Coronavirus disease 2019 (COVID-19) is an emerging outbreak caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although sharing considerable similarities with SARS, cardiac injury was more frequently reported in SARS-CoV-2 . However, the incidence and clinical significance of cardiac insufficiency in COVID-19 have not yet been well described. The purpose of our study was to purse the prevalence, risk factors and outcome of cardiac dysfunction in hospitalized patients with COVID-19.
We included 157 consecutive adult patients who were diagnosed with COVID-19. Clinical data were obtained from electronic medical records. Left ventricular (LV) and right ventricular (RV) structure and function were evaluated using bedside transthoracic echocardiography. Heart failure (HF) was classified into heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). The definitions of HF and RV dysfunction were based on the American Heart Association Guidelines [2, 3].
RV dysfunction was found in 40 (25.5%) unselected patients, 26 (28.9%) patients requiring high flow oxygen and 15 (41.7%) patients requiring mechanical ventilation. HF was presented in 28 (17.8%) unselected patients consisting of 24 (15.3%) HFpEF and 4 (2.5%) HFrEF, 22 (24.4%) patients requiring high flow oxygen and 11 (30.6%) patients requiring mechanical ventilation. 9 (5.7%) patients had biventricular dysfunction. Clinical and echocardiographic characteristics of patients with COVID-19 are shown in Supplementary Tables 1 and 2. Compared with patients without cardiac insufficiency,those with cardiac insufficiency had more comorbidities and complications as well as poorer prognosis. A multivariate logistic regression analysis revealed that acute respiratory distress syndrome (ARDS) was independently predictive of cardiac dysfunction (Supplementary Table 3), which contributed to higher mortality (Fig. 1a). Moreover, LV and RV dysfunction were more frequent in patients with elevated high-sensitivity troponin I (hs-TNI) than those without (Fig. 1b). During hospitalization, 23 patients died. The incidence of LV and RV dysfunction were higher in non-survivors than survivors (Fig. 1c). The mortality was 3.0% for patients without cardiac dysfunction and normal hs-TNI levels, 6.7% for those with cardiac dysfunction and normal hs-TNI levels, 13.3% for those without cardiac dysfunction but elevated hs-TNI levels, and 64.0% for those with cardiac dysfunction and elevated hs-TNI (Fig. 1d, e). In multivariate Cox analysis, hs-TNI elevation, mechanical ventilation and RV dysfunction were independent predictors of higher mortality (Supplementary Table 4).
Our study demonstrated that the prevalence of RV dysfunction was higher than that of LV dysfunction in patients with COVID-19. Direct viral damage, aggravation of a systemic inflammatory response, and hypoxemia may all contribute to cardiac injury. Furthermore, RV function can be worsened by increased afterload, which are likely involve ARDS, hypoxic pulmonary vasoconstriction, microthrombi within the pulmonary vasculature and microvascular injury [4, 5]. Additionally, our findings revealed that mortality was highest in patients with increased troponin associated with RV dysfunction. Elevations of cardiac troponin and RV dysfunction were independently predictive of higher mortality, highlighting the significance of closely monitoring the changes of cardiac troponin and RV function. In summary, elevated cardiac troponin together with RV dysfunction may be crucial for risk stratification of COVID-19 patients and should be taken into consideration when applying prevention and therapy.
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This work was supported by the National Natural Science Foundation of China (Grant Nos. 81727805, 81922033, 81401432).
Conflicts of interest
The authors declared no conflict of interest.
The study was approved by Union hospital Tongji Medical College, Huazhong University of Science and Technology Ethics Committee (KY-2020–02.06).
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Li, Y., Li, H., Li, M. et al. The prevalence, risk factors and outcome of cardiac dysfunction in hospitalized patients with COVID-19. Intensive Care Med 46, 2096–2098 (2020). https://doi.org/10.1007/s00134-020-06205-0