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\begin{document}

\title{Different cardiac performance in severe and mild patients with COVID-19
by standard and strain echocardiography}



\author[1]{HUi Wang}%
\author[2]{Zhiyue Liu}%
\author[1]{Jiafu Wei}%
\author[1]{Jun Lin}%
\author[1]{Yang Ge}%
\author[1]{Huanxing Li}%
\author[1]{Tao Zeng}%
\author[2]{Mei Liu}%
\author[1]{Fangyang Huang}%
\author[1]{Qi Liu}%
\author[1]{Mao Chen}%
\author[1]{He Huang}%
\affil[1]{Affiliation not available}%
\affil[2]{Sichuan University West China Hospital}%


\vspace{-1em}



  
  \date{May 24, 2024}


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\selectlanguage{english}
\begin{abstract}
Background: The initial mechanism of COVID-19 is the binding of the
virus to ACE2. Since the heart and the vessels also express ACE2, they
both could become targets of the virus. However, cardiac performance of
mild and severe patients may be different, requested individualized
treatment. The aim of this study is to explore the global and segmental
myocardial performance of the severe and mild COVID-19 patients.Methods:
45 patients with COVID-19 infection were included in this study. The
clinical history, laboratory test and standard and strain
echocardiography were performed at admission. Results: 1. All patients
showed reduced cardiac diastolic function; 2. Severe patients exhibited
exacerbated right ventricular systolic function; 3. All patients showed
impaired left ventricular strain, worse strain in severe patient. 4. The
apical longitudinal strain of mild patients was higher than basal and
middle segment. 5. There was a negative correlation between LV GLS and
log TnT-hs, as well as NT-pro BNP. 6. The EF value and strain of left
atrium of mild and severe patients decreased; 7. LV GLS, LV GCS and LA
GLS area under the ROC curve to predict the disease severity were 0.698,
0.758 and 0.782 respectively. 8. In the follow-up of severe patients,
left atrial and ventricular strain showed an increased
trend.Conclusions: These findings suggested that left ventricular
performance was subclinically impaired during COVID-9 infection
irrespective of infection severity and the strain of LV and LA may
predict the disease severity. The cardiac function had an increasing
trend for severe patients.%
\end{abstract}%



\sloppy


\textbf{1.~~~~} {}\textbf{Introduction}

The COVID-19 infection is caused by severe acute respiratory syndrome
coronavirus 2 (SARS-CoV2)\textsuperscript{1}. SARS-CoV2 as well as other
coronaviruses have been verified to transit into their host human cells
via angiotensin-converting enzyme 2 (ACE2). ACE2 is a type I integral
membrane protein with many vital physiologic functions which is highly
expressed in alveolar and cardiovascular cells\textsuperscript{2,3}.In
the published clinical studies of COVID-19, patients with acute cardiac
injury\textsuperscript{4}, shock, and arrhythmia were present in 7.2\%,
8.7\%, and 16.7\% respectively. Thus, cardiac injury has also attracted
attention in COVID-19 pneumonia.

Echocardiography is the choice of method in detecting cardiac structure
and function. Left ventricular global longitudinal strain (LVGLS) is
beneficial for both diagnosis and risk stratification in patients with
cardiac diseases\textsuperscript{5}. In the published cases, COVID-19
infected patients showed an enlarged left ventricle, diffuse myocardial
dyskinesia with a decreased left ventricular ejection fraction (LVEF),
pulmonary hypertension, as well as a reduced pulmonary artery systolic
pressure (PASP), tricuspid annular plane systolic excursion (TAPSE)
\textsuperscript{6}and a lower inferior vena cava (IVC) collapse rate.
In addition, cardiac tamponade and pericardiocentesis could also happen
in these patients\textsuperscript{7}. Besides that, there is lack of the
cohort echocardiography study to explore different cardiac performance
of different severity of disease by standard and strain echocardiography
in patients with COVID-19.{}{{}}

Therefore, this study aimed to observe 1. Different cardiac function of
patients in ICU and general ward by standard and strain
echocardiography. 2. the cardiac function change in follow-up of severe
patients in ICU with COVID-19.

\textbf{2.~~~~} {}\textbf{Methods}

\par\null

\textbf{2.1 Population}

45 patients diagnosed COVID-19 infection were included in our study
(National Health Commission: Seventh Edition Treatment plan for
COVID-19) \textsuperscript{8}. Mild patients: the clinical symptoms are
slight, and no pneumonia manifestations on imaging. Ordinary type: with
fever, respiratory tract symptoms, etc. Imaging shows pneumonia. Severe
patients: Adults with any of the following syndromes; 1. Short of
breath, RR[?] 30 times/min; 2. Oxygen saturation [?] 93\% in rest condition;
3. Arterial blood oxygen partial pressure (PaO2) / oxygen concentration
(FiO2) [?]300mmHg. Pulmonary imaging shows that the lesions progress
significantly \textgreater{} 50\% within 48 hours were treated as
severe. Critical severity: 1. Respiratory failure occurs and mechanical
ventilation is performed; 2. Shock occurs; 3. Combined organ failure
requires intensive care.

