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Cardiovascular (CV) engagement in coronavirus disease 2019 (COVID‐19) is a huge determinant of prognosis during the acute phase of the disease. However, little is known about the potential chronic implications of the late phase of COVID‐19 and about the appropriate approach to these patients. Heart failure, type 1 and type 2 myocardial infarction, arrhythmias, myocarditis, pulmonary fibrosis, and thrombosis have been shown to be related to severe acute respiratory syndrome coronavirus 2 infection, and a ‘long COVID‐19’ illness has been recognized with fatigue, chest pain, and dyspnoea among the most frequent symptoms reported after discharge from hospital. This paper focuses on some open questions that cardiologists are going to face during the next months in a general cardiology outpatient clinic, in particular how to evaluate a ‘post‐COVID’ patient during follow‐up of CV complications of the acute phase and how to manage new CV symptoms that could be the consequence, at least in part, of heart/vessels and/or lung involvement of the previous virus infection. Present symptoms and signs, history of previous CV disease (both preceding COVID‐19 and occurring during viral infection), and specific laboratory and imaging measurements during the acute phase may be of interest in focusing on how to approach the clinical evaluation of a post‐COVID patient and how to integrate in our standard of care the new information on COVID‐19, possibly in a multidisciplinary view. Dealing with the increased COVID‐associated CV risk burden and becoming acquainted with potential new e‐cardiology approaches aimed at integrating the cardiology practice are relevant new challenges brought by severe acute respiratory syndrome coronavirus 2 infection and its sequelae.

Background Severe clinical pictures and sequelae of COVID‐19 disease are immune mediated and characterized by a ‘cytokine storm’. Skeletal muscle has emerged as a potent regulator of immune system function. The aim of the present study is to define the prevalence of sarcopenia among COVID‐19 survivors and the negative impact of sarcopenia on the post‐acute COVID‐19 syndrome and its related risk factors. Methods A total of 541 subjects recovered from COVID‐19 disease were enrolled in the Gemelli Against COVID‐19 Post‐Acute Care between April 2020 and February 2021. They underwent a multidisciplinary clinical evaluation and muscle strength and physical performance assessment. Results Mean age was 53.1 years (SD 15.2, range from 18 to 86 years), and 274 (51%) were women. The prevalence of sarcopenia was 19.5%, and it was higher in patients with a longer hospital stay and lower in patients who were more physically active and had higher levels of serum albumin. Patients with sarcopenia had a higher number of persistent symptoms than non‐sarcopenic patients (3.8 ± 2.9 vs. 3.2 ± 2.8, respectively; P = 0.06), in particular fatigue, dyspnoea, and joint pain. Conclusions Sarcopenia identified according to the EWGSOP2 criteria is high in patients recovered from COVID‐19 acute illness, particularly in those who had experienced the worst clinical picture reporting the persistence of fatigue and dyspnoea. Our data suggest that sarcopenia, through the persistence of inflammation, could be the biological substrate of long COVID‐19 syndrome. Physical activity, especially if associated with adequate nutrition, seems to be an important protective factor.

Aims Patients with cirrhosis are susceptible to decompensation events, including ascites, variceal bleeding (VB), hepatic encephalopathy, or death after COVID‐19 infection. Patients may experience post‐COVID condition (PCC) with multisystem involvement that persists for at least 2 months. Methods Hospitalized patients with cirrhosis and COVID‐19 between January 2021 and January 2023 were assessed for decompensation events and mortality and compared to a propensity‐matched cohort of cirrhosis and non‐COVID‐19 sepsis. Both groups were followed for outcomes over 1 year. Results Of 252 patients with Cirrhosis+ COVID‐19 (73% men, aged 48.9 ± 13.7 years, 31%‐diabetes, 44%‐hypertension, 35%‐alcohol‐associated, 34.5%‐metabolic dysfunction‐associated steatotic liver disease; MASLD), 72 (28.6%) died in hospital and 180 (71.4%) recovered, similar to Cirrhosis+ non‐COVID‐sepsis (58/214, 27.1%). Finally,60 (33.3%) met criteria for PCC, 19 (10.5%) had no post COVID‐19 sequelae and 101 (56.1%) patients died (N = 45) or were lost to follow up (N = 56). Late Mortality was higher in Cirrhosis+ COVID‐19 than non‐COVID‐sepsis (56.1% vs. 35.3%, p = 0.026). Patients with PCC were aged 47.6 years, 63.3%‐men, Charlson Comorbidity Index > 4 (51.7%), 45%‐diabetes, 56.7%‐hypertension, with 33.3%, 23.3%, and 43.3% in Child‐Turcotte‐Pugh class A, B and C, respectively. PCC symptoms included persistent dyspnea (34, 43%), cognitive impairment (20, 25.3%), and anxiety (47, 59.4%). On multivariable analysis, predictors of the development of PCC were baseline MELDNa (HR 1.12, 95% CI: 1.05–1.17, p < 0.001) and age (HR 0.9, 95% CI: 0.91–0.99, p = 0.012). Predictors of mortality following COVID‐19 recovery were MELDNa (HR 1.03, 95% CI: 1.01–1.05, p = 0.008), age (HR 1.2, 95% CI: 1.1–1.5, p = 0.002) and hypertension (HR 1.63, 95% CI: 1.07–2.49, p = 0.025). Conclusion COVID‐19 is associated with long‐term mortality in cirrhosis even after recovery from respiratory infection. Long COVID is seen in a third of COVID‐19 survivors in patients with cirrhosis.

