Search Results (203)

Background: Natriuretic peptides, including B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), are established biomarkers of myocardial stress and circulatory overload. Although originally validated for diagnosis and exclusion of heart failure, their diagnostic and prognostic applications have expanded significantly in the context of critical illness. However, interpretation in critically ill patients is complicated by confounding factors such as systemic inflammation and renal dysfunction. Objective: This review synthesizes current evidence on the diagnostic, monitoring, and prognostic applications of natriuretic peptides in critically ill adults. It further outlines practical considerations, confounding variables, and emerging complementary biomarkers pertinent to clinical decision-making. Methods: A structured search of PubMed, Embase, and the Cochrane Library (January 2000 to October 2025) identified studies evaluating BNP, NT-proBNP, and atrial natriuretic peptide (ANP) in intensive care unit (ICU) patients. Eligible studies and review articles assessed diagnostic utility, volume status, hemodynamic monitoring, and prognostic performance. Narrative synthesis was employed using information obtained from eligible studies. Results: Twenty-four studies met the inclusion criteria. BNP and NT-proBNP facilitate differentiation between cardiogenic and noncardiogenic respiratory failure, identification of mixed shock states, and assessment of volume status when used in association with other modalities such as echocardiography and ultrasonography. Elevated natriuretic peptide concentrations consistently predict mortality, acute kidney injury, prolonged mechanical ventilation, and adverse outcomes in several disease states, including sepsis, acute respiratory distress syndrome [ARDS], postoperative cardiac dysfunction, and COVID-19-related critical illness. However, interpretation remains limited by confounders, including renal impairment, age, systemic inflammation, brain injury, mechanical ventilation, and right-ventricular strain/dysfunction. Conclusions: Natriuretic peptides serve as valuable adjuncts for diagnostic assessment, hemodynamic monitoring, and risk stratification in the ICU. When interpreted with attention to biological kinetics and clinical context, these biomarkers enhance multimodal monitoring and support individualized management. Future research should refine ICU-specific cutoffs and assess natriuretic peptide–guided therapeutic strategies in prospective multicenter trials. Full article

Background: Post-COVID-19 condition (PCC) is a complication following acute COVID-19 infection, which may lead to long-term cardiac abnormalities. This review aimed to assess the prevalence of structural/functional deviations in echocardiography in individuals with PCC compared to patients without PCC. Methods: We searched three databases. Two reviewers independently screened articles using LASER Al and extracted relevant data using a piloted Excel sheet. We performed meta-analysis using OpenMeta and RevManWeb and a subgroup analysis based on patients’ settings during acute COVID-19. We assessed the risk of bias using the Hoy et al. tool and the certainty using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. Results: We included 16 studies that reported on differences in echocardiographic findings in patients with or without PCC. Individuals with PCC were more likely to have structural/functional deviations in echocardiographic readings of unclear clinical significance, particularly those who were hospitalized during acute COVID-19. The overall certainty of the evidence was very low due to the high risk of bias, indirectness, and imprecision. Conclusions: This review provides insight into the use of echocardiograms and the frequency of test deviations in individuals with PCC. Despite existing evidence, there is a need for future studies to assess the diagnostic test accuracy of echocardiograms in PCC. Full article

