Sure. So I do want to start by just reminding listeners that talking about trauma, learning about trauma, can bring up some feelings, which is a very normal reaction to that. So I just want to remind people, if you notice that, that it’s okay to take a rain check on listening and engaging in this conversation. I also do recommend that even if you feel okay to engage with a discussion about trauma that it’s recommended that you do so in small doses, especially during these very challenging times.

Based on all of these approaches, it seems like a reasonable lower bound is that cases are at least 10x underreported, likely more than 20x underreported (according to several researchers), and potentially as much as 100x underreported.It seems reasonable, then, to assume that it’s not 1 out of every 10 people with COVID-19 who will need hospitalization -but rather 1 out of every 100 -500.Similarly, rather than 1 -4%, it seems likely that true CFR for COVID-19 will be well under half a percent, and potentially well under 0.1%for most of the population.

Long-Term Care Outbreaks

cute coronary syndrome (ACS)4/81(4.94%)

Malignant arrhythmia2/81(2.47%)

Patients presented with functional damage involving multiple vital organs, including respiratory failure (80 [94.1%]), shock (69 [81.2%]), ARDS (63 [74.1%]) arrhythmia (51 [60.0%]), acute myocardial injury (38 [44.7%]), acute liver injury (30 [35.3%]) and sepsis (28 [32.9%]) (Table 5)

Most patients had abnormal myocardial zymograms characterized by increased creatine kinase in 31 (36.5%) and increased lactate dehydrogenase in 70 (82.4%) patients.

The most common cause of death in 81 of the 85 patients was respiratory failure (38, 46.91%), followed by septic shock (16, 19.75%), multiple organ failure (13, 16.05%) and cardiac arrest (7, 8.64%).

In the epicenter of the current Italian epidemic, sudden cardiac death (SCD) likely occurred in many non-hospitalized patients with mild symptoms who were found dead home while in quarantine.

Even after hospital discharge, we should consider that myocardial injury might result in atrial or ventricular fibrosis, the substrate for subsequent cardiac arrhythmias

However, a recent pathological study found scarce interstitial mononuclear inflammatory infiltrates in heart tissue without substantial myocardial damage in a patient with COVID-19,13 suggesting that COVID-19 might not directly impair the heart.

ompared with patients without cardiac injury, patients with cardiac injury presented with more severe acute illness, manifested by abnormal laboratory and radiographic findings, such as higher levels of C-reactive protein, NT-proBNP, and creatinine levels; more multiple mottling and ground-glass opacity; and a greater proportion requiring noninvasive or invasive ventilation.

Consistently, our study also found 19.7% of patients with cardiac injury and first demonstrated that cardiac injury was independently associated with an increased risk of mortality in patients with COVID-19.

After adjusting for age, preexisting cardiovascular diseases (hypertension, coronary heart disease, and chronic heart failure), cerebrovascular diseases, diabetes mellitus, chronic obstructive pulmonary disease, renal failure, cancer, ARDS, creatinine levels greater than 133 μmol/L, and NT-proBNP levels greater than 900 pg/mL, the multivariable adjusted Cox proportional hazard regression model showed a significantly higher risk of death in patients with cardiac injury than in those without cardiac injury, either during time from symptom onset (hazard ratio [HR], 4.26 [95% CI, 1.92-9.49]) or time from admission to study end point (HR, 3.41 [95% CI, 1.62-7.16]) (Table 3).

The mortality rate was higher among patients with vs without cardiac injury (42 [51.2%] vs 15 [4.5%]; P < .001) as shown in Table 2 and the Kaplan-Meier survival curves in Figure 2. The mortality rate increased in association with the magnitude of the reference value of hs-TNI

Patients with cardiac injury vs those without cardiac injury had shorter durations from symptom onset to follow-up (mean, 15.6 [range, 1-37] days vs 16.9 [range, 3-37] days; P = .001) and admission to follow-up (6.3 [range, 1-16] days vs 7.8 [range, 1-23] days; P = .039).

