Cardiovascular Dysautonomy as a Sequel of SARS COV 2. Case Series

Abstract

The impact of COVID-19, caused by the SARS-CoV-2 virus, a pandemic that originated in Wuhan, China, can lead to serious complications, in addition to mild symptoms, with special interest in the autonomic nervous system (ANS). Damage to the ANS by SARS-CoV-2 can cause dysautonomia, an imbalance between the sympathetic and parasympathetic system, with unclear mechanisms such as cytokine storm, excessive inflammation, and virus neurotropism. A significant sequelae of COVID-19 is cardiac dysautonomia, which affects heart rate, blood pressure and other autonomic reflexes, causing postural tachycardia, orthostatic hypotension, arrhythmias and fatigue. There is decreased heart rate variability (HRV) in patients, suggesting dysautonomia. Long COVID syndrome can also include cardiac dysautonomia. To diagnose cardiac autonomic neuropathy, at least two of six criteria must be met, such as an SDNN less than 50 ms and an RMSSD less than 15 ms. The cases of cardiac dysautonomia below present several of these criteria met. Methods to evaluate cardiac dysautonomia include the COMPASS 31 scale and the orthostatic hypotension questionnaire (OHQ), but more research is still needed, especially in Mexico. The case study shows that those who followed non-pharmacological recommendations such as cardiovascular exercise, increased water intake and BMI control had improvement, while cases that did not follow these recommendations did not show significant improvements. Cardiac dysautonomia is a post-COVID-19 sequelae with high prevalence, highlighting the importance of non-invasive methods for its diagnosis. Even without symptoms, people can have this sequelae, so it is important to suspect cardiovascular disorders. The need for early intervention and monitoring of hygienic-dietary measures is emphasized to avoid the worsening and chronicity of cardiac dysautonomia, with the hope of preventing the development of chronic diseases and fatal outcomes.