Abstract:Introduction: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)-infected patients commonly have elevated troponin and D-dimer levels, but limited imaging exists to support most likely etiologies in efforts to avoid staff exposure. The purpose of this study was to report transthoracic echocardiographic (TTE) findings in SARS-CoV-2 patients with correlating troponin and D-dimer levels. Methods: We identified 66 SARS-CoV-2 patients (mean age 60 ± 15.7 years) admitted within a large, eight-hospital heal… Show more
“…Impairment of RV function was related with elevated troponin levels and clinical deterioration [ 31 ]. Similar results came from other smaller series [ 32 , 49 ]. Goerlich et al found LV diastolic impairment with elevated LV filling pressures (E/e’ ratio) in a quarter of patients admitted for COVID-19.…”
Section: During Covid-19: Myocardial Involvement In the Acute Phasesupporting
Purpose of the review
Coronavirus Disease 2019 (COVID-19) and cardiovascular (CV) disease have a close relationship that emerged from the earliest reports. The aim of this review is to show the possible associations between COVID-19 and heart failure (HF) with preserved ejection fraction (HFpEF).
Recent findings
In hospitalized patients with COVID-19, the prevalence of HFpEF is high, ranging from 4 to 16%, probably due to the shared cardio-metabolic risk profile. Indeed, comorbidities including hypertension, diabetes, obesity and chronic kidney disease — known predictors of a severe course of COVID-19 — are major causes of HFpEF, too. COVID-19 may represent a precipitating factor leading to acute decompensation of HF in patients with known HFpEF and in those with subclinical diastolic dysfunction, which becomes overt. COVID-19 may also directly or indirectly affect the heart. In otherwise healthy patients, echocardiographic studies showed that the majority of COVID-19 patients present diastolic (rather than systolic) impairment, pulmonary hypertension and right ventricular dysfunction. Such abnormalities are observed both in the acute or subacute phase of COVID-19. Cardiac magnetic resonance reveals myocardial inflammation and fibrosis in up to the 78% of patients in the chronic phase of the disease.
Summary
These findings suggest that COVID-19 might be a novel independent risk factor for the development of HFpEF, through the activation of a systemic pro-inflammatory state. Follow-up studies are urgently needed to better understand long-term sequelae of COVID-19 inflammatory cardiomyopathy.
“…Impairment of RV function was related with elevated troponin levels and clinical deterioration [ 31 ]. Similar results came from other smaller series [ 32 , 49 ]. Goerlich et al found LV diastolic impairment with elevated LV filling pressures (E/e’ ratio) in a quarter of patients admitted for COVID-19.…”
Section: During Covid-19: Myocardial Involvement In the Acute Phasesupporting
Purpose of the review
Coronavirus Disease 2019 (COVID-19) and cardiovascular (CV) disease have a close relationship that emerged from the earliest reports. The aim of this review is to show the possible associations between COVID-19 and heart failure (HF) with preserved ejection fraction (HFpEF).
Recent findings
In hospitalized patients with COVID-19, the prevalence of HFpEF is high, ranging from 4 to 16%, probably due to the shared cardio-metabolic risk profile. Indeed, comorbidities including hypertension, diabetes, obesity and chronic kidney disease — known predictors of a severe course of COVID-19 — are major causes of HFpEF, too. COVID-19 may represent a precipitating factor leading to acute decompensation of HF in patients with known HFpEF and in those with subclinical diastolic dysfunction, which becomes overt. COVID-19 may also directly or indirectly affect the heart. In otherwise healthy patients, echocardiographic studies showed that the majority of COVID-19 patients present diastolic (rather than systolic) impairment, pulmonary hypertension and right ventricular dysfunction. Such abnormalities are observed both in the acute or subacute phase of COVID-19. Cardiac magnetic resonance reveals myocardial inflammation and fibrosis in up to the 78% of patients in the chronic phase of the disease.
Summary
These findings suggest that COVID-19 might be a novel independent risk factor for the development of HFpEF, through the activation of a systemic pro-inflammatory state. Follow-up studies are urgently needed to better understand long-term sequelae of COVID-19 inflammatory cardiomyopathy.