Of patients with cardiac injury, only 22 (26.8%) underwent examination of electrocardiogram (ECG) after admission, and 14 of 22 ECGs (63.6%) were performed during the periods of elevation of cardiac biomarkers. All 14 ECGs were abnormal, with findings compatible with myocardial ischemia, such T-wave depression and inversion, ST-segment depression, and Q waves. The ECG changes in 3 patients with representative cardiac injury are shown in eFigure 2 in the

In terms of radiologic findings, bilateral pneumonia (75 of 82 patients [91.5%] vs 236 of 334 patients [70.7%]) and multiple mottling and ground-glass opacity (53 [64.6%] vs 15 [4.5%]) were more prevalent in patients with than those without cardiac injury (both P < .001, Table 1).

The duration of hospitalization before testing was longer in patients with cardiac injury than those without cardiac injury (median [range] time, 3 [1-15] days vs 2 [1-8] days; P < .001).

The laboratory and radiologic findings are shown in Table 1. In the overall study population of 416 patients, median (IQR) levels of C-reactive protein (4.5 [1.4-8.5] mg/dL; to convert to milligrams per liter, multiply by 10) and procalcitonin (0.07 [0.04-0.15] ng/L) were elevated, while the median values of other laboratory indicators were within the normal range, such as counts of leukocytes, lymphocytes, platelets, erythrocytes; hemoglobin level; cardiac indicators

In the present study, we also found that markers of inflammatory response, such as C-reactive protein, procalcitonin, and leukocytes, were significantly increased among patients who suffered from cardiac injury. The activation or enhanced release of these inflammatory cytokines can lead to apoptosis or necrosis of myocardial cells.

Thus, because of the current limited evidence, the question of whether the SARS-CoV-2 virus can directly injure the heart requires further demonstration.

In terms of laboratory findings, patients with cardiac injury compared with patients without cardiac injury showed higher median leukocyte count (median [IQR], 9400 [6900-13 800] cells/μL vs 5500 [4200-7400] cells/μL), and levels of C-reactive protein (median [IQR], 10.2 [6.4-17.0] mg/dL vs 3.7 [1.0-7.3] mg/dL), procalcitonin (median [IQR], 0.27 [0.10-1.22] ng/mL vs 0.06 [0.03-0.10] ng/mL), CK-MB (median [IQR], 3.2 [1.8-6.2] ng/mL vs 0.9 [0.6-1.3] ng/mL), myohemoglobin (median [IQR], 128 [68-305] μg/L vs 39 [27-65] μg/L), hs-TNI (median [IQR], 0.19 [0.08-1.12] μg/L vs <0.006 [<0.006-0.009] μg/L), N-terminal pro-B-type natriuretic peptide (NT-proBNP) (median [IQR], 1689 [698-3327] pg/mL vs 139 [51-335] pg/mL),

Greater proportions of patients with cardiac injury required noninvasive mechanical ventilation (38 of 82 [46.3%] vs 13 of 334 [3.9%]; P < .001) or invasive mechanical ventilation (18 of 82 [22.0%] vs 14 of 334 [4.2%]; P < .001) than those without cardiac injury.

creatinine kinase–myocardial band (median [IQR], 3.2 [1.8-6.2] vs 0.9 [0.6-1.3] ng/mL)

N-terminal pro-B-type natriuretic peptide (median [IQR], 1689 [698-3327] vs 139 [51-335] pg/mL)

Moreover, hypoxemia caused by COVID-19 may bring about atrial fibrillation, which is the most common arrhythmia among elderly individuals, and atrial fibrillation could be refractory before the pulmonary function is improved.

100 nM MLN-4760did not interfere with immunoprecipitation of ACE2 by S1-Ig,nor did this inhibitor interfere with S-protein-mediated infec-tion (Figure 4B and C)

There were numerous differences in laboratory findings between patients admitted to the ICU and those not admitted to the ICU (Table 2), including higher white blood cell and neutrophil counts, as well as higher levels of D-dimer, creatine kinase, and creatine.

Thirty-six patients (26.1%) were transferred to the intensive care unit (ICU) because of complications, including acute respiratory distress syndrome (22 [61.1%]), arrhythmia (16 [44.4%]), and shock (11 [30.6%]).

Heart rate, respiratory rate, and mean arterial pressure did not differ between patients who received ICU care and patients who did not receive ICU care. These measures were recorded on day of hospital admission for all patients, then divided into those who were later admitted to the ICU or not.