Background/Objectives: Heart failure (HF) has been associated with adverse outcomes in coronavirus disease 2019 (COVID-19), but it remains unclear whether HF independently predicts sepsis and mortality once inflammatory and cardiac biomarkers are considered. Methods: This single-center retrospective cohort analysis included 127 adult patients hospitalized with laboratory-confirmed COVID-19 at a tertiary infectious diseases hospital between March 2020 and December 2024. Pre-existing HF was defined based on cardiology records and chronic HF therapy. Baseline assessments included clinical characteristics, echocardiography, and biomarkers (NT-proBNP, high-sensitivity troponin, C-reactive protein [CRP], interleukin 6 [IL-6], procalcitonin, and D-dimer) measured within 24 h of admission. Primary outcomes were sepsis and all-cause mortality (in-hospital or 30-day). Independent associations with sepsis and mortality were examined using multivariable logistic regression incorporating demographic factors, major comorbidities, baseline disease severity, and inflammatory and cardiac biomarkers. Results: Of 127 patients (mean age 70.1 ± 14.8 years, 63.8% male), 30 (23.6%) had pre-existing HF. Patients with preexisting heart failure exhibited significantly reduced left ventricular ejection fraction and higher admission levels of NT-proBNP and high-sensitivity troponin, accompanied by a substantially increased burden of in-hospital cardiovascular complications (53.3% vs. 14.4%, p < 0.001). However, sepsis (6.7% vs. 7.2%, p = 1.000) and total mortality (20.0% vs. 17.5%, p = 0.971) did not differ significantly between HF and non-HF groups. In multivariable analyses, HF was not independently associated with sepsis (adjusted odds ratio [aOR] 0.78, 95% confidence interval [CI] 0.05–12.34, p = 0.855) or mortality (aOR 0.63, 95% CI 0.16–2.46, p = 0.506). By contrast, higher CRP (aOR 1.01 per 1 mg/L, 95% CI 1.00–1.01, p = 0.007), IL-6 (aOR 1.01 per 1 pg/mL, 95% CI 1.00–1.01, p = 0.025), and high-sensitivity troponin (aOR >999, 95% CI 138–>999, p = 0.001) were independently associated with mortality. Conclusions: In hospitalized COVID-19 patients, pre-existing HF identifies a subgroup with heightened cardiac biomarker activation and a substantially higher burden of cardiovascular complications but does not associate with sepsis or short-term mortality in this cohort after adjustment for inflammatory and cardiac biomarkers. Mortality risk appears to be driven primarily by systemic inflammation and acute myocardial injury, as reflected by CRP, IL-6, and high-sensitivity troponin. These findings support a biomarker-driven approach to risk stratification in COVID-19, in which dynamic inflammatory and cardiac injury profiles provide more prognostic information than HF status alone, while still warranting intensified cardiovascular surveillance in patients with HF. Full article

Background: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) can cause persistent, multisystem complications collectively termed long COVID. Cardiovascular sequelae are among the most clinically significant yet remain incompletely characterized. This review aimed to synthesize current evidence on objective cardiovascular outcomes in long COVID and explore underlying mechanisms. Methods: A systematic review was conducted using PubMed, Scopus, and Web of Science for studies published between January 2020 and March 2024. Search terms included “COVID-19,” “long COVID,” “post-acute sequelae,” “cardiovascular,” “echocardiography,” “biomarkers,” and “imaging.” Only studies reporting at least one cardiovascular outcome, defined as either objectively measured parameters (e.g., echocardiography, cardiac biomarkers, ECG findings, or vascular function indices) or clinically relevant cardiovascular symptoms during follow-up, were included. From 412 identified records, ten recent, high-quality studies with a primary cardiovascular focus were selected. This systematic review was conducted in accordance with the PRISMA 2020 guidelines. Results: Long COVID is associated with subclinical myocardial dysfunction, arrhythmias, endothelial injury, vascular stiffness, and a prothrombotic state. Reported findings included reduced left ventricular ejection fraction, impaired global longitudinal strain, increased arterial stiffness, elevated cardiac biomarkers, new-onset hypertension, and persistent ECG changes, even in non-hospitalized patients without prior cardiovascular disease. Proposed mechanisms include myocardial inflammation, endothelial dysfunction, renin–angiotensin–aldosterone system dysregulation, autonomic imbalance, and chronic inflammation. Secondary bacterial and fungal infections were noted in critically ill survivors but did not fully explain the breadth or persistence of symptoms. Conclusions: Long COVID is a heterogeneous entity with substantial cardiovascular implications across all levels of acute disease severity. Early detection through longitudinal monitoring, standardized definitions, and multidisciplinary care is essential to reduce long-term cardiovascular risk. Full article

Background: Cardiac arrhythmias are a frequent complication of acute SARS-CoV-2 infection. However, their long-term prevalence and clinical determinants among patients with post-COVID-19 syndrome, especially those previously hospitalized, remain poorly defined. Objectives: To assess the prevalence and types of arrhythmias in long COVID patients following hospitalization and to identify associated clinical risk factors. Methods: In this cross-sectional study, 53 patients previously hospitalized with confirmed COVID-19 were evaluated ≥3 months post-infection. All participants underwent a standardized clinical assessment, 12-lead electrocardiography, and 24 h Holter monitoring. Logistic and Cox regression analyses were performed to identify predictors of arrhythmia. Results: Arrhythmias were identified in 41.5% (n = 22) of patients. Atrial fibrillation (32%) was the most frequent arrhythmia, followed by sinus bradycardia (27%) and sinus tachycardia (18%). Age (OR 1.06, 95% CI 1.01–1.10, p = 0.01) and length of hospital stay (OR 1.1, 95% CI 1.01–1.2, p = 0.04) were independently associated with arrhythmia. Biguanide (metformin) therapy was inversely associated with the occurrence of arrhythmia (Exp(B) = 0.017, p = 0.008). Dyspnea (82.4%) and palpitations (41.5%) were the most commonly reported symptoms. Conclusions: Arrhythmias are common in patients with long COVID following severe disease. Advanced age and prolonged hospitalization are significant risk factors, while biguanide use may offer a protective effect. These findings underscore the need for targeted cardiac surveillance in this population. Full article

