Why COVID-19 is, in fact, a microvascular disease and what that means for clinicians
Michael Walter | Vascular & Endovascular
COVID-19 has impacted patients in numerous ways, making it difficult at times to properly diagnose and treat. According to a new analysis in Circulation, one key detail that cardiologists and other clinicians should keep in mind is the consistent damage it does to patients’ blood vessels. Perhaps, the authors argue, we should view COVID-19 as a microvascular disease.
“Although most patients with COVID-19 present with a mild upper respiratory tract infection and then recover, some infected patients develop pneumonia, acute respiratory distress syndrome, multiorgan failure and death,” wrote co-authors Charles J. Lowenstein, MD, of Johns Hopkins University School of Medicine in Baltimore, and Scott D. Solomon, MD, of Brigham and Women’s Hospital in Boston. “Clues to the pathogenesis of severe COVID-19 may lie in the systemic inflammation and thrombosis observed in infected patients. We propose that severe COVID-19 is a microvascular disease in which coronavirus infection activates endothelial cells, triggering exocytosis, a rapid vascular response that drives microvascular inflammation and thrombosis.”
Venous thromboembolism (VTE) and arterial thromboembolism have both been identified as significant side effects of severe COVID-19, the authors noted, with VTE impacting up to 35% of all COVID patients admitted to the ICU. Severe infections have also been associated with “laboratory findings consistent with a hypercoagulable state,” and patients entering “a hyper-inflammatory state.”
The combination of inflammation and thrombosis is crucial, suggesting that endothelial dysfunction could be at the heart of this complex infection. SARS-CoV-2, the virus behind COVID-19, appears to activate exocytosis “by binding to an endothelial surface receptor such as ACE2,” Lowenstein and Solomon wrote. Other possibilities mentioned in the analysis are that SARS-CoV-2 activates exocytosis indirectly by activating “host responses and a plethora of cytokines” or that it simply infects endothelial cells directly.