Among the 45 patients, nine patients have preexisting cardiac disease
(six patients with hypertension, one patient with coronary heart disease
and hypertension , two patients has chronic heart failure and
hypertension).The clinical history, laboratory data including
high-sensitivity troponin T(hs-TnT), N-Terminal pro-brain natriuretic
peptide (NT-pro BNP) and echocardiography data were collected at
admission to the study(baseline). Because of the small study population,
we divided the mild and ordinary type as mild group, 25 patients in
total; severe and critical severity as severe group, 20 cases in total.
The severe group in intensive care unit (ICU) were followed up for 16
days.7 severe patients recovered and were transferred out, only13 severe
patients were still in intensive care unit and received the
echocardiography at least twice(follow-up). Furthermore, 10 received
echocardiography more than 7 times during hospital. The data collection
was from February 22th to March 8th 2020. The first echocardiography in
this study was performed on admission to the study, not at hospital
admission.

23 normal people were included based on normal echocardiography and
blood test during the March 2020 in west china hospital.

\textbf{2.2 Standard Echocardiographic Examination}

Transthoracic echocardiographic examinations were performed with S5-1
probe, 1-5MHz (CX50, Phillip, Netherlands). Two-dimensional (2D) and
Doppler echocardiography were performed according to the guidelines of
the American Society of Echocardiography\textsuperscript{5}. The
following echocardiographic views were recorded over three cardiac
cycles: left parasternal long- and short axis views and apical two-
apical three- and apical four-chamber views. Images were recorded on
external hard disk and stored in digital format for offline analysis
(Q-lab 10.8.5). The right ventricular anteroposterior diameter and LV
diameter, left atrial (LA) diameter, LV interventricular septum (IVS)
and LV posterior wall (LVPW) thickness and aortic diameter were measured
at long axis view. The right atrial (RA) diameter was measured at apical
four-chamber view. The pulmonary diameter was measured at pulmonary long
axis view. LV systolic function included LV volumes, left ventricular
ejection fraction (LVEF) were measured by the modified biplane Simpson's
rule. Mitral, aortic and pulmonary artery Doppler flow profiles were
recorded, including maximum mitral inflow velocity at early (E) and late
(A) diastole. Pulsed tissue Doppler imaging was obtained with the sample
volume placed at the septum of mitral valve and free wall of tricuspid
valve at the apical 4-chamber view. Velocity of mitral annulus at early
diastole (e'), late diastolic myocardial a') velocities, and RV TDI-s
were recorded. The E/e' ratio, being recorded at the level of the septum
of the mitral annulus, was used as an index of LV filling pressure.
Tricuspid annular plane systolic excursion (TAPSE) was measured in
apical four-chamber view via placing the cursor at the tricuspid
anterior annulus and measuring the distance of systolic annular RV
excursion along a longitudinal line. All images were collected by an
experienced investigator in echocardiography who was blinded to the
clinical information.

\textbf{2.3 Strain echocardiography examination}

The images were acquired at the left parasternal short axis views,
apical long axis, apical four-chamber, and apical two-chamber views. All
off-line analyses were performed by an investigator experienced in
speckle tracking analysis using the Q-lab workstation version
10.8.5(Phillip Medical Systems). The investigator was blinded to the
patient's management and outcome information. The endocardium was
defined by manual tracing and the region of interest (ROI) was adjusted
to the compact myocardium thickness. Default settings for smoothing and
drift compensation were used. We evaluated longitudinal and
circumferential strain. LV longitudinal strain analysis was performed on
apical view. Circumferential strain was performed on short-axis views of
three segments; basal, mid and apex.Care was taken to ensure that the
basal short-axis at the level of mitral valve, and the apical plane
distal to the papillary muscle. The region of interest width was
adjusted first, to include the entire endocardium. From the analysis, we
received 18 regional longitudinal strain (RLS) and circumferential
strain (RCS). These allowed us to calculate the segmental longitudinal
and circumferential strain and the global longitudinal strain (GLS) and
circumferential strain (GCS) as well. Using the same software, the LA
endocardial border was traced in the apical 4-chamber view and apical
2-chamber view, care was taken to exclude the appendage and pulmonary
veins from the LA cavity. Then, a composite LA longitudinal strain
(LAGLS) curve throughout the cardiac cycle was generated. The frame rate
of 58 \selectlanguage{ngerman}±3 frames/sec was obtained for the LV and LA strain analysis.

