Echocardiographic assessment of the right ventricle in COVID-19: a systematic review

Ghidini, Simone; Gasperetti, Alessio; Winterton, Dario; Vicenzi, Marco; Busana, Mattia; Pedrazzini, Giovanni; Biasco, Luigi; Tersalvi, Gregorio

doi:10.1007/s10554-021-02353-6

Cited by 19 publications

(17 citation statements)

References 90 publications

(122 reference statements)

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“…Right chambers tolerate preload augmentation worse than their left counterparts. Thus, high RV pressure produces RV myocardial stress and troponin release [9].…”

Section: Discussionmentioning

confidence: 99%

Right Ventricular Assessment in Critically Ill COVID-19 Patients and its Prognostic Importance

Mohamad

Gawish²,

Abdrabo³

et al. 2022

Open Access Maced J Med Sci

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Background; Cardiac injury is a prevalent complication and is associated with worse prognosis in COVID-19 patients. The increased cardiac workload resulting from respiratory failure and hypoxemia is a common mechanism of cardiac injury and the right ventricle may bear the brunt of its impact. The aim of the present study was to determine the incidence and prognostic value of RV dysfunction in COVID-19 patients admitted to ICU using conventional echocardiography parameters.Patients were subjected to full history taking, and clinical examination, Computed Tomography of chest was done for all patients to assess severity of lung infiltration, all patients received standard treatment according to Ministry of Health and Population COVID19 treatment protocol recommendations. Echocardiographic assessment was done to all patients.The mean age of the patients was 61.10±9.64years (range 42-80years).There were 36 (60%) male and 24 (40%) female. The non-survivor group consisted of 28 patients (46.7%) and survivors consisted of 32 patients (53.3%). There was statistically significant association between mortality and RV function regarding TAPSE, FAC%, RV basal diameter and EPAP. We concluded that in COVID-19 patients, RV function must be assessed and its prognostic importance recognized. RV dysfunction is not only a symptom of high pulmonary pressures, but it also contributes to cardiac insufficiency.

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“…Right chambers tolerate preload augmentation worse than their left counterparts. Thus, high RV pressure produces RV myocardial stress and troponin release [9].…”

Section: Discussionmentioning

confidence: 99%

Right Ventricular Assessment in Critically Ill COVID-19 Patients and its Prognostic Importance

Mohamad

Gawish²,

Abdrabo³

et al. 2022

Open Access Maced J Med Sci

View full text Add to dashboard Cite

show abstract

“…Other echocardiographic parameters to evaluate the RV are the RV end-diastolic diameter (RVEDD), tricuspid annular plane systolic excursion (TAPSE), tricuspid lateral annular systolic velocity (S ′ ), RV fractional area change (RVFAC), systolic pulmonary artery pressure (sPAP) and right ventricular longitudinal strain (RVLS). 81 The RVEDD is measured in a four-chamber apical view at the level of the tip of the leaflets of the tricuspid valves at the end of diastole. Patients with an RVEDD >41 mm are more likely to progress to ARDS or need mechanical ventilation.…”

Section: Discussionmentioning

confidence: 99%

“…83 It has been hypothesized that the radial dysfunction evaluated with the RVFAC could be compensated for by the preservation of the longitudinal shortening estimated with the TAPSE and S ′ . 81 In both non-ICU patients 84 and ICU patients, 85 an sPAP > 35 mmHg is a parameter predictive of mortality in COVID-19. Finally, an RVLS with a cut-off of −20% to −21% calculated by two-dimensional speckle tracking echocardiography seems to be able to detect abnormal RV function.…”

Section: Discussionmentioning

confidence: 99%

Section: Echocardiographymentioning

confidence: 99%

Section: Echocardiographymentioning

confidence: 99%

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Coronavirus disease 2019-induced hypercoagulability and its clinical implications

Jaramillo

2021

Asian Cardiovasc Thorac Ann

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Coronavirus disease 2019 is the disease produced by severe acute respiratory syndrome-coronavirus-2, which is introduced into the host’s cell thanks to the angiotensin-converting enzyme 2 receptor. Once there, it uses the cell’s machinery to multiply itself. In this process, it generates an immune response that stimulates the lymphocytes to produce cytokines and reactive oxygen species that begin to deteriorate the endothelial cell. Complement activation, through the complement attack complex and C5a, contributes to this endothelial damage. The different mediators further promote the expression of adhesion molecules on the endothelial surface, which encourages all blood cells to adhere to the endothelial surface to form small conglomerates, called clots, which obstruct the lumen of the small blood vessels. Furthermore, the mediators of clot lysis are inhibited. All this promotes a prothrombotic environment within the pulmonary capillaries that is reflected in the elevation of D-dimer. The only solution for this cascade of events seems to be the implementation of an effective anticoagulation protocol that early counteracts the changes induced by thrombi in the pulmonary circulation and reflected in the functioning of the right ventricle.

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Inflammation and vascular remodeling in COVID-19 hearts

et al. 2022

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A wide range of cardiac symptoms have been observed in COVID-19 patients, often significantly influencing the clinical outcome. While the pathophysiology of pulmonary COVID-19 manifestation has been substantially unraveled, the underlying pathomechanisms of cardiac involvement in COVID-19 are largely unknown. In this multicentre study, we performed a comprehensive analysis of heart samples from 24 autopsies with confirmed SARS-CoV-2 infection and compared them to samples of age-matched Influenza H1N1 A (n = 16), lymphocytic non-influenza myocarditis cases (n = 8), and non-inflamed heart tissue (n = 9). We employed conventional histopathology, multiplexed immunohistochemistry (MPX), microvascular corrosion casting, scanning electron microscopy, X-ray phase-contrast tomography using synchrotron radiation, and direct multiplexed measurements of gene expression, to assess morphological and molecular changes holistically. Based on histopathology, none of the COVID-19 samples fulfilled the established diagnostic criteria of viral myocarditis. However, quantification via MPX showed a significant increase in perivascular CD11b/TIE2 + —macrophages in COVID-19 over time, which was not observed in influenza or non-SARS-CoV-2 viral myocarditis patients. Ultrastructurally, a significant increase in intussusceptive angiogenesis as well as multifocal thrombi, inapparent in conventional morphological analysis, could be demonstrated. In line with this, on a molecular level, COVID-19 hearts displayed a distinct expression pattern of genes primarily coding for factors involved in angiogenesis and epithelial-mesenchymal transition (EMT), changes not seen in any of the other patient groups. We conclude that cardiac involvement in COVID-19 is an angiocentric macrophage-driven inflammatory process, distinct from classical anti-viral inflammatory responses, and substantially underappreciated by conventional histopathologic analysis. For the first time, we have observed intussusceptive angiogenesis in cardiac tissue, which we previously identified as the linchpin of vascular remodeling in COVID-19 pneumonia, as a pathognomic sign in affected hearts. Moreover, we identified CD11b + /TIE2 + macrophages as the drivers of intussusceptive angiogenesis and set forward a putative model for the molecular regulation of vascular alterations.

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Echocardiographic assessment of the right ventricle in COVID-19: a systematic review

Cited by 19 publications

References 90 publications

Right Ventricular Assessment in Critically Ill COVID-19 Patients and its Prognostic Importance

Right Ventricular Assessment in Critically Ill COVID-19 Patients and its Prognostic Importance

Coronavirus disease 2019-induced hypercoagulability and its clinical implications

Inflammation and vascular remodeling in COVID-19 hearts

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