Search Results (132)

Burn injuries result in complex physiological and psychological sequelae, including hypermetabolism, muscle wasting, mobility impairment, scarring, and disrupted body image. While advances in acute care have improved survival, comprehensive rehabilitation strategies are critical for restoring function, appearance, and psychosocial well-being. Structured physical activity, including resistance and aerobic training, plays a central role in counteracting muscle atrophy, improving cardiovascular function, enhancing scar quality, and promoting psychological resilience and body image restoration. This narrative review synthesizes the current evidence on the effects of exercise-based interventions on post-burn recovery, highlighting their therapeutic mechanisms, clinical applications, and implementation challenges. In addition to physical training, emerging technologies such as virtual reality, aquatic therapy, and compression garments offer promising adjunctive benefits. Notably, artificial intelligence (AI) is gaining traction in burn rehabilitation through its integration into wearable biosensors and telehealth platforms that enable real-time monitoring, individualized feedback, and predictive modeling of recovery outcomes. These AI-driven tools have the potential to personalize exercise regimens, support remote care, and enhance scar assessment and wound tracking. Overall, the integration of exercise-based interventions with digital technologies represents a promising, multimodal approach to burn recovery. Future research should focus on optimizing exercise prescriptions, improving access to personalized rehabilitation tools, and advancing AI-enabled systems to support long-term recovery, functional independence, and positive self-perception among burn survivors. Full article

Post-acute sequelae of COVID-19 have been associated with an elevated risk of thromboembolism and adverse cardiovascular events (CVEs). We aim to evaluate whether alterations in poorly studied hemostatic and endothelial proteins are associated with CVEs in patients previously admitted to the ICU and evaluated one year post-discharge. We carried out a cross-sectional study involving 63 COVID-19 patients previously admitted to the ICU one year post-discharge. Plasma levels of factor IX (coagulation factor), protein C, protein S (natural anticoagulant), and von Willebrand factor (VWF, an endothelial marker) were measured using a Luminex 200™ analyzer. Generalized linear models (GLMs) were used to assess the association of these coagulation proteins with CVEs and N-terminal pro-B-type natriuretic peptide (NT-proBNP). We found that lower levels of factor IX (p = 0.011), protein C (p = 0.028), and protein S (p = 0.008) were associated with CVEs one year after ICU discharge. Additionally, at the one-year follow-up, we found lower levels of factor IX (p = 0.002) and higher levels of VWF (p = 0.006) associated with higher levels of NT-proBNP, underscoring the involvement of both hemostatic imbalance and persistent endothelial dysfunction. Our findings revealed a gender-specific pattern of associations with NT-proBNP levels. These findings highlight the significant role of persistent hemostatic imbalance and endothelial dysfunction in the development of cardiovascular abnormalities among COVID-19 survivors discharged from the ICU. Full article

Rising morbidity and mortality from cardiovascular disease (CVD) have increased interest in precision and preventive management to reduce long-term sequelae. While retinal imaging has traditionally been recognized for identifying vascular changes in systemic conditions such as hypertension and type 2 diabetes mellitus, a new ophthalmologic field, cardiac-oculomics, has associated retinal biomarker changes with other cardiovascular diseases with retinal manifestations. Several imaging modalities visualize the retina, including color fundus photography (CFP), optical coherence tomography (OCT), and OCT angiography (OCTA), which visualize the retinal surface, the individual retinal layers, and the microvasculature within those layers, respectively. In these modalities, imaging-derived biomarkers can present due to CVD and have been linked to the presence, progression, or risk of developing a range of CVD, including hypertension, carotid artery disease, valvular heart disease, cerebral infarction, atrial fibrillation, and heart failure. Promising artificial intelligence (AI) models have been developed to complement existing risk-prediction tools, but standardization and clinical trials are needed for clinical adoption. Beyond risk estimation, there is growing interest in assessing real-time cardiovascular status to track vascular changes following pharmacotherapy, surgery, or acute decompensation. This review offers an up-to-date assessment of the cardiac-oculomics literature and aims to raise awareness among cardiologists and encourage interdepartmental collaboration. Full article

