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Review
. 2022 Nov;24(11):1711-1726.
doi: 10.1007/s11886-022-01786-2. Epub 2022 Sep 30.

Long-COVID Syndrome and the Cardiovascular System: A Review of Neurocardiologic Effects on Multiple Systems

Affiliations
Review

Long-COVID Syndrome and the Cardiovascular System: A Review of Neurocardiologic Effects on Multiple Systems

Nicholas L DePace et al. Curr Cardiol Rep. 2022 Nov.

Abstract

Purpose of review: Long-COVID syndrome is a multi-organ disorder that persists beyond 12 weeks post-acute SARS-CoV-2 infection (COVID-19). Here, we provide a definition for this syndrome and discuss neuro-cardiology involvement due to the effects of (1) angiotensin-converting enzyme 2 receptors (the entry points for the virus), (2) inflammation, and (3) oxidative stress (the resultant effects of the virus).

Recent findings: These effects may produce a spectrum of cardio-neuro effects (e.g., myocardial injury, primary arrhythmia, and cardiac symptoms due to autonomic dysfunction) which may affect all systems of the body. We discuss the symptoms and suggest therapies that target the underlying autonomic dysfunction to relieve the symptoms rather than merely treating symptoms. In addition to treating the autonomic dysfunction, the therapy also treats chronic inflammation and oxidative stress. Together with a full noninvasive cardiac workup, a full assessment of the autonomic nervous system, specifying parasympathetic and sympathetic (P&S) activity, both at rest and in response to challenges, is recommended. Cardiac symptoms must be treated directly. Cardiac treatment is often facilitated by treating the P&S dysfunction. Cardiac symptoms of dyspnea, chest pain, and palpitations, for example, need to be assessed objectively to differentiate cardiac from neural (autonomic) etiology. Long-term myocardial injury commonly involves P&S dysfunction. P&S assessment usually connects symptoms of Long-COVID to the documented autonomic dysfunction(s).

Keywords: Autonomic dysfunction; Inflammation; Long-COVID; Neuro-cardiovascular effects; Oxidative stress; Quality of life; Symptoms; Treatment.

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Conflict of interest statement

Dr. Colombo reports the following: inventor of P&S Monitoring technology and officer of Physio PS, Inc. NeuroCardiology Research Corp. has no interest or involvement in this work. The other author has no disclosures to report.

Figures

Fig. 1
Fig. 1
The cytokine storm involved in COVID-19 infections is a source of oxidative stress. Viruses and traumas (mental or physical) in general may lead to oxidative stress, which may lead to parasympathetic or sympathetic dysfunction(s), known as dysautonomias (adapted from Rasa et al. [••])
Fig. 2
Fig. 2
Classification of Long-COVID (reprinted from Raveendran AV et al. Diabetes Metab Syndr. 2021 May to Jun;15(3):869–875, with permission from Elsevier) [51]

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