\textbf{2.4 Statistical analysis}

Quantitative data are presented as Mean±SD, qualitative data as
frequency number (\%). Comparisons among the groups were performed by
one-way ANOVA. If there was a difference, then S-N-K test was used.
T\selectlanguage{english}-test was used to compare between two groups. Chi-square test was used
to compare binary variables. Since values of NT-pro BNP and hs-TnT were
not normally distributed, data were log-transformed for multivariate
analyses. Pearson's correlation was used to test the association between
LV GLS and log hs-TnT, as well as NT-pro BNP. The Receiver Operating
Characteristic (ROC) curve was performed to evaluate the GLS's and GCS's
ability to predict the severity of the disease. Area under the
curve(AUC)\textless{}0.5 has no diagnostic value,
0.5\textless{}AUC\textless{}0.7 has low diagnostic value,
0.7\textless{}AUC\textless{}0.9 has medium diagnostic value, and
AUC\textgreater{}0.9 has high diagnostic value.\textsuperscript{9} when
AUC\textgreater{}0.9, according to Youden Index, combining sensitivity
and specificity, find the best diagnostic cut point.\emph{P}
\textless{}0.05 was considered significant. All statistical tests were
analyzed with SPSS (version 19.0) software.

\textbf{3.Results}

\textbf{3.1 The cardiac structure and function in patients with COVID-19
at baseline}

The mean age of the patients with COVID-19 was 55.33+-19.65 years old,
with a range from 20 to 87. There were 23 men and 22 women in this
study. Nine patients had hypertension, in whom one had coronary heart
disease and two had chronic heart disease. (Table 1)

None of the patients had significant valvular lesions. Trace to mild
tricuspid regurgitation was found in 8 mild patients (32\%), and in 6
severe patients (30\%). No significant pulmonary hypertension was found.
Table 2 showed the echocardiographic data at mild and severe patients.
Significantly thicker interventricular septum (IVS) (\emph{P\textless{}}
0.05) and posterior wall of left ventricle (LVPW)(\emph{P\textless{}}
0.05) , higher E /e'(\emph{P\textless{}} 0.05) , were observed in severe
patients when compared with control group, IVS and LVPW was
thicker(\emph{P\textless{}} 0.05)in severe patients than in mild
patients. E/e' was larger in mild group than controls.
(\emph{P\textless{}} 0.05).

larger right atrium(\emph{P\textless{}} 0.05), lower
TAPSE(\emph{P\textless{}} 0.05) and TDI-s (\emph{P\textless{}} 0.05)
were observed in severe patients when compared with control group. The
size of RA was larger in mild group than controls. (\emph{P\textless{}}
0.05). Moreover, TDI-s was significantly lower(\emph{P\textless{}} 0.05)
in the group of severe patients than in mild patients. LAEF decreased in
patients with COVID-19 and no difference in LAESV among these three
groups.

\textbf{3.2 Left atrial strain and left ventricular strain in patients
with COVID-19 at baseline}

GLS and GCS patterns of left ventricle and GLS of left atrium during the
cardiac cycle were reported in Table 3. LA GLS in severe and mild
patients with COVID-19 were lower than controls(\emph{P\textless{}}
0.05). LV GLS, LV GCS and LA GLS in severe and mild patients with
COVID-19 were lower than controls(\emph{P\textless{}} 0.05). LVGLS,
LVGCS in severe patients were lower than mild
patients(\emph{P\textless{}} 0.05).

Basal, middle and apical segment of circumferential strain (CS) and
longitudinal strain (LS) in severe and mild patients were presented in
Table 4. No significant difference was observed among basal, middle and
apical segments in LV CS and LV LS in severe group. No difference in
three segments in LV CS in mild patients, however, apical LS was higher
than LS in the other two segments in mild patients.

In severe patients with COVID-19(n=20), the value of log (NT-pro BNP)
and log (hs-TnT) were 2.50+-0.94 pg/ml and 1.12+-0.57 pg/ml respectively.
There was a negative correlation between LV GLS and log TnT-hs as well
as NT pro-BNP in severe patients with COVID -19 (figure 1).

We analyzed the relation between the severity of COVID-19 patients and
LV GLS, LV GCS and LA GLS through ROC curve and defined the mild
condition as positive status (Figure2).The results showed that the URC
of LV GLS, LV GCS and LA GLS to predict the severity were
0.698(0.543-0.826), 0.758(0.607-0.873) and 0.782(0.634-0.891)
respectively. LV GLS, LV GCS and LA GLS may had a low or medium
diagnostic performance for the severity of COVID-19 patients
(all\emph{P} \textless{}0.05).

\textbf{3.3 The cardiac function in severe patients with COVID-19 during
follow-up}

There was no statistical difference in the size of both atria and
ventricle, thickness of interventricular septum, left ventricular
posterior wall, diameter of aorta and pulmonary between the baseline and
follow-up results. No difference was also observed in left ventricular
systolic function (LVEF) and diastolic function (E/e'), LAEF, IVC
collapse rate and systolic (TAPSE, TDI-S) function of right ventricle.
(Table 5)

The GCS of left ventricle was significantly higher (\emph{P\textless{}}
0.05) at follow-up when compared with baseline. However, there was no
statistical difference in LV GLS of severe patients at baseline and
follow-up, neither in LA GLS (Table 6).