Cardiovascular complications are a hallmark of Post-Acute Sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection (PASC), yet the mechanisms driving persistent cardiac dysfunction remain poorly understood. Emerging evidence implicates mitochondrial dysfunction in immune cells as a key contributor. This study investigated whether CD14⁺⁺ monocytes from long COVID patients exhibit bioenergetic impairment, mitochondrial DNA (mtDNA) damage, and defective oxidative stress adaptation, which may underlie cardiovascular symptoms in PASC. CD14⁺⁺ monocytes were isolated from 14 long COVID patients with cardiovascular symptoms (e.g., dyspnea, angina) and 10 age-matched controls with similar cardiovascular risk profiles. Mitochondrial function was assessed using a Seahorse Agilent Analyzer under basal conditions and after oxidative stress induction with buthionine sulfoximine (BSO). Mitochondrial membrane potential was measured via Tetramethylrhodamine Ethyl Ester (TMRE) assay, mtDNA integrity via qPCR, and reactive oxygen species (ROS) dynamics via Fluorescence-Activated Cell Sorting (FACS). Parallel experiments exposed healthy monocytes to SARS-CoV-2 spike protein to evaluate direct viral effects. CD14⁺⁺ monocytes from long COVID patients with cardiovascular symptoms (n = 14) exhibited profound mitochondrial dysfunction compared to age-matched controls (n = 10). Under oxidative stress induced by buthionine sulfoximine (BSO), long COVID monocytes failed to upregulate basal respiration (9.5 vs. 30.4 pmol/min in controls, p = 0.0043), showed a 65% reduction in maximal respiration (p = 0.4035, ns) and demonstrated a 70% loss of spare respiratory capacity (p = 0.4143, ns) with significantly impaired adaptation to BSO challenge (long COVID + BSO: 9.9 vs. control + BSO: 54 pmol/min, p = 0.0091). Proton leak, a protective mechanism against ROS overproduction, was blunted in long COVID monocytes (3-fold vs. 13-fold elevation in controls, p = 0.0294). Paradoxically, long COVID monocytes showed reduced ROS accumulation after BSO treatment (6% decrease vs. 1.2-fold increase in controls, p = 0.0015) and elevated mitochondrial membrane potential (157 vs. 113.7 TMRE fluorescence, p = 0.0179), which remained stable under oxidative stress. mtDNA analysis revealed severe depletion (80% reduction, p < 0.001) and region-specific damage, with 75% and 70% reductions in amplification efficiency for regions C and D (p < 0.05), respectively. In contrast, exposure of healthy monocytes to SARS-CoV-2 spike protein did not recapitulate these defects, with preserved basal respiration, ATP production, and spare respiratory capacity, though coupling efficiency under oxidative stress was reduced (p < 0.05). These findings suggest that mitochondrial dysfunction in long COVID syndrome arises from maladaptive host responses rather than direct viral toxicity, characterized by bioenergetic failure, impaired stress adaptation, and mitochondrial genomic instability. This study identifies persistent mitochondrial dysfunction in long COVID monocytes as a critical driver of cardiovascular complications in PASC. Key defects—bioenergetic failure, impaired stress adaptation and mtDNA damage—correlate with clinical symptoms like heart failure and exercise intolerance. The stable elevation of mitochondrial membrane potential and resistance to ROS induction suggest maladaptive remodeling of mitochondrial physiology. These findings position mitochondrial resilience as a therapeutic target, with potential strategies including antioxidants, mtDNA repair agents or metabolic modulators. The dissociation between spike protein exposure and mitochondrial dysfunction highlights the need to explore host-directed mechanisms in PASC pathophysiology. This work advances our understanding of long COVID cardiovascular sequelae and provides a foundation for biomarker development and targeted interventions to mitigate long-term morbidity. Full article

SARS-CoV-2 infection has resulted in more than 700 million cases and nearly 7 million deaths worldwide. Although vaccination efforts have effectively reduced mortality and transmission rates, a significant proportion of recovered patients—up to 40%—develop long COVID syndrome (LC) or post-acute sequelae of COVID-19 infection (PASC). LC is characterized by the persistence or emergence of new symptoms following initial SARS-CoV-2 infection, affecting the cardiovascular, neurological, respiratory, gastrointestinal, reproductive, and immune systems. Despite the broad range of clinical symptoms that have been described, the risk factors and pathogenic mechanisms behind LC remain unclear. This review, the first of a two-part series, is distinguished by the discussion of the role of the SARS-CoV-2 spike protein in the primary mechanisms underlying the pathophysiology of LC. Full article