Introduction Although most patients recover within several weeks after acute COVID‐19, some of them develop long‐lasting clinical symptoms. Renal transplant recipients have an increased mortality risk from COVID‐19. We aimed to describe complications occurring after COVID‐19 in this group of patients. Methods A prospective single‐center cohort study was conducted at University Hospital Centre Zagreb. Patients with two negative reverse transcriptase‐polymerase chain reaction (RT‐PCR) tests for SARS‐CoV‐2 after COVID‐19 were eligible for further follow‐up at our outpatient clinic. They underwent detailed clinical and laboratory assessments. The primary outcome was the development of complications after COVID‐19. Results Only 11.53% of renal transplant recipients who survived acute COVID‐19 were symptomless and free from new‐onset laboratory abnormalities during the median follow‐up of 64 days (range: 50–76 days). Three patients died from sepsis after discharge from the hospital. In 47 patients (45.2%), clinical complications were present, while 74 patients (71.2%) had one or more laboratory abnormalities. The most common clinical complications included shortness of breath (19.2%), tiredness (11.5%), peripheral neuropathy (7.7%), self‐reported cognitive impairments (5.7%), and dry cough (7.7%). Most common laboratory abnormalities included shortened activated partial thromboplastin time (50%), elevated D‐dimers (36.5%), elevated fibrinogen (30.16%), and hypogammaglobulinemia (24%). Positive RT‐PCR for cytomegalovirus (8.7%), Epstein–Barr virus (26%), or BK virus (16.3%). Multivariate analysis identified the history of diabetes mellitus and eGFR CKD‐EPI as predictors for the development of post‐COVID clinical complications. Six months after acute COVID‐19, elevated D‐dimers persisted with normalization of other laboratory parameters. Twenty‐nine patients were hospitalized, mostly with several concomitant problems. However, initially reported clinical problems gradually improved in the majority of patients. Conclusion Post‐COVID‐19 clinical and laboratory complications are frequent in the renal transplant population, in some of them associated with significant morbidity. All patients recovered from acute COVID‐19 should undergo long‐term monitoring for evaluation and treatment of complications. Although most patients recover within several weeks after acute COVID‐19, some of them develop chronic injury of different organs or have nonspecific long‐lasting clinical symptoms. Renal transplant recipients have clinical and laboratory complications after acute COVID‐19.

Coronavirus disease (COVID‐19) has been shown to impact the central nervous system, leading to various neurological complications. Arterial spin labeling (ASL), a non‐invasive magnetic resonance imaging technique, enables the measurement of cerebral blood flow and perfusion abnormalities. This systematic review aims to synthesize ASL findings in patients with COVID‐19 and assess the potential role of ASL in diagnosing and managing neurological complications. A comprehensive search was conducted on PubMed and Scopus for studies related to ASL in individuals with COVID‐19 or post‐COVID‐19 syndrome published between December 2019 and August 2024. Extracted data encompassed study characteristics, ASL protocols, cognitive assessments, and principal findings. The most consistent observation across studies was hypoperfusion detected in various brain regions, particularly within the frontal lobes, which may correlate with cognitive impairment and olfactory dysfunction. Additionally, some investigations reported hyperperfusion localized to the leptomeninges. These results may reflect underlying mechanisms such as hypoxic–ischemic injury, inflammation, vascular dysfunction, and neuronal damage attributable to COVID‐19. In conclusion, ASL has emerged as a valuable tool for evaluating brain perfusion among patients affected by or recovering from COVID‐19 since it offers critical insights into cerebral hemodynamics and metabolism. Further research is warranted to validate these ASL findings and elucidate whether post‐COVID‐19 syndrome contributes to persistent brain perfusion issues. Coronavirus disease (COVID‐19) and long COVID can result in changes in brain perfusion, which may contribute to impaired cognition and hindered recovery. Arterial spin labeling (ASL), as a non‐invasive magnetic resonance imaging technique, proves useful for investigating the effects of COVID‐19 on cerebral function. This review emphasizes that both COVID‐19 and long COVID may induce alterations in brain perfusion.

Key Clinical Message Good's syndrome (GS) in conjunction with a severe COVID‐19 infection, shedding light on the complexities of managing this rare condition that combines thymoma and immunodeficiency. This study delves into the clinical presentation and management of a 63‐year‐old male diagnosed with Good's syndrome (GS) amid a severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection. GS, an uncommon association between thymoma and immunodeficiency, remains a clinical mystery, necessitating increased awareness and understanding. Our patient's intricate clinical course, marked by recurrent COVID‐19 symptoms and multiple hospitalizations, exemplifies the challenges posed by GS. Through a systematic review of GS cases globally, we highlight its worldwide distribution, with a substantial proportion reported in Europe. Notably, the diagnosis of thymoma often precedes immunodeficiency, emphasizing the importance of vigilance in clinical assessments.