Influenza has long been a well-documented contributor to cardiovascular morbidity and mortality, particularly among high-risk groups. COVID-19 has notably altered the seasonality and natural history of pandemic influenza, with broad implications for related cardiac complications. This review examines the interaction between influenza and cardiovascular illness, especially myocardial infarction, congestive heart failure, stroke, and other acute cardiac events. We review the impact of the COVID-19 pandemic on influenza transmission dynamics, public health policy, and the evolving burden of cardiovascular complications. New evidence indicates that both diseases exacerbate endothelial dysfunction, systemic inflammation, and prothrombotic states, thereby increasing cardiovascular risk. A comparative analysis of pre- and post-COVID-19 influenza-related cardiac complications clarifies evolving trends and guides future preventive strategies. In light of the recent resurgence of influenza following the relaxation of COVID-19 mitigation measures, maximizing vaccine coverage and collaborating to manage viral infections in patients with cardiovascular disease are critical. This review focuses on key research needs to understand long-term cardiac consequences and the urgent requirement for targeted public health strategies to counter viral-mediated cardiovascular threats. In the post-COVID era, integrating influenza and COVID-19 vaccination strategies into cardiovascular risk management may represent a critical opportunity to reduce virus-triggered cardiovascular morbidity and mortality. Full article

Background: Chronically non-healing thoracic wounds after cardiac and non-cardiac thoracotomy, including cases when coronary artery bypass grafting (CABG) is performed, represent a great clinical challenge. It is often that a conservative treatment of the wounds does not provide effective regeneration of the damaged tissues. It is especially critical in patients with infected wounds, in patients owning a systemic infection, and in elderly people. Methods: The article presents a case report of successful treatment of a 63-year-old man with refractory chronic osteomyelitis of the sternum and mediastinitis four years after CABG, complicated by COVID-19 at the time of reconstructive surgery. Due to the low effectiveness of conservative treatment methods, a two-stage approach was applied: radical surgical wound debridement followed by infiltration of the wound with allogenic mesenchymal stromal cells (MSCs) of Wharton’s jelly (WJ-MSCs). Results: This double-stage therapy successfully modulated the inflammatory environment and stimulated granulation, facilitating final thoracoplasty and osteosynthesis. The patient achieved complete healing of the sternum, demonstrating benefits of WJ-MSCs in treating conservative treatment-resistant infections in the surgical wound. Conclusions: The advantages of using perinatal mesenchymal stem cells, with WJ-MSCs as a type of this class of MSCs, were demonstrated in treating chronically infected sternal surgical wounds. We also compared their regenerative properties to other stem cell types like bone marrow MSCs. Full article

Post-COVID cardiac complications have emerged as a significant and persistent clinical concern, yet their underlying mechanisms remain poorly understood. Animal models can act as proxies to investigate the pathophysiology of the human, post-acute sequelae of SARS-CoV-2 infection (PASC). The aim of this experimental study was to evaluate the expression of inflammatory biomarkers in cardiac tissue 28 days after SARS-CoV-2 infection in a female hACE2 mouse model, with a focus on chemokine-mediated immune activation. Twelve female C57BL/6 hACE2 mice were infected with the Omicron variant (BA.1.17 lineage) of SARS-CoV-2, and eleven non-infected mice served as controls. Cardiac tissue was analyzed via Western blot for markers of innate immune activation (TLR4, MyD88, NF-κB) and pro-inflammatory cytokines (IL-6, IL-18, IL-1β, TNF-α, CD11d). Cardiac tissue injury markers (iNOS, PAI-1 and Connexin43) were also analyzed. Compared to non-infected mice, cardiac tissue from infected mice showed significantly higher expression of IL-6 (p = 0.028), indicating an inflammatory state, and CD11d (p = 0.016), suggesting an inflammatory stage accompanied by sustained activation of chemokine-mediated inflammatory signaling. No significant differences in TLR4 (p = 0.340), MyD88 (p = 0.410), NF-κB p65 (p = 0.780), IL-18 (p = 0.548), IL-1β (p = 0.455), and TNF-α (p = 0.125) expressions were observed Similarly, no changes in cardiac damage markers (iNOS: p = 0.4684; PAI-1: p = 0.5345; Connexin 43: p = 0.2879) were found. The results of this experimental study would support the hypothesis of persistent low-grade inflammation as a contributor to post-COVID cardiac sequelae in females that is not accompanied by severe tissue damage, as also observed in clinical studies. This study also reinforces the need for studies evaluating the functional and structural evolution of the myocardium after an acute SARS-CoV-2 infection. Full article