Only 10 severe patients received echocardiography examination more than
7 times during hospitalization. The patient number was small, thus we
drew a line chart to show the strain in left atrium and left ventricle.
The results showed that the LA GLS, LV GCS and LV GLS tended to rise
gradually. (Figure 3).

\textbf{Discussion}

Acute myocardial injury has been demonstrated in 7.2\%-12\% of patients
with COVID-19 in preliminary reports, with a higher prevalence among
those requiring intensive care \textsuperscript{10}. Mortality data from
44672 cases of COVID-19 released by the Chinese Centre for Disease
Control and Prevention demonstrate that patients with cardiovascular
comorbidities show a much higher mortality\textsuperscript{11}.

But there still lack a systematic and comprehensive study including mild
and severe patients in the assessment of left ventricular, left atrial
and right ventricular function.

The aim of the present study was to evaluate the cardiac function by
standard and strain echocardiography including mild and severe patients
with COVID-19. We observed that: 1. Both mild and severe COVID-19
infected patients showed reduced left ventricular diastolic function
compared with control group; 2. Severe patients with COVID-19 exhibited
exacerbated right ventricular systolic function; 3. Both mild and severe
patients with COVID-19 showed impaired left ventricular strain, and the
strain in severe patients even worse, suggesting all the patients may
had early systolic function. 4. The strain in apical segment of mild
patients with COVID-19 was elevated compared with basal and middle
segment. 5.There was a negative correlation between LV GLS and log
TnT-hs, as well as NT-pro BNP. 6. The EF value and strain of left atrium
of mild and severe patients with COVID-19 decreased; 7.LV GLS, LV GCS
and LA GLS might predict the severity of COVID-19. 8. In the follow-up
of severe COVID-19 infected patients, their cardiac structure and
function had no change, while left atrial and ventricular strain
exhibited an increased trend.

In the present study, there was no difference in the size of LV and
LVEF, among the 3 groups. IVS and LVPW in severe patients with COVID-19
were thicker than mild patients and the controls. There were 8 severe
patients with hypertension. However, only one mild patient with
hypertension. That might contribute to thicker IVS and
LVPW\textsuperscript{12}. In addition, the age may also have an effect
on this cardiac performance\textsuperscript{13}. In our investigation,
E/e' in severe patients with COVID-19 were higher than mild and control
groups, probably suggesting elevated LV filling pressure. Furthermore,
no difference in RV among the 3 groups. TDI-s and TAPSE, the index of
right ventricular systolic function, in severe patients were lower than
that in the other two groups, suggesting right ventricular systolic
dysfunction, which was seen, particularly in the context of severe
parenchymal lung disease and acute respiratory
disease\textsuperscript{13}. Previous study also demonstrated that
compared with survivors, nonsurvivors displayed enlarged right heart
chambers, diminished RV function, and elevated pulmonary artery systolic
pressure.\textsuperscript{14} 7 of 17 (42\%) needed prone positioning
for severe Hypoxia had RV dysfunction(RV FAC \textless{}
35\%).\textsuperscript{15}

LA is considered to modulate left ventricular \selectlanguage{english}filling and cardiovascular
performance as (i) a reservoir for pulmonary venous return during
ventricular systole,(ii) a conduit for pulmonary venous return during
early ventricular diastole, and (iii) a booster pump that augments
ventricular \selectlanguage{english}filling during late ventricular
diastole.\textsuperscript{16}LA size is strong predictor of
cardiovascular morbidity and death\textsuperscript{17}.LA size
correlates with both LA and left ventricular(LV) function. Previous
study found no difference in LA dimension between survivors and
nonsurvivors with COVID-19\textsuperscript{14}, and there is still lack
of study on left atrial strain for now. In our study, higher LA volume
and lower LAEF were observed in severe and mild patients with COVID-19
than control group. Further, LA myocardial deformation is assessed as
global longitudinal strain. \textsuperscript{18}In addition, the results
showed that LAGLS decreased in severe and mild patients, suggesting the
LA systolic dysfunction. All LA volume, LAEF and LAGLS showed LA
systolic dysfunction, contributing to LV dysfunction.

Strain image is superior to standard echocardiography for myocardial
injury detection in patients and reflects the complex deformation
pattern of the heart during systole\textsuperscript{19}. Previous study
showed that LV GLS measurement are stable and repeatable, which have
additional predictive value for evaluating the rest cardiac function of
patients.\textsuperscript{20} The normal LV GLS measured by Qlab is
18.9+-2.5\%\textsuperscript{21}. Though there was no significant change
in LVEF and LV volumes, significantly lower LV GLS and LV GCS were
observed in severe and mild patients with COVID-19 compared with control
group, especially in severe group. Although in severe patients, 2
patients with coronary heart disease and 1 with chronic heart disease
may contribute to worse GLS. Patients with hypertension may also lead to
lower GLS\textsuperscript{22}. This result showed subclinical cardiac
systolic dysfunction in patients with COVID-19. Troponin and NT-pro BNP
is a widely accepted biomarker of myocardial injury, and elevated serum
levels have been a notable feature during recent epidemics of
respiratory virus infections.\textsuperscript{20}Accordingly, we
observed the troponin and NT-pro BNP were negatively correlated with LV
GLS in severe patients. Previous data indicated a decreased myocardial
longitudinal strain in fulminat myocarditis especially decreased in the
basal and middle segments\textsuperscript{4,23},which was similar to our
results, our results observed the apical LS in mild patients was higher
than middle and basal segment, however, no significant difference among
basal, middle and apical LS,CS in severe patients, as shown in table 4.
Previous study showed that GLS can predict functional capacity in
patients with preserved LVEF heart failure and to assess prognosis in
reduced LVEF heart failure\textsuperscript{24}. And it could classify HF
patients according to the functional capacity.\textsuperscript{25} In
this study, we found that GLS had a low predicted value of the disease
severity, which may stratify the patients with unknown condition and
therefore to deserve more differentiated treatment.