Common complications among the 138 patients included shock (12 [8.7%]), ARDS (27 [19.6%]), arrhythmia (23 [16.7%]), and acute cardiac injury (10 [7.2%]). Patients who received care in the ICU were more likely to have one of these complications than non-ICU patients.

The mortality during hospitalization was 7.62% (8 of 105) for patients without underlying CVD and normal TnT levels,

for those without underlying CVD but elevated TnT levels, and 69.44% (25 of 36) for those with underlying CVD and elevated TnTs.

Plasma TnT levels demonstrated a high and significantly positive linear correlation with plasma high-sensitivity C-reactive protein levels (β = 0.530, P < .001) and N-terminal pro–brain natriuretic peptide (NT-proBNP) levels (β = 0.613, P < .001). Plasma TnT and NT-proBNP levels during hospitalization (median [interquartile range (IQR)], 0.307 [0.094-0.600]; 1902.00 [728.35-8100.00]) and impending death (median [IQR], 0.141 [0.058-0.860]; 5375 [1179.50-25695.25]) increased significantly compared with admission values (median [IQR], 0.0355 [0.015-0.102]; 796.90 [401.93-1742.25]) in patients who died (P = .001; P < .001), while no significant dynamic changes of TnT (median [IQR], 0.010 [0.007-0.019]; 0.013 [0.007-0.022]; 0.011 [0.007-0.016]) and NT-proBNP (median [IQR], 352.20 [174.70-636.70]; 433.80 [155.80-1272.60]; 145.40 [63.4-526.50]) was observed in survivors

During hospitalization, patients with elevated TnT levels had more frequent malignant arrhythmias, and the use of glucocorticoid therapy (37 [71.2%] vs 69 [51.1%]) and mechanical ventilation (41 [59.6%] vs 14 [10.4%]) were higher compared with patients with normal TnT levels.

that the levels of the last test of neutrophils (14/16, 87.5%), PCT (11/11, 100%), CRP (11/13, 84.6%), cTnI (7/9, 77.8%),

In severe cases, COVID-19 may present as pneumonia, the acute respiratory distress syndrome (ARDS), with or without both distributive and cardiogenic shock, to which elderly populations with preexisting medical comorbidities are the most vulnerable

No study has described the incidence of ST-segment elevation myocardial infarction in COVID-19, but it appears to be low. Similarly, the incidence of left ventricular systolic dysfunction, acute left ventricular failure and cardiogenic shock have also not been described.

However, an elevation of high-sensitivity cardiac troponin I (cTnI) above 99th percentile upper reference limit is the most commonly used definition

We describe the first case of acute cardiac injury directly linked to myocardial localization of severe acute respiratory syndrome coronavirus (SARS‐CoV‐2) in a 69‐year‐old patient with flu‐like symptoms rapidly degenerating into respiratory distress, hypotension, and cardiogenic shock.

An intra‐aortic balloon pump (IABP) was placed on top of adrenaline (0.07 μg/kg/min), and noradrenaline (0.1 μg/kg/min) was added for worsening hypotension (systolic blood pressure: 80/67/60 mmHg).

The first echocardiography showed a dilated left ventricle [left ventricular (LV) end‐diastolic diameter 56 mm], severe and diffuse LV hypokinesia (LV ejection fraction 34%). Three hours later, LV ejection fraction dropped to 25% and estimated cardiac index was 1.4 L/min/m2. Coronary angiography findings were unremarkable.

Vice versa, we did not observe viral particles in cardiac myocytes and, therefore, we cannot infer on viral cardiotropism. Cardiac myocytes showed non‐specific damage that was mainly characterized by focal myofibrillar lysis. In addition, we did not observe cytopathic endothelia and small intramural vessel inflammation or thrombosis. Other cases are needed to confirm this observation.

