Q: We have heard reports of delayed arrhythmia and cardiovascular collapse as patients begin to recover from respiratory symptoms. Have you seen this and do you have special recommendations for rhythm management?


In our hospital, about 20% of patients will have cardiovascular damage,  It is caused by hypoxia, or by the direct damage of virus. In particular, we need to be alert to the occurrence of fulminant myocarditis. Even among the recovered  patients, we have also observed that some patients have heart function decline. This is worthy of further study. Therefore, we should pay attention to the treatment of myocardial protection while we treated the novel coronavirus pneumonia.

Q: Why is thrombolysis preferred over in PCI in patients with myocardial infarction?


A) Almost all medical staff join in the treatment of COVID-19, including cardiovascular intervention experts. 

B) It is recommended to operate in the negative pressure operating room. 

C) Patient transport: transport of patients increases the risk of disease spread. Due to traffic control, patient transport is not as fast as usual. 

So, thrombolysis is the first choice for patients with myocardial infarction.

Q: What was your criteria for doing echocardiograms in COVID19 patients?


The following COVID19 patients should be considered for echocardiography:

1.  Patients who have basic cardiovascular disease before admission. 

2.  Patients with high risk factors for cardiovascular disease. 

3.  Patients with manifestations of heart failure. 

4.  Patients who have chest pain, palpitation and other symptoms. 

5.  Other tests, such as an electrocardiogram, which suggest heart damage. 

6.  Lab tests suggest cTnI or BNP are significant increased.

Q: Is there a increase in arrhythmias, and if yes, which types of arrhythmia?


Higher incidence of arrythmias have been noticed in patients with COVID-19 infection, especially in those critical patients who have sepsis, hypoxia, or underlying cardiovascular disease. Sinus tachyarrythmia and atrium fibrillation were more frequently to be seen.

Q: Have you seen episodes of isolated or predominantly myocarditis without major lung involvement?


There are no such reports.The clinical evidence of direct myocardial injury by COVID-19 is not sufficient. The use of VV mode in most ECMO patients is a good evidence, and the autopsy results do not support it.

Q: At hospitals able to perform primary PCI for STEMI, is it your experience to use thrombolytic as the primary treatment - reserving PCI for thrombolytic failure?


Thrombolysis is currently the main treatment for STEMI patients. Interventional catheter room with negative pressure is required during PCI, but the conditions of negative pressure catheter room are not present in Wuhan, so thrombolysis is currently recommended. I think PPCI can still does if thrombolysis fails. The risk of exposure in a short period of time is not particularly high as long as you have tertiary protection .

Q: Should cardiac troponin measurements be obtained routinely for risk stratification in these patients?


TnI or TnT has been routinely tested after admission to monitor myocardial ischemia. Elevation of cardiac troponin has also been found in many COVID-19 patients. We have done a retrospective study about the relationship between fatal outcomes and elevation of TnT for COVID-19 patients. The results imply that elevation of TnT plays a crucial role in the fatal outcome of COVID-19. Elevation of TnT results in the impairment of cardiac function and malignant arrhythmia. Furthermore, the mortality of COVID-19 patients with elevation of TnT is high. So we think that cardiac troponin can be used as a stratified management test for COVID-19 patients.

Q: Please discuss if you saw a positive or negative effect of ACE inhibitor or ARB therapy.


This is a controversial topic. I was infected with COVID-19 in January 2020. To study this problem, I took 4 mg perindopril 5 days after the onset of the disease.  A few hours later, I continued to have high fever and a severe cough. Theoretically, COVID-19 invades the cells through ACE2, and some ACEI / ARB up-regulate ACE2, which may be beneficial to virus replication. Therefore, the consensus of cardiovascular experts in Hubei Province suggests that ACEI / ARB should be replaced with other antihypertensive drugs in the early stage of COVID-19.

Q: Is there any data on the incidence of death in patients with HTN on ACE/ARB versus those not on ACE/ARB? That is, is the cause of increased mortality in HTN patients due not to the disease but the medications we are usin


A retrospective analysis in our hospital found that there was no statistical difference in ACEI / ARB utilization rate (18 / 95 vs 4 / 17) between the cured group and the dead group. But this is only a cross-sectional study, which is not enough to answer this question

Q: I noticed that there is high elevated of D-dimer in all patients, especially in severe cases and in patients who have died. What is the mechanism of thrombrosis and that it impacts the whole body with the onseet of COVID


Pathological anatomy has confirmed the existence of thrombosis.  We also found that some patients have deep vein thrombosis in the lower extremity. In some COVID-19 patients, the disease worsened suddenly, D-dimer increased significantly, and patients even died suddenly. In this regard, we should pay attention to whether there is pulmonary thromboembolism (PTE) after the fall off of deep vein thrombosis (DVT). It is suggested that in the process of prevention and treatment of COVID-19, the risk of venous thromboembolism (VTE) should be assessed, and effective prevention should be carried out for high-risk patients. Patients with sudden deterioration of oxygenation, respiratory distress, blood pressure drop and other clinical manifestations should be alert to the occurrence of PTE and be treated in time.

