We present one of the first detailed analyses of echocardiographic changes in patients with COVID-19. Valvular regurgitation was the commonest abnormality observed. Patients with an abnormal TTE were more likely to die in hospital.
Our data is consistent with many previous studies suggesting that patients with abnormal TTE were more likely to die in hospital (13, 14, 20–22). Peng et al. have shown that abnormal echocardiography features were linked to the severity of disease and consequent cardiovascular sequelae (23).
Ours is one of the first studies to assess echocardiographic findings in admitted COVID-19 patients, irrespective of severity and its relationship to several biomarkers. Previous studies have detailed cardiac injury associated with COVID-19 based on troponin levels, ECG findings and echocardiogram features (13–15). The aetiology of cardiac dysfunction as it relates to abnormal TTE is likely to be multifactorial as shown in our study with no relation between troponin and abnormal TTE. Although direct invasion of the virus into the myocardium is one reason; it is likely that in the majority of the cases, myocardial infarction (Type II mainly) due to reduced oxygen perfusion and respiratory failure, microangiopathy secondary to cytokine storm and stress cardiomyopathy are potential causes (8, 24–30).
Participants in our groups were well-matched for age, sex and comorbidities. The commonest echocardiogram abnormality noted in our study was TR, similar to findings from another study (31), and under one third of our patients demonstrated RV dysfunction. The latter could be secondary to the acute respiratory distress syndrome seen in critically ill COVID-19 patients, which results in RV systolic dysfunction (8, 32, 33). Despite not being overly sensitive for a pulmonary embolism (PE), echocardiographic features of right heart strain and right heart dysfunction can indicate the presence of a pulmonary embolus (PE) or Pulmonary Intravascular Coagulation (PIC) which has been hypothesised to be one of the causative mechanisms leading to respiratory distress in COVID-19 patients (34).
Although RV dysfunction relates to poor outcomes, RV longitudinal strain is more highly predictive of mortality in COVID-19 patients (32, 35, 36). Despite the advantages of RV longitudinal strain, time constraints and increased risk of exposure to the SARS-CoV-2 virus for the sonographer limits its usage in the COVID-19 positive patients. Patients with disproportionately enlarged RV and reduced left ventricle (LV) systolic function need to be monitored closely with early goal-directed therapies as this has been shown to guide management of the critically ill (23, 37–39).
Our data also showed that elevated PASP on echocardiogram was an independent predictor of death. Our study corroborates with other literature which suggests that elevated PASP was related to morbidity (32). A case series also noted elevated PASP in their patients, which could be explained by pulmonary hypertension or recurrent pulmonary-embolic disease (37, 40). High PASP relates to pulmonary hypertension, whether underlying or as a consequent result of SARS-CoV-2-related lung injury, pulmonary hypercoagulable state or cardiomyopathy, confers significant mortality and morbidity (41, 42).
Anecdotal evidence has demonstrated that elevation of PASP and then a sudden depreciation in COVID-19 fulminant myocarditis was likely linked to right heart functional decline secondary to sustained overload (43). In concordance with other studies, elevated PASP and right heart enlargement was significantly predictive of mortality (31). In fact, taking into consideration the crucial role of right heart function, the German Society of Cardiology concluded that optimum RV functioning was essential for COVID-19 patients’ prognosis (44).
We also found that LDH was significantly raised in COVID-19 patients with an abnormal TTE. It is well known that raised LDH, although non-specific, correlates well with cardiac dysfunction (45, 46). Furthermore, we noted that mean haemoglobin in patients with abnormal TTE was significantly lower than in patients with normal TTE and predicted abnormal TTE. There appears to be no data that shows a relationship between SARS-CoV-2 and anaemia. However, one can hypothesise that as anaemia results in reduced oxygen perfusion, the consequent compensatory cardiovascular response can induce diastolic dysfunction and left ventricular remodelling observed on TTE.
Strengths and limitations
Our study does have several limitations. Our study is a retrospective observational study over a limited period of time from a single centre and with modest sample sizes. The latter raises the potential for a type II error, which may contribute to the small number of independent associations seen in our analysis. Also, we included patients who had already been hospitalised prior to their diagnosis of COVID-19 and therefore this may have been a confounding factor as their underlying primary diagnosis could have influenced their echocardiographic changes. Furthermore, the decision to perform the echocardiogram was likely due to specific symptoms or concerns and thus, we cannot completely exclude the possibility of selection bias. A few of the patients tested were critically unwell, and some requiring ventilator support at the time of the TTE; this could have influenced the TTE findings. Therefore, we cannot conclude that abnormal TTE findings were directly attributed to COVID-19, even though we did not find any significant differences between the two groups. For definite conclusions, a larger cohort or multicentre analysis is required. We suggest that biomarkers such as Hb and LDH can be used as a screening tool in COVID-19 patients to perform an echocardiogram.