Cardiac myocytes showed non‐specific features consisting of focal myofibrillar lysis, and lipid droplets. We did not observe viral particles in myocytes and endothelia. Small intramural vessels were free from vasculitis and thrombosis. EMB did not show significant myocyte hypertrophy or nuclear changes; interstitial fibrosis was minimal, focal, and mainly perivascular

The pathologic study showed low‐grade interstitial and endocardial inflammation (Figure 1A and 1B). Large (>20 μm), vacuolated, CD68‐positive macrophages were seen with immune‐light microscopy (Figure 1C and 1D); they were ultrastructurally characterized by cytopathy, with membrane damage and cytoplasmic vacuoles (Figure 1E). The ultrastructural study demonstrated single or small groups of viral particles with the morphology (dense round viral envelope and electron‐dense spike‐like structures on their surface) and size (variable between 70 and 120 nm) of coronaviruses (Figure 2). COVID‐19 infected Vero cells were used as control. The viral particles were observed in cytopathic, structurally damaged interstitial cells that demonstrated loss of the cytoplasmic membrane integrity (Figure 3)

By the end of Jan 25, 31 (31%) patients had been discharged and 11 (11%) patients had died; all other patients were still in hospital (table 1). The first two deaths were a 61-year-old man (patient 1) and a 69-year-old man (patient 2). They had no previous chronic underlying disease but had a long history of smoking.

The clinical effects of pneumonia have been linked to increased risk of cardiovascular disease up to 10-year follow-up16 and it is likely that cases infected via respiratory virus outbreaks will experience similar adverse outcomes. Therapeutic use of corticosteroids further augments the possibility of adverse cardiovascular events. However, long-term follow-up data concerning the survivors of respiratory virus epidemics are scarce. Lipid metabolism remained disrupted 12 years after clinical recovery in a metabolomic study amongst 25 SARS survivors,17 whereas cardiac abnormalities observed during hospitalisation in eight patients with H7N9 influenza returned to normal at 1-year follow-up.

The final diagnosis was acute virus-negative lymphocytic myocarditis associated with SARS-CoV-2 respiratory infection

EMB (Panel E, day 7) documented diffuse T-lymphocytic inflammatory infiltrates (CD3+ >7/mm2) with huge interstitial oedema and limited foci of necrosis. No replacement fibrosis was detected, suggesting an acute inflammatory process. Molecular analysis showed absence of the SARS-CoV-2 genome within the myocardium. No contraction band necrosis or TTS-associated microvascular abnormalities were observed.

CMR (day 7) showed a recovery of systolic function (from 52% by CTA to 64% by CMR), although with persistence of a mild hypokinesia at basal and mid left ventricular segments; at the same sites, diffuse myocardial oedema, determining wall pseudo-hypertrophy, was observed on short T1 inversion recovery (STIR) sequences (Panel D) and confirmed by T1 and T2 mapping (average native T1 = 1188 ms, normal value <1045; average T2 = 61 ms, normal value <50). Late gadolinium enhancement sequences demonstrated absence of detectable myocardial scar/necrotic foci.

Although the first clinical suspicion was myocarditis, coronary computed tomography angiography (CTA) was acquired to rule out coronary artery disease (CAD). Baseline chest scan (Panel B) confirmed bilateral patchy ground-glass opacities; CTA showed no aortic dissection, pulmonary embolism, or epicardial CAD (Panel C). Dynamic 3D volume-rendering reconstruction demonstrated a clear hypokinesia of the left ventricle mid and basal segments, with normal apical contraction, suggesting a reverse Tako-Tsubo syndrome (TTS) pattern

ECG (Panel A) showed low atrial ectopic rhythm, mild ST-segment elevation in leads V1–V2 and aVR, reciprocal ST depression in V4–V6, and QTc 452 ms with diffuse U-waves. The high-sensitivity troponin T curve was 135–107–106 ng/L (normal value <14), NT-proBNP 512 pg/mL (normal value <153), and C-reactive protein 18 mg/L (normal value <6). Transthoracic echocardiogram showed mild left ventricular systolic dysfunction (LVEF 43%) with inferolateral wall hypokynesis; neither ventricle was dilated and there was no pericardial effusion.

Itis likely that cardiac troponin measurements wererequested in those who were more unwell or where there wasreasonable suspicion of myocardial ischemia or myocardial dysfunction. Only systematic testing of both symptomatic and asymptomatic patients infected with SARS-CoV-2 will provide an accurate estimate of the prevalence of myocardial injuryin this condition.

In a cohort of 191 patients with confirmed COVID-19 based on SARS-CoV-2 RNA detection, the univariable odds ratio for death when hs-cTnI concentrations were above the 99thpercentile upper reference limit was 80.1 (95% confidence interval [CI]10.3 to 620.4, P<0.0001).[4]This was higher than the odds ratios observed for all other biomarkerstested,including D-Dimer and lymphocyte count.