Background: Pediatric SARS-CoV-2 infection is usually mild, but in rare cases may lead to severe complications. Early recognition and comprehensive management are critical for favorable outcomes. Case Presentation: We present the case of a 2-year-old girl, previously healthy and unvaccinated against Streptococcus Pneumoniae (S. pneumoniae), who developed SARS-CoV-2 infection and acute otitis media. Initial laboratory evaluation revealed leukocytosis with neutrophilia and increased inflammatory markers. Antiviral and antibiotic treatment was initiated, but she remained febrile, polypneic, and tachycardic. The diagnosis of MIS-C was excluded; there was no involvement of two organs, and infection with S. pneumoniae serotype 19 F was identified. Given the unfavorable evolution, corticosteroid therapy and immunoglobulin were instituted, and subsequently, following the antibiogram result, antibiotic therapy was escalated to Meropenem and Linezolid. Clinical and laboratory parameters improved, but pericarditis with a small fluid slide and ECG changes were associated. The evolution was favorable with complete cardiac recovery at 30 days. Conclusion: This case highlights the importance of vigilant assessment for secondary bacterial infections and cardiac complications in pediatric COVID-19. Prompt recognition and targeted treatment are essential, and pneumococcal vaccination remains a fundamental preventive measure. Moreover, the scarcity of literature documenting SARS-CoV-2 infections complicated by pericarditis further underscores the uniqueness of this case and its relevance for specialists in the field. Full article

The coronavirus disease 2019 (COVID-19) pandemic has revealed a close and multifaceted relationship between viral infection, systemic inflammation, and cardiovascular health. Among the cardiac complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), atrial fibrillation (AF)—especially new-onset atrial fibrillation (NOAF)—has emerged as a major determinant of disease severity and prognosis. Clinical studies and meta-analyses show that 5–10% of hospitalized COVID-19 patients develop AF, with markedly higher rates in critically ill individuals. Both pre-existing and NOAF are independently associated with increased risks of intensive care admission, mechanical ventilation, thromboembolic events, and mortality. The underlying mechanisms involve a combination of cytokine-mediated inflammation, endothelial dysfunction, microvascular injury, and dysregulation of the renin–angiotensin–aldosterone system (RAAS). Viral downregulation of angiotensin-converting enzyme 2 (ACE2) receptors contributes to myocardial fibrosis, while hypoxia, oxidative stress, and autonomic imbalance further promote electrical remodeling and arrhythmogenesis. Post-infectious studies indicate that atrial structural changes and autonomic dysfunction may persist for months, predisposing survivors to recurrent arrhythmias. Technological advances in telecardiology and digital medicine have provided new tools for early detection and long-term monitoring. Wearable electroencephalography (ECG) devices, implantable loop recorders (ILRs), and artificial intelligence (AI)-based diagnostic algorithms enable continuous rhythm surveillance and individualized management, improving outcomes in post-COVID patients. This review summarizes current evidence on the epidemiology, pathophysiology, clinical implications, and monitoring strategies of AF in COVID-19. It underscores the importance of integrating telemedicine and AI-assisted diagnostics into cardiovascular care to mitigate the long-term arrhythmic and systemic consequences of SARS-CoV-2 infection. Full article