In our study, only 13 severe patients in ICU received echocardiography
one more time. Compared with the first examination, no change in cardiac
structure on follow-up. For the strain, our results showed only LV GCS
increased (30.40+-7.51 vs 23.05+-8.56, \emph{P\textless{}} 0.05) in severe
patients when compared with the first echocardiography, while the LV GLS
and LA GLS exhibited an increased trend. Furthermore, the line chart
based on 10 patients for 16 days also showed steadily rising trend.
Alleviating myocardial injury was implied, although which needed longer
observation. Previous study showed cardiac impairment caused by SARS-CoV
in the more critically ill patients may be reversible on
recovery\textsuperscript{26}.

\textbf{Study Limitations}

Outbreak of COVID-19 was abrupt, the study was an observational, 'not
well-designed' one in highly contagious COVID-19 patients, lasting only
16 days. The study population number in our study was small.

\textbf{Conclusions}

These findings suggested that left ventricular performance was
subclinically impaired during COVID-9 infection irrespective of
infection severity and the strain of LV and LA may predict the disease
severity. The cardiac function had an increasing trend for severe
patients treated in ICU. Whether the myocardial injury may be reversible
on clinical recovery needs longer follow-up.

\textbf{Acknowledgements}

We thank the COVID-9 Clinical Taskforce, Sichuan Province, and all the
health care providers and institutions involved in the management of
patients with COVID-9.

\textbf{Disclosures}

All authors declare that they have no conflict of interest to disclose.

\textbf{ORCID} https://orcid.org/0000-0001-9192-1419

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24. Hasselberg NE, Haugaa KH, Sarvari SI, et al. Left ventricular global
longitudinal strain is associated with exercise capacity in failing
hearts with preserved and reduced ejection fraction. Eur Heart J
Cardiovasc Imaging 2015;16:217-24.

25. Maia RJC, Brandao SCS, Leite J, et al. Global Longitudinal Strain
Predicts Poor Functional Capacity in Patients with Systolic Heart
Failure. Arquivos brasileiros de cardiologia 2019;113:188-94.

26. Li SS, Cheng CW, Fu CL, et al. Left ventricular performance in
patients with severe acute respiratory syndrome: a 30-day
echocardiographic follow-up study. Circulation 2003;108:1798-803.

\textbf{Figure legends}

\textbf{Figure 1. a. Correlation between LV GLS and log hs-TnT; b.
Correlation between LV GLS and log NT-pro BNP. (n=20 in each
group).}hs-TnT, high-sensitivity toponin T; NT-pro BNP, N-Terminal
pro-brain natriuretic peptide; LV, left ventricular; GLS global
longitudinal strain;

\begin{CJK}{UTF8}{gbsn}\textbf{Figure2. LV GLS、LV GCS an LA GLS as a predictor of severity of
the COVID-19 patients.}\end{CJK}\selectlanguage{english} LV, left ventricular; LA, left atrial; GLS,
global longitudinal strain; GCS, global circumferential strain.

\textbf{Figure3. The change of LAEF(a), LA GLS(b), LV GLS(c) and LV
GCS(d) post onset.} LV, left ventricular; LA, left atrial; EF, ejection
fraction; GLS, global longitudinal strain; GCS, global circumferential
strain.

\textbf{Tables}

\textbf{Table 1. Study population}\selectlanguage{english}
\begin{longtable}[]{@{}lllll@{}}
\toprule
\begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
Control(n=23)\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
Mild(n=25)\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
Severe(n=20)\strut
\end{minipage} & \begin{minipage}[b]{0.17\columnwidth}\raggedright\strut
\emph{P} value\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Male (\%)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
13(57)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
13(52)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
10(50)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0.91\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
Age (years old)\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
42.17\selectlanguage{ngerman}±14.72 20\textasciitilde{}70\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
48.44\selectlanguage{ngerman}±16.10 20\textasciitilde{}82\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
63.95\selectlanguage{ngerman}±20.64*\# 20\textasciitilde{}87\strut
\end{minipage} & \begin{minipage}[t]{0.19\columnwidth}\raggedright\strut
\textless{}0.001\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Duration of observation(days)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
8\selectlanguage{ngerman}±9.1\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
8.1\selectlanguage{ngerman}±6.2\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0.661\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
SBP (mmHg)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
123.17\selectlanguage{ngerman}±14.21\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
124.92\selectlanguage{ngerman}±15.72\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
141.55\selectlanguage{ngerman}±18.70*\#\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0.014\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
DBP (mmHg)\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
79.61\selectlanguage{ngerman}±10.22\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
81.42\selectlanguage{ngerman}±7.90\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
79.82\selectlanguage{ngerman}±13.88\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0.717\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Hypertension\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
8\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Coronary heart disease\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
1\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
Chronic heart failure\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
0\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
2\strut
\end{minipage} & \begin{minipage}[t]{0.17\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