While the spectrum of clinical manifestation is highly related to the inflammation process of the respiratory tract, this case provides evidence of cardiac involvement as a possible late phenomenon of the viral respiratory infection. This process can be subclinical with few interstitial inflammatory cells, as reported by an autopsy study,10 or can present with overt manifestations even without respiratory symptoms, as in the present case.

A 12-lead electrocardiogram (ECG) showed low voltage in the limb leads, minimal diffuse ST-segment elevation (more prominent in the inferior and lateral leads), and an ST-segment depression with T-wave inversion in lead V1 and aVR

Chest radiography was repeated on day 4 and showed no thoracic abnormalities. Transthoracic echocardiography, performed on day 6, revealed a significant reduction of LV wall thickness (interventricular septum, 11 mm; posterior wall, 10 mm), an improvement of LVEF to 44%, and a slight decrease of pericardial effusion (maximum, 8-9 mm). At the time of submission, the patient was hospitalized with progressive clinical and hemodynamic improvement.

During the first days of her hospitalization, the patient remained hypotensive (systolic blood pressure less than 90 mm Hg) and required inotropic support (dobutamine) in the first 48 hours, during which there was a further increase in levels of NT-proBNP (8465 pg/mL), high-sensitivity troponin T (0.59 ng/mL), and creatine kinase–MB (39.9 ng/mL), with a progressive stabilization and reduction during the following days (Table). Blood pressure progressively stabilized, although systolic pressure remained less than 100 mm Hg, and dobutamine treatment was weaned on day 4.

Transthoracic echocardiography revealed normal left ventricular (LV) dimensions with an increased wall thickness (interventricular septum, 14 mm, posterior wall, 14 mm) and a diffuse echo-bright appearance of the myocardium. There was diffuse hypokinesis, with an estimated LV ejection fraction (LVEF) of 40%. There was no evidence of heart valve disease. Left ventricular diastolic function was mildly impaired with mitral inflow patterns, with an E/A ratio of 0.7 and an average E/e′ ratio of 12. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers (maximum, 11 mm) without signs of tamponade. Cardiac magnetic resonance imaging (MRI) confirmed the increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe LV dysfunction (LVEF of 35%) (Video 1 and Video 2). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema. Phase-sensitive inversion recovery sequences showed diffuse late gadolinium enhancement extended to the entire biventricular wall (Figure 2). The myocardial edema and pattern of late gadolinium enhancement fulfilled all the Lake Louise criteria for the diagnosis of acute myocarditis.6 The circumferential pericardial effusion was confirmed, especially around the right cardiac chambers (maximum, 12 mm).

Cardiac magnetic resonance imaging showed increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe left ventricular dysfunction (left ventricular ejection fraction of 35%). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema, and there was also diffuse late gadolinium enhancement involving the entire biventricular wall. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers. These findings were all consistent with acute myopericarditis.

In addition, repeated floods of catecholamines due to anxiety and the side effects of medication can also lead to myocardial damage.

Third, Huang’s study noted that high concentration of IL-1β, IFN-γ, IP-10 and MCP-1 could be detected in patients infected with 2019-nCoV, which might lead to activated T-helper-1 (Th1) cell responses [4]. Furthermore, they also found that ICU patients had much higher concentrations of inflammatory factors than those non-ICU patients, suggesting that the cytokine storm was associated with disease severity

Second, hypoxaemia may be also an important reason of cardiac injury. In Huang’s study, 32% COVID-19 patients had various degree of hypoxaemia and need required high-flow nasal cannula or higher-level oxygen support. In Chen’s study, up to 76% of patients require oxygen therapy. Due to severe 2019-nCoV infection, the pneumonia may cause significant gas exchange obstruction, leading to hypoxaemia, which significantly reduces the energy supply by cell metabolism, and increases anaerobic fermentation, causing intracellular acidosis and oxygen free radicals to destroy the phospholipid layer of cell membrane. Meanwhile, hypoxia-induced influx of calcium ions also leads to injury and apoptosis of cardiomyocytes.