Although the acute phase of the COVID-19 pandemic has subsided, the emergence of the post-COVID-19 condition presents a new and complex public health challenge, characterized by persistent, multisystem symptoms that can endure for weeks or months after the initial infection with the SARS-CoV-2 virus, significantly affecting survivors’ quality of life. Among the most concerning sequelae are cardiovascular complications, which encompass a broad spectrum of conditions, including arrhythmias, myocardial damage, or postural orthostatic tachycardia syndrome. This narrative review explores the burden of the SARS-CoV-2 infection on cardiovascular health by reviewing the latest and most relevant findings in the literature and highlighting different aspects of COVID-19’s cardiovascular involvement. This review investigates the pathophysiological mechanisms underlying cardiovascular involvement in the post-COVID-19 condition, with a focus on direct viral invasion via ACE2 receptors, immune-mediated cardiovascular injury, cytokine storm, systemic inflammation, endothelial dysfunction, and mitochondrial injury. The interplay between pre-existing cardiovascular diseases, such as hypertension, atherosclerosis, diabetes, and atrial fibrillation, and COVID-19 is also explored, revealing that individuals with such conditions are at heightened risk for both severe acute illness and long-term complications. Long-term immune activation and the persistence of viral antigens are increasingly recognized as contributors to ongoing cardiovascular damage, even in individuals with mild or asymptomatic initial infections. As the healthcare system continues to adapt to the long-term consequences of the SARS-CoV-2 pandemic, a deeper understanding of these cardiovascular manifestations is essential. This knowledge will inform the development of targeted strategies for prevention, clinical management, and rehabilitation of affected patients. Furthermore, the insights gained from the intersection of COVID-19 and cardiovascular health will be instrumental in shaping responses to future viral epidemics, highlighting the necessity for multidisciplinary approaches to patient care and public health preparedness. Full article

Infective endocarditis (IE) is a relatively rare but potentially life-threatening disease characterized by substantial mortality and long-term sequelae among the survivors. In recent decades, a dramatic change in the profile of patients diagnosed with IE has been observed primarily in developed countries, most likely due to an aging population and a recent increase in invasive medical procedures. Nowadays, the typical IE patient is usually older, with complex comorbidities, and a history significant for cardiac disease, including degenerative heart valve disease, prosthetic valves, or cardiovascular implantable electronic devices (CIEDs). Moreover, as patient risk factors change, predisposing them to more healthcare-associated IE, the microbiology of IE is also shifting; there are growing concerns regarding the rise in the incidence of IE caused by difficult-to-treat resistance (DTR) bacteria in at-risk patients with frequent healthcare contact. The present review aims to explore the evolving landscape of IE and summarize the current knowledge on novel diagnostics to ensure timely diagnosis and outline optimal therapy for DTR bacterial IE. Full article

Acute aortic dissection (AAD) is a critical cardiovascular emergency marked by the rupture of the aortic intima, resulting in blood infiltration into the media and the formation of a false lumen. AAD incidence varies by area, emphasizing the need for better diagnostics and epidemiological investigations. Bucharest University Emergency Hospital’s Emergency Department conducted this retrospective cohort analysis from May 2021 to May 2023. We examined 26 Stanford Type A aortic dissection patients to establish in-hospital mortality and one-year survival rates. The primary objective was to analyze demographic, clinical, and paraclinical factors and their impact on patient outcomes. A total of 57.7% of the study group was male and had a mean age of 58.2 years, and 69.2% of patients had hypertension, indicating its importance as a risk factor. Acute chest discomfort was reported by 53.8%, neurological problems by 30.8%, and syncope or hypotension by 42.3%. CT angiography and transthoracic echocardiogram (TTE) confirmed the diagnosis and assessed dissection severity. Pericardial effusion (19.2%) and moderate to severe aortic regurgitation (26.9%) were notable. Management varied by dissection intensity and location. Emergency surgery was performed in 61.5% of patients within 24 h of diagnosis, resulting in a 12.5% in-hospital death rate. Conservatively managed patients had a 60.0% in-hospital death rate. Timely intervention is crucial, since the surgical cohort had an 87.5% one-year survival rate compared to 30% for the conservatively managed cohort. Acute renal damage (25%), protracted mechanical ventilation (31.3%), and advanced supportive care infections were postoperative sequelae. Conservative care exacerbated visceral ischemia (20%) and heart failure (10%). Advanced age and hypotension upon admission were independent mortality predictors, emphasizing the need for early risk assessment and personalized treatment. Multimodal imaging, timely surgical referral, and excellent postoperative care improve AAD outcomes, according to this study. Full article