“…RV dysfunction correlated with troponin levels. • During follow-up, 50% of patients showing clinical deterioration revealed also further worsening of RV parameters, whereas the LV function remains normal in all those patients Schott et al [ 63 ] • ECHO revealed RV dilation and increased RV/LV ratio in the majority of hospitalized patients (74% and 82%, respectively), whereas reduction of LVEF was detected only in 3% of the patients Rivinius et al [ 64 ] • In mechanically ventilated heart transplant recipients with COVID-19, the mortality of can reach 87% and appeared associated with RV dysfunction accompanied by increased PAP, whereas none of them showed LVEF reduction Caravita et al [ 65 ] • The prevalence of PH (mean PAP ≥ 25 mmHg) was 4 times higher in ventilated COVID-19 patients with ARDS compared to those without the need for mechanical ventilation (76% vs. 19%, p < 0.001) Doyen et al [ 66 ] • Patients with cardiac injury (increased hs-TnI) experienced 3.6 times more RV than LV systolic dysfunction (47% and 13%, respectively) RV right ventricle, ICU intensive care unit, ECHO echocardiography, PAPs systolic pulmonary arterial pressure, LV left ventricle, EF ejection fraction, RVLS right ventricular longitudinal strain, FAC RV right ventricular fractional area change, TAPSE tricuspid annulus peak systolic excursion, PH pulmonary hypertension, PAP pulmonary arterial pressure, ARDS acute respiratory distress syndrome, hs-TnI high-sensitive troponin I Fig. 1 Pathophysiologic role of heart–lung interactions for the development and progression of life-threatening RV dysfunction during SARS-COV-2 infection.…”
Section: Major Covid-related Pulmonary and Cardiovascular Injuriesmentioning
confidence: 99%
“…Among the patients developing clinical deterioration during follow-up, 50% showed further deterioration of RV parameters, whereas the LV function remains normal in all those patients [ 39 ]. An ECHO study on hospitalized COVID-19 patients revealed RV dilation in 74% of them and the RV/LV ratio, which was increased in 82% of the patients, reached 0.9 ± 0.3 [ 63 ]. In that study, the LVEF was 60% (52–74%) and reduction of LVEF was detected in only 3% of the patients.…”
Section: Relevance Of Right Heart Dysfunction In Covid-19mentioning
Due to the SARS-CoV-2 infection–related severe pulmonary tissue damages associated with a relative specific widespread thrombotic microangiopathy, the pathophysiologic role of heart–lung interactions becomes crucial for the development and progression of right ventricular (RV) dysfunction. The high resistance in the pulmonary circulation, as a result of small vessel thrombosis and hypoxemia, is the major cause of right heart failure associated with a particularly high mortality in severe COVID-19. Timely identification of patients at high risk for RV failure, optimization of mechanical ventilation to limit its adverse effects on RV preload and afterload, avoidance of medication-related increase in the pulmonary vascular resistance, and the use of extracorporeal membrane oxygenation in refractory respiratory failure with hemodynamic instability, before RV failure develops, can improve patient survival. Since it was confirmed that the right-sided heart is particularly involved in the clinical deterioration of patients with COVID-19 and pressure overload-induced RV dysfunction plays a key role for patient outcome, transthoracic echocardiography (TTE) received increasing attention. Limited TTE focused on the right heart appears highly useful in hospitalized COVID-19 patients and particularly beneficial for monitoring of critically ill patients. In addition to detection of right-sided heart dilation and RV dysfunction, it enables assessment of RV-pulmonary arterial coupling and evaluation of RV adaptability to pressure loading which facilitate useful prognostic statements to be made. The increased use of bedside TTE focused on the right heart could facilitate more personalized management and treatment of hospitalized patients and can contribute towards reducing the high mortality associated with SARS-CoV-2 infection.
“…In a report of echocardiographic findings from 66 high-risk cases, Schott et al described frequent right ventricle dilation and increased wall thickness [ 84 ]. The American College of Cardiology and American Society of Echocardiography recommend that echocardiographic examinations in the context of COVID-19 are performed in a manner that reduces sonographer exposure time and are conducted only if it is likely that results will change clinical management [ 85 ].…”
Section: Clinical Recommendations For Cardiovascular Screening and Trmentioning
First documented in China in early December 2019, the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spread rapidly and continues to test the strength of healthcare systems and public health programs all over the world. Underlying cardiovascular disease has been recognized as a risk factor for coronavirus disease 2019 (COVID-19)-related morbidity and mortality since the early days of the pandemic. In addition, evidence demonstrates cardiac and endothelial damage in somewhere between one-third and three-quarters of individuals with COVID-19, regardless of symptom severity. This damage is thought to be mediated by direct viral infection, immunopathology and hypoxemia with the additional possibility of exacerbation via medication-induced cardiotoxicity. Clinically, the cardiovascular consequences of COVID-19 may present as myocarditis with or without arrhythmia, endothelial dysfunction and thrombosis, acute coronary syndromes and heart failure. Presentation can vary widely and may or may not be typical of the condition in an individual without COVID-19. There is evidence to support the prognostic utility of cardiac biomarkers (e.g., cardiac troponin) and imaging studies (e.g., echocardiography, cardiac magnetic resonance imaging) in the context of COVID-19 and building evidence suggests that cardiovascular screening may be warranted even among those with asymptomatic or mild infection and those without traditional cardiovascular risk factors. In addition, evidence suggests the potential for long-term cardiovascular consequences for those who recover from COVID-19 with implications for the field of cardiology long into the future. Even among those without COVID-19, disruption of infrastructure and changes in human behavior as a result of the pandemic also have an upstream role in cardiovascular outcomes, which have already been documented in multiple locations. This review summarizes what is currently known regarding the pathogenic mechanisms of COVID-19-related cardiovascular injury and describes clinical cardiovascular presentations, prognostic indicators, recommendations for screening and treatment, and long-term cardiovascular consequences of infection. Ultimately, medical personnel must be vigilant in their attention to possible cardiovascular symptoms, take appropriate steps for clinical diagnosis and be prepared for long-term ramifications of myocardial injury sustained as a result of COVID-19.
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