA or the Kruskal–Wallis test for continuous data. Results: Marked organ pathology was significantly more frequent in the highest D-dimer group (≥2000 ng/mL). Pulmonary microthrombi and bronchopneumonia increased stepwise across ascending D-dimer strata (p < 0.05). Myocardial and renal lesions similarly showed higher prevalence in patients with elevated D-dimer. Correlation analysis revealed that severe lung and heart pathologies were strongly associated with high inflammatory markers and a greater risk of ICU admission and mortality. Conclusions: Our findings underscore that COVID-19-related organ damage is magnified in patients with significantly elevated D-dimer. By integrating pathology reports with clinical and laboratory data, we highlight the prognostic role of hypercoagulability and systemic inflammation in the pathogenesis of multi-organ complications. Stratifying patients by D-dimer may inform more tailored management strategies, particularly in those at highest risk of severe pathology and adverse clinical outcomes.

The emergence of SARS-CoV2 has presented itself as a significant global health crisis. The prevalence of thrombotic events is known to be high in these patients, affecting various organ systems, sometimes leading to cutaneous thrombosis, pulmonary embolism (PE), stroke, or coronary thrombosis. The available evidence suggests that thromboembolism, hypercoagulability, and the excessive production of proinflammatory cytokines play a significant role in the development of multiorgan failure. Methodology: This retrospective single-centre study was conducted at “Victor Babes” University of Medicine and Pharmacy from Timisoara, Romania, involving a total of 420 patients diagnosed with COVID-19. We separated them into a CONTROL group that included 319 patients, and an intervention group (PE) with 101 patients that, subsequent to infection with the virus, developed pulmonary embolism. The study included the reporting of demographic data, laboratory findings, and comorbidities. Results: Out of a total of 420 patients, 24% experienced pulmonary embolism, while 21.42% died. Arterial thrombotic events were found to be associated with factors such as age, cardiovascular disease, levels of white blood cells, D-dimers, and albumin in the blood. The findings of the study indicate that there is an independent association between pulmonary thrombosis and hypertension (odds ratio (OR): 1.1; 95% confidence interval (CI): 0.7 to 1.7; p = 0.6463), cancer (OR: 1.1; 95% CI: 0.6 to 2.3; p = 0.6014), and COPD (OR: 1.2; 95% CI: 0.6 to 2.3; p = 0.4927). On the other hand, there is a stronger correlation between PE and obesity (OR: 2.8; 95% CI: 1.7 to 4.6; p < 0.0001), diabetes (OR: 3.3; 95% CI: 2 to 5.3; p < 0.0001), and dyslipidemia (OR: 3.6; 95% CI: 2.3 to 5.8; p < 0.0001) in a multivariable regression logistic model. Conclusions: Patients diagnosed with severe forms of COVID-19 display a comparable incidence of arterial thrombotic events, which have been linked to poor survival rates.

The COVID-19 pandemic has significantly impacted global health, with pulmonary embolism (PE) emerging as a critical complication due to the hypercoagulable state induced by SARS-CoV-2 infection. Despite advancements in prevention and treatment, PE remains a major cause of morbidity and mortality in COVID-19 patients. This study analyzes the trends, outcomes, and contributing factors of PE across ten pandemic waves in Romania, highlighting the evolving clinical burden and management approaches. This retrospective observational study was conducted on confirmed COVID-19 patients that also developed PE, who were admitted to “Victor Babeș” Hospital and Municipal Emergency Hospital in Timișoara, Romania. Data on demographics, clinical features, inflammatory markers, comorbidities, and treatment were collected from medical records. Statistical analyses, including ANOVA and Kaplan–Meier survival analysis, were conducted to evaluate trends and survival outcomes over time. The study included 166 patients, with a mean age of 67.26 ± 13.57 years. Mortality peaked at 50% in Wave 1, declined to 12% in Wave 7, and increased again to 28% in Wave 10. Intubation rates varied, with a high of 29% in Wave 6 and a low of 12% in Wave 8. Lung involvement was the most severe in Wave 4 (mean 0.54 ± 0.18) but improved in later waves, reaching a mean of 0.24 ± 0.12 in Wave 8. This study highlights the dynamic trends in PE during the COVID-19 pandemic in Romania. Improved clinical management, vaccination, and adaptive healthcare strategies contributed to better outcomes in later waves.

Background and Objectives: Coronavirus disease 2019 (COVID-19) triggers a dysregulated host response that may culminate in refractory hypoxaemic shock. Whether veno-venous ECMO modifies the inflammatory cascade more effectively in COVID-19 than in other septic states, and how it compares with conventional ventilatory support for COVID-19, remains uncertain. We compared three groups: COVID-19 patients supported with ECMO (COVID-ECMO, n = 25), non-COVID-19 septic shock patients on ECMO (SEPSIS-ECMO, n = 19) and critically ill COVID-19 patients managed without ECMO (COVID-CONV, n = 74). Methods: This retrospective study (January 2018–January 2025) extracted demographic, laboratory and clinical data at baseline, 48 h and 72 h. The primary end-point was the 72 h change in SOFA score (ΔSOFA). The secondary end-points included the evolution of interleukin-6 (IL-6), C-reactive protein (CRP), D-dimer and ferritin; haemodynamic variables; and 28 day mortality. A post hoc inverse-probability-of-treatment weighting (IPTW) sensitivity analysis adjusted for between-group severity imbalances. Results: Baseline APACHE II differed significantly (29.5 ± 5.8 COVID-ECMO, 27.4 ± 6.1 SEPSIS-ECMO, 18.2 ± 4.9 COVID-CONV; p < 0.001). At 48 h, IL-6 fell by 51.8% in COVID-ECMO (−1 116 ± 473 pg mL⁻¹) versus 32.4% in SEPSIS-ECMO and 18.7% in COVID-CONV (p < 0.001). The ΔSOFA values at 72 h were −4.6 ± 2.2, −3.1 ± 2.5 and −1.4 ± 1.9, respectively (p < 0.001). ECMO groups achieved larger mean arterial pressure rises (+16.8 and +14.2 mmHg) and greater norepinephrine reduction than COVID-CONV. The twenty-eight-day mortality was 36.0% (COVID-ECMO), 42.1% (SEPSIS-ECMO) and 39.2% (COVID-CONV) (p = 0.88). Across all patients, IL-6 clearance correlated with ΔSOFA (ρ = 0.48, p < 0.001) and with vasopressor-free days (ρ = 0.37, p = 0.002). Conclusions: ECMO, regardless of aetiology, accelerates inflammatory-marker decline and organ failure recovery compared with conventional COVID-19 management, but survival advantage remains elusive. COVID-19 appears to display a steeper cytokine-response curve to ECMO than bacterial sepsis, suggesting phenotype-specific benefits that merit confirmation in prospective trials.