PMC:7102662 / 6290-10949 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7102662","sourcedb":"PMC","sourceid":"7102662","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7102662","text":"2.1 Pathogenic considerations\nSARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias.\n\n2.1.1 Role of underling CV comorbidities\nThe patients with pre-existing CVD appear to have heightened vulnerability to develop COVID-19 and tend to have more severe disease with worse clinical outcomes [1,4,6,8]. Various CV risk factors also adversely affect porgnosis of these patients, although they do not seem to increase likleihood of developing the infection. A meta-analysis of six published studies from China including 1527 patients with COVID-19 reported 9.7%, 16.4% and 17.1% prevalence of diabetes, cardio-cerebrovascular disease and hypertension respectively [4]. Although the prevalence of diabetes and hypertension in this cohort was same as in the Chinese general population, the prevalence of cardio-cerebrovascular disease was considerably higher. More importantly, the presence of diabetes, cardio-cerebrovascular disease and hypertension was associated with a 2-fold, 3-fold and 2-fold greater risk of severe disease or requiring intensive care unit (ICU) admission, suggesting prognostic impact of these comorbidities. A much larger report from the Chinese Center for Disease Control and Prevention described clinical outcomes in 44672 confirmed cases of COVID-19 [1]. The overall case fatality rate (CFR) was 2.3% in the entire cohort but significantly higher (6%, 7.3% and 10.5% respectively) in patients with hypertension, diabetes and CVD.\nAlthough data is lacking, the prevalence of various CV comorbidities and their impact on clinical outcomes seem to vary considerably across different geographic locations. The CFRs have been lower in China outside Hubei province and many other countries but much higher in some European nations [2]. A small report including 21 patients from Washington, United States of America presented a particularly grim scenario [9]. Comorbidities were common in this cohort, with diabetes present in 33.3% and congestive heart failure in 42.9%. Acute cardiac dysfunction occurred in 33.3% patients and 52.4% patients died. However, the overall CFR in the United States seems to be much lower (201 deaths out of 15219 confirmed cases) [2], although it is likely to rise as many of the patients are currently hospitalized and have not yet had the definite 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