SBP indicates systolic blood pressure; DBP diastolic blood pressure. *
compared with control group , \emph{P\textless{}} 0.05; \# compared with
mild patients, \emph{P} \textless{}0.05.

\textbf{Table 2.} \textbf{Standard echocardiography at baseline in
patients with COVID-19}\selectlanguage{english}
\begin{longtable}[]{@{}lllll@{}}
\toprule
& Control(n=23) & Mild(n=25) & Severe(n=20) & \emph{P}
value\tabularnewline
\midrule
\endhead
LV (mm) & 40.04\selectlanguage{ngerman}±3.80 & 40.88\selectlanguage{ngerman}±3.30 & 41.30\selectlanguage{ngerman}±10.35 & 0.78\tabularnewline
LA (mm) & 29.70\selectlanguage{ngerman}±2.80 & 30.92\selectlanguage{ngerman}±3.01 & 29.80\selectlanguage{ngerman}±3.81 & 0.35\tabularnewline
RV (mm) & 20.87\selectlanguage{ngerman}±1.78 & 20.24\selectlanguage{ngerman}±2.09 & 20.10\selectlanguage{ngerman}±3.33 & 0.53\tabularnewline
RA (mm) & 33.57\selectlanguage{ngerman}±3.27 & 38.80\selectlanguage{ngerman}±4.51* & 37.95\selectlanguage{ngerman}±4.71* &
\textless{}0.001\tabularnewline
IVS (mm) & 8.43\selectlanguage{ngerman}±1.73 & 8.96\selectlanguage{ngerman}±1.86 & 10.70\selectlanguage{ngerman}±2.08*\# & 0.001\tabularnewline
LVPW (mm) & 7.87\selectlanguage{ngerman}±0.69 & 7.72\selectlanguage{ngerman}±1.72 & 8.95\selectlanguage{ngerman}±1.47*\# & 0.009\tabularnewline
AAO (mm) & 29.70\selectlanguage{ngerman}±2.80 & 29.68\selectlanguage{ngerman}±4.30 & 29.55\selectlanguage{ngerman}±3.30 & 0.98\tabularnewline
PA (mm) & 19.26\selectlanguage{ngerman}±2.07 & 20.40\selectlanguage{ngerman}±1.63 & 19.70\selectlanguage{ngerman}±2.89 & 0.20\tabularnewline
LV EDV (ml) & 83.35\selectlanguage{ngerman}±22.94 & 85.70\selectlanguage{ngerman}±28.09 & 87.56\selectlanguage{ngerman}±14.07 &
0.44\tabularnewline
LV ESV (ml) & 32.78\selectlanguage{ngerman}±12.49 & 29.52\selectlanguage{ngerman}±5.16 & 28.50\selectlanguage{ngerman}±13.97 &
0.21\tabularnewline
LVEF (\%) & 69.12\selectlanguage{ngerman}±6.85 & 69.12\selectlanguage{ngerman}±6.85 & 61.96\selectlanguage{ngerman}±5.42 & 0.23\tabularnewline
AV(m/s) & 1.27\selectlanguage{ngerman}±0.17 & 1.23\selectlanguage{ngerman}±0.27 & 1.28\selectlanguage{ngerman}±0.20 & 0.75\tabularnewline
E (m/s) & 0.76\selectlanguage{ngerman}±0.16 & 0.69\selectlanguage{ngerman}±0.19 & 0.67\selectlanguage{ngerman}±0.25 & 0.27\tabularnewline
e'(cm/s) & 10.52\selectlanguage{ngerman}±3.00 & 8.04\selectlanguage{ngerman}±3.26* & 6.75\selectlanguage{ngerman}±3.02* & 0.001\tabularnewline
E/ e' & 7.57\selectlanguage{ngerman}±2.21 & 9.57\selectlanguage{ngerman}±3.82* & 11.53\selectlanguage{ngerman}±1.42* & 0.015\tabularnewline
TAPSE (mm) & 22.43\selectlanguage{ngerman}±3.06 & 21.04\selectlanguage{ngerman}±2.95 & 20.30\selectlanguage{ngerman}±3.25* & 0.03\tabularnewline
TDI-s(cm/s) & 13.61\selectlanguage{ngerman}±2.53 & 14.28\selectlanguage{ngerman}±2.70 & 11.85\selectlanguage{ngerman}±5.51*\# &
0.032\tabularnewline
LAEF (\%) & 67.9\selectlanguage{ngerman}±8.06 & 47.73\selectlanguage{ngerman}±7.84\textsuperscript{*} &
42.72\selectlanguage{ngerman}±2.58\textsuperscript{*} & \textless{}0.001\tabularnewline
LA ESV (ml) & 36.56\selectlanguage{ngerman}±13.91 & 28.35\selectlanguage{ngerman}±7.53 & 30.15\selectlanguage{ngerman}±14.96 &
0.536\tabularnewline
LA EDV (ml) & 5.69\selectlanguage{ngerman}±2.29 & 14.65\selectlanguage{ngerman}±4.06\textsuperscript{*} &
17.88\selectlanguage{ngerman}±11.02\textsuperscript{*} & 0.002\tabularnewline
\bottomrule
\end{longtable}

