Long COVID: post-acute sequelae of COVID-19 with a cardiovascular focus

Abstract

Emerging as a new epidemic, long COVID or post-acute sequelae of coronavirus disease 2019 (COVID-19), a condition characterized by the persistence of COVID-19 symptoms beyond 3 months, is anticipated to substantially alter the lives of millions of people globally. Cardiopulmonary symptoms including chest pain, shortness of breath, fatigue, and autonomic manifestations such as postural orthostatic tachycardia are common and associated with significant disability, heightened anxiety, and public awareness. A range of cardiovascular (CV) abnormalities has been reported among patients beyond the acute phase and include myocardial inflammation, myocardial infarction, right ventricular dysfunction, and arrhythmias. Pathophysiological mechanisms for delayed complications are still poorly understood, with a dissociation seen between ongoing symptoms and objective measures of cardiopulmonary health. COVID-19 is anticipated to alter the long-term trajectory of many chronic cardiac diseases which are abundant in those at risk of severe disease. In this review, we discuss the definition of long COVID and its epidemiology, with an emphasis on cardiopulmonary symptoms. We further review the pathophysiological mechanisms underlying acute and chronic CV injury, the range of post-acute CV sequelae, and impact of COVID-19 on multiorgan health. We propose a possible model for referral of post-COVID-19 patients to cardiac services and discuss future directions including research priorities and clinical trials that are currently underway to evaluate the efficacy of treatment strategies for long COVID and associated CV sequelae.

The Impact of Metabolic Syndrome and Obesity on the Evolution of Diastolic Dysfunction in Apparently Healthy Patients Suffering from Post-COVID-19 Syndrome

“…(c) To appreciate the systolic pressure in the pulmonary artery (sPAP), we determined the peak tricuspid regurgitation velocity (TRV) in continuous-wave Doppler, from the apical window at the level of the tricuspid valves, and we employed Bernouli's equation to calculate the pressure gradient, to which we added the estimated right atrial pressure, based on the inferior vena cava diameter, and its respiratory variations. We considered that sPAP values of ≥35 mmHg at rest indicated pulmonary hypertension (PH), with severities ranging from mild (35)(36)(37)(38)(39)(40)(41)(42)(43)(44) to moderate (45-60 mmHg) to severe (>60 mmHg) [23,27]. (d) To evaluate DD, the apical 4-chamber view was employed to determine the left atrial volume index (LAVI), then pulsed Doppler was used to register the peak early diastolic velocity (E), and the late diastolic velocity (A) at the level of the mitral valve annulus, and, subsequently, the E/A ratio was calculated.…”

The Provision of Dental Care to COVID-19 Survivors: A Concise Review

“…They need close monitoring, even after discharge, as the ongoing systemic inflammation may lead to ventricular dysfunction and malignant arrythmia 46 . Persistent symptoms may include hypotension, tachycardia, palpitations, dyspnoea and arrhythmias 47 , 48 , 49 , 50 , with some requiring hospital readmission 51 . There are increased risks of incident cardiovascular disease, such as cerebrovascular disorders (stroke/transient ischaemic attacks), dysrhythmia (atrial fibrillation/sinus tachycardia), ischaemic heart disease (acute coronary disease/myocardial infarction/angina), thromboembolic disease (pulmonary embolism/deep vein thrombosis), heart failure, pericarditis, myocarditis, cardiac arrest and cardiogenic shock 49 , 52 , 53 , 54 , 55 , 56 .…”

“…Persistent symptoms may include hypotension, tachycardia, palpitations, dyspnoea and arrhythmias 47 , 48 , 49 , 50 , with some requiring hospital readmission 51 . There are increased risks of incident cardiovascular disease, such as cerebrovascular disorders (stroke/transient ischaemic attacks), dysrhythmia (atrial fibrillation/sinus tachycardia), ischaemic heart disease (acute coronary disease/myocardial infarction/angina), thromboembolic disease (pulmonary embolism/deep vein thrombosis), heart failure, pericarditis, myocarditis, cardiac arrest and cardiogenic shock 49 , 52 , 53 , 54 , 55 , 56 . Long-term sequelae may include increased cardiometabolic demand, myocardial fibrosis or scarring, arrhythmias, tachycardia and autonomic dysfunction, as in POTS described above 6 .…”

Direct mechanisms of SARS-CoV-2-induced cardiomyocyte damage: an update

“…Omicron has become the current dominant variant worldwide, including in China [ 1 , 2 ]. Although predominantly characterized by viral pneumonia, cardiac involvement could be prevalent during COVID-19 progression, which is reportedly associated with disease severity and mortality [ 3 , 4 ].…”

“…Given the current convincing evidence that myocardial injury intensifies the severity of COVID-19, cardiac management should be a priority for physicians. In addition, the long-term effects of COVID-19 on cardiovascular health are still a major global concern [ 4 ]. We have previously proposed several pathogenic mechanisms explaining the association of COVID-19 with myocardial injury, including SARS-CoV-2 host cell invasion, myocardial oxygen supply/demand imbalance, abnormal coagulation, and excessive immune reaction [ 11 ].…”