This study aimed at: (1) Reporting COVID‐19 symptoms and duration in professional football players; (2) comparing players’ pulmonary function before and after COVID‐19; (3) comparing players’ metabolic power (Pmet) before and after COVID‐19. Thirteen male players (Age: 23.9 ± 4.0 years, V̇O2peak: 49.7 ± 4.0 mL/kg/min) underwent a medical screening and performed a running incremental step test and a spirometry test after COVID‐19. Spirometric data were compared with the ones collected at the beginning of the same season. Players’ mean Pmet of the 10 matches played before COVID‐19 was compared with mean Pmet of the 10 matches played after COVID‐19. Players completed a questionnaire on COVID‐19 symptoms and duration 6 months following the disease. COVID‐19 positivity lasted on average 15 ± 5 days. “General fatigue” and “muscle fatigue” symptoms were reported by all players during COVID‐19 and persisted for 77% (general fatigue) and 54% (muscle fatigue) of the players for 37 ± 28 and 38 ± 29 days after the disease, respectively. No significant changes in spirometric measurements were found after COVID‐19, even though some impairments at the individual level were observed. Conversely, a linear mixed‐effects model analysis showed a significant reduction of Pmet (−4.1 ± 3.5%) following COVID‐19 (t = −2.686, p < 0.05). “General fatigue” and “muscle fatigue” symptoms may persist for several weeks following COVID‐19 in professional football players and should be considered for a safer return to sport. Players’ capacity to compete at high intensities might be compromised after COVID‐19. “General fatigue” and “muscle fatigue” symptoms were the most common long‐term COVID‐19 symptoms reported. Players’ capability to exercise at high intensity was compromised following COVID‐19. Players’ pulmonary function was not affected by COVID‐19, even though some impairments were observed at the individual level.

Introduction Long COVID is a life‐limiting condition that affects 65 million people worldwide. It devastates lives with uncertain illness trajectories, and yet, there are many research uncertainties as there is a lack of understanding of its causes, effective treatments and management plans. We set out to identify current research priorities for people with Long COVID, carers, healthcare professionals and researchers. Methods A systematic literature review and previous Long COVID priority‐setting exercises identified three broad under‐researched areas of Long COVID research within the fields of Public Health and Health Services Research: symptoms; managing day‐to‐day life; and the emotional impact of Long COVID. We disseminated an elicitation survey that asked for research questions in these areas; responses were analysed and summarised into 42 research questions. A survey was then disseminated, asking respondents to prioritise these 42 questions. Workshops were held with people with Long COVID, carers, healthcare professionals and researchers to analyse responses and agree the top 10 priorities. Results The top priorities in order were pharmacological treatment of Long COVID; understanding the pathophysiology; nonpharmacological symptom management; improving public and professional understanding of Long COVID; understanding of the long‐term risks of Long COVID; improving financial and social supports; improving understanding of postviral syndromes; diagnostics; service redesign/pathways; and the well‐being of children with Long COVID. Conclusion Four years into the pandemic, there is an emphasis on the need for research on treatment, understanding and support for people living with Long COVID. Patient and Public Contribution People with Long COVID and carers were involved in the study design, survey design, dissemination, data analysis, interpretation and reviewing and editing the manuscript.

Background Long coronavirus disease (COVID), characterized by persistent and sometimes debilitating symptoms following a severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, has garnered increasing attention as a potential public health crisis. Emerging evidence indicates a higher incidence of hearing loss in individuals who have had COVID 2019 (COVID‐19) compared to the general population. However, the conclusions were inconsistent, and the causal relationship between COVID‐19 and sensorineural hearing loss remains unknown. Methods To addresses this outstanding issue, we performed Mendelian randomization analysis to detect the causal association between COVID‐19 and hearing loss using the largest genome‐wide association study data to date in the European population and confirmed the results in the East Asian population. Comprehensively sensitive analyses were followed, including Cochran's Q test, Mendelian randomization (MR)‐Egger intercept test, MR‐pleiotropy residual sum and outlier, and leave‐one‐out analysis, to validate the robustness of our results. Results Our results suggested that there is no causal association between COVID‐19 and the risk of hearing loss in the European population. Neither the susceptibility, hospitalization, and severity of COVID‐19 on hearing loss (inverse variance weighted method: odds ratio (OR) = 1.046, 95% confidence interval (CI) = 0.907–1.205, p = .537; OR = 0.995, 95% CI = 0.956–1.036, p = .823; OR = 0.995, 95% CI = 0.967–1.025, p = .76). Replicated analyses in the East Asian population yielded consistent results. No pleiotropy and heterogeneity were found in our results. Conclusion In conclusion, our MR results do not support a genetically predicted causal relationship between COVID‐19 and sensorineural hearing loss. Thus, the associations observed in prior observational studies may have been influenced by confounding factors rather than a direct cause‐and‐effect relationship. More clinical and mechanism research are needed to further understand this association in the future.