Background/Objectives: Whether a remote history of SARS-CoV-2 infection independently affects early haemodynamic stability after elective cardiopulmonary bypass (CPB) remains uncertain. We evaluated whether prior COVID-19 (>7 weeks before surgery) was associated with postoperative vasopressor requirements or early complications in adults undergoing elective CPB. Methods: We conducted a single-centre prospective cohort study including adults (≥18 years) scheduled for elective on-pump coronary, valve, or combined cardiac surgery between 1 August 2022 and 30 October 2023. Patients undergoing emergency procedures or surgery < 7 weeks after infection were excluded. The exposure was a documented history of COVID-19 for >7 weeks preoperatively. The primary outcome was postoperative vasopressor use within 24 h of ICU admission; secondary outcomes included inotrope use, arrhythmias, acute cardiac or respiratory failure, pneumonia, acute kidney injury (KDIGO), delirium, stroke, length of stay, and mortality. Multivariable logistic regression adjusted for age, CPB duration, obesity, anaemia, chronic kidney disease, sex, EuroSCORE I, left ventricular ejection fraction, and procedure type. Results: Of 351 screened patients, 280 elective CPB cases were analyzed; 101 (36.1%) had prior COVID-19. Vasopressor use occurred in 151/280 (53.9%) patients, with no difference between COVID and non-COVID groups (53.5% vs. 54.2%; p = 1.00). Prior COVID-19 was not associated with vasopressor requirement (adjusted OR 0.94, 95% CI 0.56–1.59). Independent predictors were longer CPB duration (aOR 2.80 per hour; p < 0.001) and older age (aOR 1.028 per year; p = 0.02). Secondary outcomes, including organ dysfunction and mortality, did not differ between groups. Conclusions: In adults undergoing elective CPB ≥ 7 weeks after SARS-CoV-2 infection, prior COVID-19 did not increase early vasopressor needs or short-term postoperative complications. Haemodynamic requirements were primarily driven by CPB duration and age. Further research using dose-standardized vasoactive metrics and formal COVID-19 severity stratification is warranted. Full article

Background/Objectives: An increasing number of older individuals require general anaesthesia for major non-cardiac surgery, with 20% displaying postoperative complications. Regional cerebral oxygen saturation (rSO₂) correlates with the gold standard of mixed venous oxygen saturation, indicating global perfusion. We hypothesised that rSO₂-based anaesthesia reduces organ dysfunction and morbidity after major non-cardiac surgery. Methods: In Singapore and Toronto, we conducted a prospective, double-blind, randomised controlled trial in elderly patients undergoing major non-cardiac surgery, after obtaining research ethics board permission and informed consent. This RCT followed the CONSORT guidelines. Patients received bilateral cerebral oximetry sensors, and the control group received standard care. In the intervention group, an algorithm restored rSO₂ if it dropped 10% below baseline for >15 s by adjusting cerebral perfusion pressure, inspired oxygen concentration, end-tidal carbon dioxide, depth of anaesthesia, haemoglobin, and cardiac index. Postoperative complications and outcomes were noted. Categorical data were analysed using Chi-square or Fisher’s exact tests and continuous data using a t-test or a Mann–Whitney U test. The study was powered for 394 patients, but due to the COVID-19 pandemic and funding constraints, this study was terminated at 101 patients. Results: Of 101 patients, 49 were randomised to the control and 52 to the intervention group. A total of 31 (63%) patients in the control group and 30 (58%) in the interventional exhibited bilateral cerebral desaturation. Time of cumulative cerebral desaturation was longer in the control group (23 ± 48 min vs. 9 ± 15 min, respectively, p = 0.01). A total of 142 algorithm-based treatments were employed, restoring rSO₂ in 29 (86%) patients. Both groups displayed equal postoperative outcomes. Conclusions: In major non-cardiac surgery, cerebral desaturation is prevalent in over 85% of patients. Although algorithm-guided therapy restored rSO₂ in the majority of patients, it did not result in reduced postoperative morbidity. Full article

