Abstract
Long coronavirus disease 2019 (COVID-19) was described in patients recovering from COVID-19, with dyspnea being a frequent symptom. Data regarding the potential mechanisms of long COVID remain scarce. We investigated the presence of subclinical cardiac dysfunction, assessed by transthoracic echocardiography (TTE), in recovered COVID-19 patients with or without dyspnea, after exclusion of previous cardiopulmonary diseases. A total of 310 consecutive COVID-19 patients were prospectively included. Of those, 66 patients (mean age 51.3 ± 11.1 years, almost 60% males) without known cardiopulmonary diseases underwent one-year follow-up consisting of clinical evaluation, spirometry, chest computed tomography, and TTE. From there, 23 (34.8%) patients reported dyspnea. Left ventricle (LV) ejection fraction was not significantly different between patients with or without dyspnea (55.7 ± 4.6 versus (vs.) 57.6 ± 4.5, p = 0.131). Patients with dyspnea presented lower LV global longitudinal strain, global constructive work (GCW), and global work index (GWI) compared to asymptomatic patients (−19.9 ± 2.1 vs. −21.3 ± 2.3 p = 0.039; 2183.7 ± 487.9 vs. 2483.1 ± 422.4, p = 0.024; 1960.0 ± 396.2 vs. 2221.1 ± 407.9, p = 0.030). GCW and GWI were inversely and independently associated with dyspnea (p = 0.035, OR 0.998, 95% CI 0.997–1.000; p = 0.040, OR 0.998, 95% CI 0.997–1.000). Persistent dyspnea one-year after COVID-19 was present in more than a third of the recovered patients. GCW and GWI were the only echocardiographic parameters independently associated with symptoms, suggesting a decrease in myocardial performance and subclinical cardiac dysfunction.
Highlights
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), rapidly spread across the globe with more than 260 million cases worldwide, overwhelming the healthcare systems [1,2,3].Clinical manifestations occur predominantly due to lung involvement, there is a growing body of evidence showing the presence of cardiovascular complications attributed to SARS-CoV2 infection [4,5].COVID-19 pneumonia is characterized by a wide spectrum of symptoms including fever, cough, dyspnea or chest pain as well as headache, ageusia or anosmia [6,7]
Advanced age and a history of cardiovascular or respiratory diseases are well established risk factors for a more severe course of COVID-19 [2,8]. It is considered primarily a respiratory disease, several other organs may be involved via angiotensin converting enzyme 2 (ACE2) receptors which are located at the level of the endothelial cells, explaining the complexity of symptoms and complications including myocardial injury [9,10]
Base4lionfe9 characteristics including clinical data, laboratory values, spirometry and chest computer tomography (CT) parameters are available in Supplementary Materials Table S1
Summary
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), rapidly spread across the globe with more than 260 million cases worldwide, overwhelming the healthcare systems [1,2,3].Clinical manifestations occur predominantly due to lung involvement, there is a growing body of evidence showing the presence of cardiovascular complications attributed to SARS-CoV2 infection [4,5].COVID-19 pneumonia is characterized by a wide spectrum of symptoms including fever, cough, dyspnea or chest pain as well as headache, ageusia or anosmia [6,7]. Clinical manifestations occur predominantly due to lung involvement, there is a growing body of evidence showing the presence of cardiovascular complications attributed to SARS-CoV2 infection [4,5]. Advanced age and a history of cardiovascular or respiratory diseases are well established risk factors for a more severe course of COVID-19 [2,8]. It is considered primarily a respiratory disease, several other organs may be involved via angiotensin converting enzyme 2 (ACE2) receptors which are located at the level of the endothelial cells, explaining the complexity of symptoms and complications including myocardial injury [9,10]. Earlier reports showed an increased prevalence of high cardiac troponin levels, a surrogate biomarker for myocardial injury, which was further associated with impaired left ventricular relaxation and reduced right ventricle function leading to higher morbidity and mortality rates, including possible long-term consequences [11,12,13,14,15]
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