LV indicates left ventricular; LA left atrium; RV right ventricular; RA
right atrium; IVS interventricular septum; LVPW left ventricular
posterior wall; AAO ascending aorta; PA pulmonary artery; EDV
end-diastolic volume; ESV end-systolic volume; EF ejection fraction; AV
aortic blood flow velocity; E peak mitral inflow early filling velocity;
e', early diastolic myocardial velocity; TAPSE Tricuspid annulus
systolic displacement; TDI-s early systolic myocardial velocity; *
compared with control group ,\emph{P\textless{}} 0.05; \# compared with
mild patients,\emph{P\textless{}} 0.05.

\textbf{Table 3 LAGLS, LVGCS, LV GLS by strain echocardiography}\selectlanguage{english}
\begin{longtable}[]{@{}lllll@{}}
\toprule
& Control(n=23) & Mild(n=25) & Severe(n=20) & \emph{P}
value\tabularnewline
\midrule
\endhead
LA GLS & 40.13\selectlanguage{ngerman}±10.09 & 18.83\selectlanguage{ngerman}±6.32\textsuperscript{*} &
14.88\selectlanguage{ngerman}±6.23\textsuperscript{*} & \textless{}0.001\tabularnewline
LV GCS & 37.43\selectlanguage{ngerman}±5.95 & 27.13\selectlanguage{ngerman}±4.51\textsuperscript{*} &
21.06\selectlanguage{ngerman}±8.78\textsuperscript{*\#} & \textless{}0.001\tabularnewline
LV GLS & 20.43\selectlanguage{ngerman}±3.50 & 18.79\selectlanguage{ngerman}±3.73\textsuperscript{*} &
15.82\selectlanguage{ngerman}±4.39\textsuperscript{*\#} & \textless{}0.001\tabularnewline
\bottomrule
\end{longtable}

LV indicted left ventricular; LA left atrium; EDV end-diastolic volume;
ESV end-systolic volume; EF ejection fraction; GLS global longitudinal
strain; GCS global circumferential strain. * compared with control group
,\emph{P\textless{}} 0.05; \# compared with mild
patients,\emph{P\textless{}} 0.05.

\textbf{Table 4 Regional LV strains}\selectlanguage{english}
\begin{longtable}[]{@{}lllll@{}}
\toprule
& Basal segment & Middle segment & Apical segment & \emph{P}
Value\tabularnewline
\midrule
\endhead
LV RCS (severe) & 16.29\selectlanguage{ngerman}±8.06 & 22.49\selectlanguage{ngerman}±10.55 & 24.39\selectlanguage{ngerman}±11.31 &
0.082\tabularnewline
LV RLS (severe) & 14.07\selectlanguage{ngerman}±3.82 & 15.72\selectlanguage{ngerman}±5.24 & 17.68\selectlanguage{ngerman}±6.11 &
0.170\tabularnewline
LV RCS (mild) & 25.55\selectlanguage{ngerman}±6.49 & 27.47\selectlanguage{ngerman}±5.68 & 28.38\selectlanguage{ngerman}±5.13 &
0.297\tabularnewline
LV RLS (mild) & 17.11\selectlanguage{ngerman}±5.25 & 17.77\selectlanguage{ngerman}±4.58 &
21.49\selectlanguage{ngerman}±4.90\textsuperscript{*\#} & 0.015\tabularnewline
\bottomrule
\end{longtable}

LV indicted left ventricular; RLS regional longitudinal strain; RCS
regional circumferential strain. * compared with basal segment,
\emph{P\textless{}} 0.05; \# compared with middle segment,
\emph{P\textless{}} 0.05.