The utilisation of cardiopulmonary bypass (CPB) during cardiac surgery is often associated with complex haemostatic perturbations, frequently manifesting as a paradoxical risk of both bleeding and thrombosis. This is postulated to be driven by systemic inflammation, endothelial activation and contact activation of the coagulation cascade due to extracorporeal circulation. However, the coronavirus disease 2019 (COVID-19) pandemic revealed a unique hypercoagulable state, termed COVID-19-associated coagulopathy (CAC), also observed in those vaccinated against COVID-19. CAC displays similar physiological manifestations to those of disseminated intravascular coagulation (DIC), characterised by elevated fibrinogen and D-dimer values. The precise pathogenesis of CAC requires further elucidation though proposed mechanisms include: an exaggerated inflammatory response to COVID-19 infection or antibody proliferation due to vaccination, direct epithelial cell damage mediated by angiotensin converting enzyme 2, and ‘hypoxithrombosis’. CAC has since provided a unique framework to understand and potentially mitigate coagulation complications encountered during CPB in the post-pandemic era, as it is no longer sufficient to view COVID-19 as a transient influence on surgical risk. Rather, it must be recognized as a persistent modifier of the haemostatic environment across the population, with direct implications upon patient selection, intraoperative management and postoperative care in cardiac surgery. This review examines the pathological drivers behind CAC alongside the insights obtained from CAC management during ECMO deployment, to investigate the potential translation of such knowledge into improved anticoagulation strategies and monitoring during cardiac surgery. The use of alternative anticoagulants including factor XI inhibitors and the modulation of heparinase activity offers promising avenues to attenuate coagulopathies more commonly observed during CPB in the post-pandemic climate, whilst anti-Xa assays and viscoelastic testing have offered applicability to modern perfusion practices. By bridging the knowledge gained during the pandemic with that of conventional CPB, this review aims to inform future strategies for haemostasis management in cardiac surgery in a novel cohort of surgical patients. Full article

The SARS-CoV-2 pandemic has posed global medical challenges due to its ability to affect multiple organ systems. Among the post-COVID-19 complications, multisystem inflammatory syndrome has emerged as a severe condition affecting both children (MIS-C) and adults (MIS-A). This review aims to compile and analyze published data to investigate clinical characteristics, laboratory findings, and outcomes of MIS post-COVID-19. A comprehensive search of various databases was conducted to identify studies reporting MIS-related complications in pediatric and adult populations post-COVID-19 infection. Screening, data extraction, and cross-checking were performed by two independent reviewers. Only 64 studies met our inclusion criteria, and compiled results revealed that cardiac complications were the predominant manifestation followed by gastrointestinal, hematologic, neurological, and mucocutaneous involvement. Laboratory findings consistently demonstrated elevated inflammatory markers including CRP, ferritin, D-dimer, and IL-6. Most patients required hospitalization, and many needed intensive care; treatment typically involved IVIG, corticosteroids, and biologic therapies. While most patients recovered, a subset experienced persistent complications. These findings highlight the importance of early recognition, multidisciplinary management, and structured follow-up for MIS. Future research is warranted to clarify the underlying mechanisms, risk factors, and long-term outcomes associated with MIS in post-COVID-19 patients. Full article

Background/Objectives: Sudden cardiac arrest (SCA) accounts for ~50% of cardiovascular mortality in the U.S. Cardiovascular complications are common in acute and post-acute COVID-19 infection. We aimed to examine nationwide trends in SCA-related hospitalizations in the United States before and during the COVID-19 outbreak. Methods: Using data from the National Inpatient Sample, we conducted a retrospective analysis of hospitalizations for SCA in the U.S. between 2016 and 2020. Sociodemographic and clinical characteristics and in-hospital mortality were compared between the pre-COVID (2016–2019) and COVID (2020) eras. Multivariable analysis was performed to identify factors associated with mortality. Results: Among a weighted total of 153,100 SCA hospitalizations between 2016 and 2020, the median age was 65 years, 62.7% were male, and 66.6% were white. There was a trend towards fewer hospitalizations in 2020 compared to prior years (n = 28,585 vs. n_average = 32,129, p = 0.07). In-hospital mortality remained unchanged between the pre-COVID and COVID eras (47.7% vs. 47.3%, p = 0.66). Increased mortality was associated with female sex (OR: 1.21; 95% CI: 1.15–1.28; p < 0.001), non-white race (OR: 1.24; 95% CI: 1.15–1.28; p < 0.001), history of renal failure (OR: 1.08; 95% CI: 1.02–1.15; p = 0.007), and diabetes (OR: 1.32; 95% CI: 1.25–1.39; p < 0.001). In 2020, 1.5% of the study population was diagnosed with COVID-19 infection, which was found to be independently associated with increased in-hospital mortality (OR: 1.57; 95% CI: 1.27–1.95; p < 0.001). Conclusions: In 2020, there was a trend towards a decrease in hospitalizations for SCA, while COVID-19 infection was independently associated with higher in-hospital mortality among patients admitted with SCA. Full article