Background/Objectives: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has caused post-acute sequelae, especially for people with pre-existing conditions, including chronic kidney disease (CKD), which may impact the cardiovascular system. Yet, despite the preliminary description of the general population’s long-COVID-19 consequences, data on CKD patients is scarce. The aim of this study was to investigate the longitudinal effects of COVID-19 on echocardiographic parameters of cardiac function and on cardiac biomarkers in patients with CKD. Methods: A total of 163 patients were included in this observational prospective trial (listed under NCT05125913 code): 88 in the COVID-19 group and 75 in the control group. The serial echocardiographic characteristics in patients who survived beyond one year, focused on left and right ventricular systolic function, together with cardiac biomarkers evolution, were compared between the two groups. Results: At baseline, there were no significant differences in left ventricular (LV) function parameters, except for a higher Tei Index in the COVID-19 group (p < 0.01). Right ventricular (RV) systolic dysfunction was more frequent in the COVID-19 group, with worse fractional area change (FAC) (p = 0.01), RV free wall longitudinal strain (RVFWLS) (p = 0.01), and RV Tei Index (p = 0.01). Over time, the control group showed a decline in LV ejection fraction (EF), while the COVID-19 group slightly improved. RV global systolic function was better preserved in the COVID-19 group. To the best of our knowledge, this is the first study that demonstrates a statistically significant increase in LAVi in patients with COVID-19. Conclusions: Prior COVID-19 infection influenced the trajectory of LV and RV function in CKD patients over 12 months, suggesting potential transient myocardial adaptations. While overall cardiac function did not differ significantly between groups, COVID-19 survivors exhibited better preservation of some ventricular function parameters. Full article

Orexins (OXs) are critical for regulating circadian rhythms, arousal, appetite, energy metabolism, and electrolyte balance, affecting both the autonomic nervous system (ANS) and the cardiovascular system (CVS). Disruption of the OX system can result in symptoms similar to those observed in post-acute sequelae of COVID-19 (PASC). This review emphasizes the adverse effects of OX dysregulation on autonomic and cardiometabolic functions in patients with PASC. Additionally, we highlight the potential of anti-OX therapies to provide neuroprotective, anti-inflammatory, and immunoregulatory benefits, offering hope for alleviating some of the debilitating symptoms associated with PASC. Full article

Background/Objectives: Non-invasive respiratory support and invasive mechanical ventilation are critical interventions that can induce significant changes not only in the lungs but also in extra-pulmonary organs, which are often overlooked. Understanding the extra-pulmonary effects of non-invasive respiratory support and invasive mechanical ventilation is crucial since it can help prevent or mitigate complications and improve outcomes. This narrative review explores these consequences in detail and highlights areas that require further research. Main Text: Non-invasive respiratory support and invasive mechanical ventilation can significantly impact various extrapulmonary organs. For instance, some ventilation strategies can affect venous return from the brain, which may lead to neurological sequelae. In the heart, regardless of the chosen ventilation method, increased intrathoracic pressure (ITP) can also reduce venous return to the heart. This reduction in turn can decrease cardiac output, resulting in hypotension and diminished perfusion of vital organs. Conversely, in certain situations, both ventilation strategies may enhance cardiac function by decreasing the work of breathing and lowering oxygen consumption. In the kidneys, these ventilation methods can impair renal perfusion and function through various mechanisms, including hemodynamic changes and the release of stress hormones. Such alterations can lead to acute kidney injury or exacerbate pre-existing renal conditions. Conclusions: This review emphasizes the critical importance of understanding the extensive mechanisms by which non-invasive respiratory support and invasive mechanical ventilation affect extrapulmonary organs, including neurological, cardiovascular, and renal systems. Such knowledge is essential for optimizing patient care and improving outcomes in critical care settings. Full article

Post-acute sequelae of COVID-19 (PASC) are a diverse set of symptoms and syndromes driven by dysfunction of multiple organ systems that can persist for years and negatively impact the quality of life for millions of individuals. We currently lack specific therapeutics for patients with PASC, due in part to an incomplete understanding of its pathogenesis, especially for non-pulmonary sequelae. Here, we discuss three animal models that have been utilized to investigate PASC: non-human primates (NHPs), hamsters, and mice. We focus on neurological, gastrointestinal, and cardiovascular PASC and highlight advances in mechanistic insight that have been made using these animal models, as well as discussing the sequelae that warrant continued and intensive research. Full article