\textbf{Table 5 Echocardiographic Data at Baseline and Follow-Up in
severe patients with COVID-19}\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
& Baseline(n=13) & Follow-up(n=13) & \emph{P} value\tabularnewline
\midrule
\endhead
LV (mm) & 45.62\selectlanguage{ngerman}±4.234 & 44.77\selectlanguage{ngerman}±6.57 & 0.422\tabularnewline
LA (mm) & 30\selectlanguage{ngerman}±4.22 & 32\selectlanguage{ngerman}±2.80 & 0.128\tabularnewline
RV (mm) & 20.46\selectlanguage{ngerman}±3.38 & 20.00\selectlanguage{ngerman}±3.03 & 0.475\tabularnewline
RA (mm) & 36.92\selectlanguage{ngerman}±4.31 & 35.00\selectlanguage{ngerman}±12.0 & 0.505\tabularnewline
IVS (mm) & 11.31\selectlanguage{ngerman}±1.80 & 11.31\selectlanguage{ngerman}±1.80 & 1\tabularnewline
LVPW (mm) & 9.31\selectlanguage{ngerman}±1.65 & 9.62\selectlanguage{ngerman}±1.61 & 0.436\tabularnewline
AAO (mm) & 30.08\selectlanguage{ngerman}±3.04 & 30.00\selectlanguage{ngerman}±3.05 & 0.337\tabularnewline
PA (mm) & 19.77\selectlanguage{ngerman}±3.27 & 19.69\selectlanguage{ngerman}±2.11 & 0.943\tabularnewline
LV EDV (ml) & 96.08\selectlanguage{ngerman}±25.36 & 94.46\selectlanguage{ngerman}±32.68 & 0.807\tabularnewline
LV ESV (ml) & 32.92\selectlanguage{ngerman}±16.62 & 32.46\selectlanguage{ngerman}±22.04 & 0.943\tabularnewline
LV EF (\%) & 65.85\selectlanguage{ngerman}±10.89 & 66.15\selectlanguage{ngerman}±10.21 & 0.929\tabularnewline
AV(m/s) & 1.35\selectlanguage{ngerman}±0.20 & 1.40\selectlanguage{ngerman}±0.29 & 0.495\tabularnewline
E peak(m/s) & 0.71\selectlanguage{ngerman}±0.33 & 0.69\selectlanguage{ngerman}±0.21 & 0.842\tabularnewline
e'(cm/s) & 6.38\selectlanguage{ngerman}±2.93 & 6.62\selectlanguage{ngerman}±3.10 & 0.785\tabularnewline
E/e' & 0.13\selectlanguage{ngerman}±0.72 & 0.11\selectlanguage{ngerman}±0.03 & 0.547\tabularnewline
TAPSE (mm) & 20.08\selectlanguage{ngerman}±3.69 & 19.69\selectlanguage{ngerman}±3.20 & 0.706\tabularnewline
TDI-s(cm/s) & 9.77\selectlanguage{ngerman}±4.57 & 10.31\selectlanguage{ngerman}±4.37 & 0.470\tabularnewline
IVC (mm) & 16.15\selectlanguage{ngerman}±4.08 & 17\selectlanguage{ngerman}±2.83 & 0.523\tabularnewline
Collapse rate\textgreater{}50\%(n/\%) & 10(77\%) & 11(85\%) &
0.618\tabularnewline
LAEF (\%) & 39.98\selectlanguage{ngerman}±6.36 & 44.67\selectlanguage{ngerman}±5.01 & 0.185\tabularnewline
\bottomrule
\end{longtable}

LV indicates left ventricular; LA left atrium; RV right ventricular; RA
right atrium; IVS interventricular septum; LVPW left ventricular
posterior wall; AAO ascending aorta; PA pulmonary artery; EDV
end-diastolic volume; ESV end-systolic volume; EF ejection fraction; AV
aortic blood flow velocity; E peak mitral inflow early filling velocity;
e', early diastolic myocardial velocity; TAPSE Tricuspid annulus
systolic displacement; TDI-s early systolic myocardial velocity; IVC
inferior vena cava; * compared with control group ,\emph{P\textless{}}
0.05; \# compared with mild patients,\emph{P\textless{}} 0.05.

\textbf{Table 6 LAGLS, LV GCS and LVGLS in severe patients at baseline
and follow-up}\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
& Baseline(n=13) & Follow-up(n=13) & \emph{P} value\tabularnewline
\midrule
\endhead
LA GLS & 14.17\selectlanguage{ngerman}±4.04 & 18.36\selectlanguage{ngerman}±4.89 & 0.084\tabularnewline
LV GCS & 23.05\selectlanguage{ngerman}±8.56 & 30.40\selectlanguage{ngerman}±7.51 & 0.042\tabularnewline
LV GLS & 16.47\selectlanguage{ngerman}±5.23 & 19.78\selectlanguage{ngerman}±8.11 & 0.068\tabularnewline
\bottomrule
\end{longtable}

LV indicted left ventricular; LA left atrium; EF ejection fraction; GLS
global longitudinal strain; GCS global circumferential strain. *
compared with control group, \emph{P\textless{}} 0.05; \# compared with
mild patients, \emph{P\textless{}} 0.05\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/figure1/figure1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/ROCFen-Xi-2/ROCFen-Xi-2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/figure3/figure3}

\end{center}
\end{figure}

\selectlanguage{english}
\FloatBarrier
\end{document}