The data again showed a significant higher incidence of acute cardiac injury in ICU/severe patients compared to the non-ICU/severe patients [RR = 13.48, 95% CI (3.60, 50.47), Z = 3.86, P = 0.0001]

Another two studies only gave the data of creatine kinase, if it can be seen as a biomarker of cardiac injury, the proportion might be 11.5% (95% CI 7.8–15.2%).

Two studies that gave clear data were statistically analyzed, and the data showed that 8.0% (95% CI 4.1–12.0%) patients might be suffered from an acute cardiac injury.

It is reasonable to expect that severe and critical cases have more severe effects on the cardiovascular system owing to more robust inflammatory response. At this early stage, our knowledge is mainly based on available numerators data, and the exact population-level denominators are not known. Also, it is likely that the asymptomatic and mildly symptomatic cases are missing from most reports, which further skews our understanding of the disease.

There were no obvious histological changes seen in heart tissue, suggesting that SARS-CoV-2 infection might not directly impair the heart

There were a few interstitial mononuclear inflammatory infiltrates, but no other substantial damage in the heart tissue

Based on the analysis of the clinical data, we confirmed that some patients died of fulminant myocarditis. In this study, we first reported that the infection of SARS-CoV-2 may cause fulminant myocarditis.

Among the 68 fatal cases, 36 patients (53%) died of respiratory failure, five patients (7%) with myocardial damage died of circulatory failure, 22 patients (33%) died of both, and five remaining died of an unknown cause

There were a few interstitial mononuclear inflammatory infiltrates, but no other substantial damage in the heart tissue

Among survivors, secondary infection, acute kidney injury, and acute cardiac injury were observed in one patient each, occurring 9 days (acute kidney injury), 14 days (secondary infection), and 21 days (acute cardiac injury) after illness onset.

Creatine kinase, U/L≤1851 (ref)......>1852·56 (1·03–6·36)0·043....High-sensitivity cardiac troponin I, pg/mL≤281 (ref)......>2880·07 (10·34–620·36)<0·0001....

In this study, increased high-sensitivity cardiac troponin I during hospitalisation was found in more than half of those who died.

Heart failure44 (23%)28 (52%)16 (12%)<0·0001Septic shock38 (20%)38 (70%)0<0·0001Coagulopathy37 (19%)27 (50%)10 (7%)<0·0001Acute cardiac injury33 (17%)32 (59%)1 (1%)<0·0001Acute kidney injury28 (15%)27 (50%)1 (1%)<0·0001

COVID‐19 prognosis is related to age and sex. The expression of ACE2 decreases with increasing age. ACE2 expression is higher in young people than in elderly individuals and higher in females than in males.11, 12 This pattern does not match the characteristic of severely ill COVID‐19 patients being mostly elderly males. We believe that whether the level of ACE2 expression is high or low is not a key factor affecting the prognosis of patients with COVID‐19. The relationship between sex and prognosis requires additional data to verify.

Duration from onset of symptoms to radiological confirmation of pneumonia, days5 (3–9)5 (3–7)Duration from onset of symptoms to ICU admission, days9 (6–12)11 (7–14)Heart rate, beats per min89 (20)89 (15)Systolic blood pressure, mm Hg133 (20)140 (21)

Cardiac injury3 (15%)9 (28%)12 (23%)

By Jan 26, 2020, 710 patients had been admitted to Wuhan Jin Yin-tan hospital with confirmed SARS-CoV-2 pneumonia, of whom 658 (93%) were considered ineligible, including three patients who had cardiac arrest immediately after admission.

A raised troponin (hypersensitive-troponin I (hs-cTnI)) was detected in five patients, possibly suggestive of virus-associated myocardial injury.

The mechanism of acute myocardial injury caused by SARS-CoV-2 infection might be related to ACE2. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system and, therefore, ACE2-related signalling pathways might also have a role in heart injury.

Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells

Among the people who died from COVID-19 reported by the NHC, 11.8% of patients without underlying CVD had substantial heart damage, with elevated levels of cTnI or cardiac arrest during hospitalization.

and respiratory dysfunction and hypoxaemia caused by COVID-19, resulting in damage to myocardial cells.

some of the patients first went to see a doctor because of cardiovascular symptoms. The patients presented with heart palpitations and chest tightness rather than with respiratory symptoms, such as fever and cough, but were later diagnosed with COVID-19.