Background/Objectives: The long-term consequences of intensive treatment for Hodgkin lymphoma (HL), including metabolic syndrome (MetS) and cardiovascular diseases, but also deteriorated quality of life (QoL), are present in many survivors of childhood HL. Methods: Adolescents and young adults diagnosed with HL who continued the follow-up after successful treatment for HL were included. Anthropometric parameters, body composition, laboratory data, blood pressure values, compliance to the Mediterranean diet (MD), QoL and lifestyle habits were evaluated at the follow-up. Available data were also extracted retrospectively at the time of diagnosis. The primary objective was to determine metabolic sequelae in the early post-treatment period in adolescents treated for HL. Additionally, QoL and compliance with MD were explored, and the correlation of MetS with QoL was investigated. Results: Sixty percent of patients had at least one risk factor for metabolic syndrome, with obesity/abdominal obesity, high blood pressure and low HDL being most commonly observed, present in 66.7%, 44.4% and 44.4% of patients, respectively. The number of obese patients increased from 6.3% at the diagnosis to 31.3% at the follow-up. The majority of patients (53.3%) had low adherence to the MD. Participants had comparable quality-of-life domains to those of the healthy population at the follow-up. The physical health domain of QoL was positively correlated with compliance to the MD in young adults (r = 0.8, p = 0.032) and negatively correlated with obesity/overweight in adolescents (r = −0.85, p = 0.008). Conclusions: Healthy lifestyle choices can impact not only the metabolic health of survivors but also their quality of life, and therefore should be encouraged in these patients. Full article

Coronavirus disease 19 (COVID-19) is responsible for one of the worst pandemics in human history. The causative virus, the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), can invade host cells in multiple organs by binding the angiotensin-converting enzyme (ACE) II expressed on the cell surface. Once inside the host cell, viral replication takes place, leading to cellular disruption and the release of signal molecules that are recognised by the innate immune system. Innate immunity activation leads to the release of proinflammatory cytokines and primes the adaptive immune system. The proinflammatory environment defends against further viral entry and replication. SARS-CoV-2 infection is thought to lead to myocardial injury through several mechanisms. Firstly, direct viral-mediated cellular invasion of cardiomyocytes has been shown in in vitro and histological studies, which is related to cellular injury. Secondly, the proinflammatory state during COVID-19 can lead to myocardial injury and the release of protein remnants of the cardiac contractile machinery. Thirdly, the hypercoagulable state of COVID-19 is associated with thromboembolism of coronary arteries and/or other vascular systems. COVID-19 patients can also develop heart failure; however, the underlying mechanism is much less well-characterised than for myocardial injury. Several questions remain regarding COVID-19-related heart failure, including its potential reversibility, the role of anti-viral medications in its prevention, and the mechanisms underlying heart failure pathogenesis in long COVID-19. Further work is required to improve our understanding of the mechanism of cardiac sequelae in COVID-19, which may enable us to target SARS-CoV-2 and protect patients against longer-lasting cardiovascular complications. Full article

Background/objectives: A significant number of COVID-19 cases experience persistent symptoms after the acute infection phase, a condition known as long COVID or post-acute sequelae of COVID-19. Approved prevention and treatment options for long COVID are currently lacking. Given the heterogeneous nature of long COVID, a personalized medicine approach is essential for effective disease management. This study aimed to describe trends in pharmacotherapy from pre-COVID to post-COVID phases to gain insights into COVID-19 treatment strategies and assess whether pre-COVID pharmacotherapy can predict long COVID symptoms as a health status indicator. Methods: In the Precision Medicine for more Oxygen (P4O2) COVID-19 study, 95 long COVID patients were comprehensively evaluated through post-COVID outpatient clinics and study visits. This study focused on descriptive analysis of the pharmacotherapy patterns across different phases: pre-COVID-19, acute COVID, and post-COVID. Furthermore, associations between pre-COVID medication and long COVID outcomes were analyzed with regression analyses. Results: We observed peaks in the use of certain medications during the acute infection phase, including corticosteroids and antithrombotic agents, with a decrease in the use of renin–angiotensin system inhibitors. Consistently high use of alimentary tract medications was found across all phases. Pre-COVID respiratory medications were associated with fatigue symptoms, while antiinfectives and cardiovascular drugs were linked to fewer persisting long COVID symptom categories. Conclusion: Our findings provide longitudinal, descriptive pharmacotherapy insights and suggest that medication history can be a valuable health status indicator in characterizing patients for personalized disease management strategies, considering the heterogeneous nature of long COVID. Full article