Long Covid Land Toolbox
How the virus behind COVID-19 can harm your blood vessels and your heart
By Laura Williamson, American Heart Association News
It started as a respiratory illness – or so everyone thought. But it quickly became apparent that SARS-CoV-2, the virus that causes COVID-19, was so much more.
“Since the beginning, the virus showed a very dramatic ability to affect different organs and systems beyond the respiratory system,” said Dr. Chiara Giannarelli, an associate professor in the departments of medicine and pathology at NYU Grossman School of Medicine. “Early on, there was some evidence the virus was damaging the heart, causing an increased risk of heart attacks and strokes in these patients. But no one was looking at the vasculature,” the blood vessels that carry the virus throughout the body and in and out of the heart.
From her lab in New York City, Giannarelli had front-row seats in the spring of 2020 to the epicenter of COVID-19 infections in the U.S. Because her research already focused on the complex relationship between inflammatory and immune cells in the arteries and their role in atherosclerosis – the root of cardiovascular disease – she felt well positioned to investigate.
Meanwhile, other research teams were looking into what the virus was doing to the heart muscle. Cases of myocarditis, an inflammation of the heart muscle, were being identified as the cause of death in some people with COVID-19.
Choroid plexus volume is enlarged in long COVID and associated with cognitive and brain changes
Patients with post-COVID condition (PCC) present with diverse symptoms which persist at long-term after SARS-CoV-2 infection. Among these symptoms, cognitive impairment is one of the most prevalent and has been related to brain structural and functional changes. The underlying mechanisms of these cognitive and brain alterations remain elusive but neuroinflammation and immune mechanisms have been majorly considered. In this sense, the choroid plexus (ChP) volume has been proposed as a marker of neuroinflammation in immune-mediated conditions and the ChP epithelium has been found particularly susceptible to the effects of SARS-CoV-2. The objective was to investigate the ChP in PCC and evaluate its relationships with cognition, brain, and immunological alterations. One-hundred and twenty-nine patients with PCC after a mean of 14.79 ± 7.17 months of evolution since the infection and 36 healthy controls were recruited. Participants underwent a neuropsychological, and neuroimaging assessment and immunological markers evaluation. Results revealed ChP volume enlargement in PCC compared to healthy controls. The ChP enlargement was associated with cognitive dysfunction, grey matter volume reduction in frontal and subcortical areas, white matter integrity and diffusivity changes and functional connectivity changes. These ChP changes were also related to intermediate monocytes levels. Findings suggest that the ChP integrity may play a relevant role in the pathophysiology of cognitive deficits and the observed brain changes in PCC. The previously documented function of the ChP in maintaining brain homeostasis and regulating the entry of immune cells into the brain supports the presence of neuroinflammatory mechanisms in this disorder.
Neurological post-COVID syndrome is associated with substantial impairment of verbal short-term and working memory
In 2020, severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) triggered one of the most severe pandemics in human history. The World Health Organization (WHO) estimates that by the end of 2023, approximately 773 million people had contracted acute SARS-CoV-2 infection, resulting in the multi-organ coronavirus disease 19 (COVID-19). Many of these affected patients continue to suffer from persistent or new symptoms, even 12 weeks after acute infection. This condition, in which symptoms persist or new symptoms develop at least three months after the acute infection and persist for at least two months without the finding of any causal relationship, is subsumed under the terms post COVID-19 condition or post-COVID syndrome (PCS). In the following, the term PCS refers to COVID-19 symptoms or new symptoms that cannot be attributed to any other etiology and persist more than 12 weeks after the acute COVID-19 infection. Symptoms commonly found and included in the symptom complex of PCS are hair loss, chronic kidney disease, thromboembolism, palpitations and chest pain, headache, cognitive impairment, post-traumatic stress disorder, sleep disturbances, anxiety and depressive symptoms, cough, shortness of breath, arthralgias, myalgias, and frequently and most importantly, chronic fatigue.
Total long COVID symptoms scores, prior to COVID (Pre COVID), during the long COVID phase (Post COVID), after vaccination (Post Vaccine), and after infusion of monoclonal antibodies (Post MCA) for Patient 1, Patient 2 and Patient 3, respectively. Note: Patient 3 did not receive a vaccine.
Remission of severe forms of long COVID following monoclonal antibody (MCA) infusions: A report of signal index cases and call for targeted research
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Digital Download: Request for Covid Accommodation in Health Care Facilities
Everyone deserves safe access to health care, but we know many people are facing resistance to simple, reasonable requests for Covid accommodations like respirators and air filters cleaners.
So we’re making it easier for you to request accommodations from your primary care doctor, dentist, specialists, or other health care workers, with a fillable PDF form that clearly lays out your requested accommodations and your legal rights to them.
Download our Request for Accommodation in Health Care Facilities PDF today.
Neurological, psychological, psychosocial complications of long-COVID and their management
Since it first appeared, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has had a significant and lasting negative impact on the health and economies of millions of individuals all over the globe. At the level of individual health too, many patients are not recovering fully and experiencing a long-term condition now commonly termed ‘long-COVID’. Long-COVID is a collection of symptoms which must last more than 12 weeks following initial COVID infection, and which cannot be adequately explained by alternate diagnoses. The neurological and psychosocial impact of long-COVID is itself now a global health crisis and therefore preventing, diagnosing, and managing these patients is of paramount importance. This review focuses primarily on: neurological functioning deficits; mental health impacts; long-term mood problems; and associated psychosocial issues, among patients suffering from long-COVID with an eye towards the neurological basis of these symptoms.
Neurological complications caused by SARS-CoV-2
SARS-CoV-2 can not only cause respiratory symptoms but also lead to neurological complications. Research has shown that more than 30% of SARS-CoV-2 patients present neurologic symptoms during COVID-19 (A. Pezzini and A. Padovani, Nat Rev Neurol 16:636–644, 2020, https://doi.org/10.1038/s41582-020-0398-3). Increasing evidence suggests that SARS-CoV-2 can invade both the central nervous system (CNS) (M.S. Xydakis, M.W. Albers, E.H. Holbrook, et al. Lancet Neurol 20: 753–761, 2021 https://doi.org/10.1016/S1474-4422(21)00182-4 ) and the peripheral nervous system (PNS) (M.N. Soares, M. Eggelbusch, E. Naddaf, et al. J Cachexia Sarcopenia Muscle 13:11–22, 2022, https://doi.org/10.1002/jcsm.12896), resulting in a variety of neurological disorders. This review summarized the CNS complications caused by SARS-CoV-2 infection, including encephalopathy, neurodegenerative diseases, and delirium. Additionally, some PNS disorders such as skeletal muscle damage and inflammation, anosmia, smell or taste impairment, myasthenia gravis, Guillain-Barré syndrome, ICU-acquired weakness, and post-acute sequelae of COVID-19 were described.
Endothelial inflammation in COVID-19
Disrupted endothelial function underlies the multiorgan complications of COVID-19
The vascular endothelium forms a crucial interface between tissues and the blood stream and maintains normal blood flow (1). In its homeostatic state, the endothelium resists blood clotting, vasoconstriction, and inflammation and maintains selective barrier functions. This tightly regulated suite of properties can shift rapidly to unleash a series of functions vital to stanch blood loss from wounds or mobilize innate and adaptive immune defenses to repair injury and fight pathogenic microorganisms. But these defensive actions of endothelial cells can, if overexuberant, aggravate disease. Infection with severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) has highlighted how altered endothelial functions contribute to multiorgan health effects during the acute phase of COVID-19 and potentially to the longer-term consequences associated with Long Covid.