Background The COVID-19 pandemic has placed unprecedented strain on health-care systems. Frailty is being used in clinical decision making for patients with COVID-19, yet the prevalence and effect of frailty in people with COVID-19 is not known. In the COVID-19 in Older PEople (COPE) study we aimed to establish the prevalence of frailty in patients with COVID-19 who were admitted to hospital and investigate its association with mortality and duration of hospital stay.Methods This was an observational cohort study conducted at ten hospitals in the UK and one in Italy. All adults (≥18 years) admitted to participating hospitals with COVID-19 were included. Patients with incomplete hospital records were excluded. The study analysed routinely generated hospital data for patients with COVID-19. Frailty was assessed by specialist COVID-19 teams using the clinical frailty scale (CFS) and patients were grouped according to their score (1-2=fit; 3-4=vulnerable, but not frail; 5-6=initial signs of frailty but with some degree of independence; and 7-9=severe or very severe frailty). The primary outcome was in-hospital mortality (time from hospital admission to mortality and day-7 mortality).
In the treatment of mitral stenosis, balloon valvuloplasty and open surgical commissurotomy have comparable initial results and low rates of restenosis, and both produce good functional capacity for at least three years. The potential complications associated with balloon valvuloplasty should be noted. The better hemodynamic results at three years, lower cost, and elimination of the need for thoracotomy suggest that balloon valvuloplasty should be considered for all patients with favorable mitral-valve anatomy.
Takotsubo syndrome (TTS) is caused by catecholamine surge, which is also observed in COVID-19 disease due to the cytokine storm. We performed a systematic literature search using PubMed/Medline, SCOPUS, Web of Science, and Google Scholar databases to identify COVID-19-associated TTS case reports and evaluated patient-level demographics, clinical attributes, and outcomes. There are 12 cases reported of TTS associated with COVID-19 infection with mean age of 70.8 ± 15.2 years (range 43–87 years) with elderly (66.6% > 60 years) female (66.6%) majority. The time interval from the first symptom to TTS was 8.3 ± 3.6 days (range 3–14 days). Out of 12 cases, 7 reported apical ballooning, 4 reported basal segment hypo/akinesia, and 1 reported median TTS. Out of 12 cases, during hospitalization, data on left ventricular ejection fraction (LVEF) was reported in only 9 of the cases. The mean LVEF was 40.6 ± 9.9% (male, 46.7 ± 5.7%, and female, 37.7 ± 10.6%). Troponin was measured in all 12 cases and was elevated in 11 (91.6%) without stenosis on coronary angiography except one. Out of 11 cases, 6 developed cardiac complications with 1 case each of cardiac tamponade, heart failure, myocarditis, hypertensive crisis, and cardiogenic shock in 2. Five patients required intubation, 1 patient required continuous positive airway pressure, and 1 patient required venovenous extracorporeal membrane oxygenation. The outcome was reported in terms of recovery in 11 (91.6%) out of 12 cases, and a successful recovery was noted in 10 (90.9%) cases. COVID-19-related TTS has a higher prevalence in older women. Despite a lower prevalence of cardiac comorbidities in COVID-19 patients, direct myocardial injury, inflammation, and stress may contribute to TTS with a high complication rate.
Background C-reactive protein (CRP) is a non-specific acute phase reactant elevated in infection or inflammation. Higher levels indicate more severe infection and have been used as an indicator of COVID-19 disease severity. However, the evidence for CRP as a prognostic marker is yet to be determined. The aim of this study is to examine the CRP response in patients hospitalized with COVID-19 and to determine the utility of CRP on admission for predicting inpatient mortality. Methods Data were collected between 27 February and 10 June 2020, incorporating two cohorts: the COPE (COVID-19 in Older People) study of 1564 adult patients with a diagnosis of COVID-19 admitted to 11 hospital sites (test cohort) and a later validation cohort of 271 patients. Admission CRP was investigated, and finite mixture models were fit to assess the likely underlying distribution. Further, different prognostic thresholds of CRP were analysed in a time-to-mortality Cox regression to determine a cut-off. Bootstrapping was used to compare model performance [Harrell’s C statistic and Akaike information criterion (AIC)]. Results The test and validation cohort distribution of CRP was not affected by age, and mixture models indicated a bimodal distribution. A threshold cut-off of CRP ≥40 mg/L performed well to predict mortality (and performed similarly to treating CRP as a linear variable). Conclusions The distributional characteristics of CRP indicated an optimal cut-off of ≥40 mg/L was associated with mortality. This threshold may assist clinicians in using CRP as an early trigger for enhanced observation, treatment decisions and advanced care planning.
The coronavirus disease 2019 pandemic is an issue of global significance that has taken the lives of many across the world. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus responsible for its pathogenesis. The pulmonary manifestations of COVID-19 have been well described in the literature. Initially, it was thought to be limited to the respiratory system; however, we now recognize that COVID-19 also affects several other organs, including the nervous system. Two similar human coronaviruses (CoV) that cause severe acute respiratory syndrome (SARS-CoV-1) and Middle East respiratory syndrome (MERS-CoV) are also known to cause disease in the nervous system. The neurological manifestations of SARS-CoV-2 infection are growing rapidly, as evidenced by several reports. There are several mechanisms responsible for such manifestations in the nervous system. For instance, post-infectious immune-mediated processes, direct virus infection of the central nervous system (CNS), and virus-induced hyperinflammatory and hypercoagulable states are commonly involved. Guillain-Barré syndrome (GBS) and its variants, dysfunction of taste and smell, and muscle injury are numerous examples of COVID-19 PNS (peripheral nervous system) disease. Likewise, hemorrhagic and ischemic stroke, encephalitis, meningitis, encephalopathy acute disseminated encephalomyelitis, endothelialitis, and venous sinus thrombosis are some instances of COVID-19 CNS disease. Due to multifactorial and complicated pathogenic mechanisms, COVID-19 poses a large-scale threat to the whole nervous system. A complete understanding of SARS-CoV-2 neurological impairments is still lacking, but our knowledge base is rapidly expanding. Therefore, we anticipate that this comprehensive review will provide valuable insights and facilitate the work of neuroscientists in unfolding different neurological dimensions of COVID-19 and other CoV associated abnormalities.
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