Q: You gave an example of people with chest pain, so naturally we would be thinking about the heart. But your Chinese colleagues are reporting to us a very high rate of cardiac involvement. I think most cardiologists in th


Our routine detection of cTnI and BNP changes in patients did find that these indicators were increased in many patients. But heart events are not common. Autopsy results also do not support direct myocardial damage caused by  COVID-19.  At present, the mechanism of myocardial damage (elevated NT-Pro-BNP and cTnI) caused by COVID-19 infection is not much clear. The possible reasons are as follows: 

1) Direct damage: viral infection can directly cause damage to myocardial cells

2)  Immune damage: the excessive activation of the immune system results in an extreme immune response, releasing a large number of cytokines, and the conversion into a triggered cytokine storm may be one of the mechanisms of myocardial damage

3) Hypoxemia: severe COVID-19 patients affected blood gas due to diffuse alveolar injury and pulmonary clear film formation, leading to severe hypoxemia, sustained hypoxia will increase anaerobic fermentation, cause acidosis, increase intracellular oxygen free radicals, intracellular calcium overload, and cause damage to myocardial cells

4) Angiotensin converting enzyme 2 (ACE2): currently known as ACE2, an important target for COVID-19 infection, and ACE2 receptors are widely expressed in the cardiovascular system. Therefore, ACE2-related signaling pathways may also cause myocardial damage.

Q: When you face with someone who with heart failure who also has COVID-19, have you stopped the use of ACI or ARBs or continued what they are?


Most acute heart failure patients admitted in ICU when complicated with COVID-19, usually had hypotension and need inotropic and vasoconstrictive agents. There was no opportunity for ACEI or ARBs. It has been a great concern or controversy on ACEI or ARBs usage in mild COVID-19 patients with hypertension and chronic heart failure, since it may increase ACE2 receptor on basic research, but nobody knows right or wrong. My personal opinion is that, daily usage of ACEI/ARBs might increase the possibility of novel coronavirus infection theoretically, but for patients who already have confirmed COVID-19 for more than 3-4 weeks, it’s not a big concern. Because most patients will have swab tests negative and develop antibody at that time.

Q: Have you seen patients develop cardiomyopathy with COVID-19?


1. Increase in cardiac troponin (>28 pg/mL)

2. Significantly higher blood pressure (145 mm Hg)

3. Increase in Creatinine Kinase

4. Some patients have FIRST symptom as CV presentation

5. Heart palpitations and/or tightness in the chest, with no respiratory symptoms

6. Pathological findings from limited autopsies and biopsy studies showed below regarding to the heart:

    Degenerated or necrosed myocardial cells are present, along with mild infiltration of monocytes, lymphocytes and/or neutrophils in the cardiac interstitium. Endothelial desquamation, endovasculitis and thrombi are seen in some blood vessels.

Q: Have you seen any COVID-19 patients with ventricular fibrillation/cardiac arrest?


Absolutely yes. We have observed several cases of that. Some patients were related with previous myocardial infarction or severe triple-vessels coronary artery disease. Some had cardiac arrest related with significant hypoxia when intubation. And some patients had severe hyperkalemia or hypokalemia.

Q: It is interesting because we have seen a couple of patients already develop a new cardiomyopathy. I wonder if the elevated troponins you are seeing are more from demand ischemia? Are you doing echocardiograms and seeing


Among my patients, the elevated troponin is one of the most important negative prognostic indicators. However, the patients who have elevated troponins don’t show hypokinesis related to myocardial infarction and ECG changes from demand ischemia. I think the myocardial injury is another manifestation of multiple organ dysfunction caused by coronavirus. On the other hand, I do suspect that the coronavirus may have a predilection for attacking the myocardium over the liver and kidney. Additionally, the general duration of the virus is about 30-40 days, while the elevation of troponin always begin at the 10th day. Greater elevation in troponins is also clearly correlated with a worsening prognosis, so the protection of heart is necessary. 

Q: Are you doing echocardiograms and seeing new hypokinesis and reduced ejection fraction on COVID19 patients? We are finding this I think in a couple of the initial patients.


We did do echocardiograms for almost every patient, but most patients have normal echocardiograms with no evidence of new hypokinesis or reduced ejection fraction at all. Only individual patients had reduced ejection fraction. There were isolated patients with reduced ejection fraction, but these recovered rapidly as troponins decreased. So most ECG are normal, with isolated cases showing sinus tachycardia, or T wave inversion in precordial leads, but no dynamic evolution. 

Q: How was the diastolic function? In this case, could the patient with hypoxia be experiencing diastolic dysfunction causing evidence of acute HF? Could this be explained by diastolic heart failure? High ProBNP with norma


It is a good question. Yes, diastolic dysfunction is presented in some patients with severe hypoxia. However, not only diastolic dysfunction, but also directly damage of heart by virus, cytokine storm or the patient was associated with cardiovascular disease could cause acute heart failure. COVID-19 currently has a crude mortality rate of 4% in China but a mortality rate of more than 10% in patients combined with cardiovascular disease. Though BNP is not fit for evaluation of diastolic dysfunction, it is still useful for explaining the abnormal systolic function and pulmonary edema in patients with acute heart failure.

Q: When would you consider Angiogram in MI II, and what measures of hemodynamic support would you consider such as Impala or IABP?


Increased serum troponin I/T concentrations without recognizable acute coronary syndromes are well described in critically ill and deceased cases. We will not perform coronary angiogram for patients with Tape 2 MI. For COVID-19 patients who concomitant or complicated with STEMI or NSTEMI, if the patients without respiratory failure but the hemodynamic status is unstable, IABP is preferred. If the patients have respiratory and circulatory failure, V-A ECMO is routinely used. For a few patients who had respiratory failure complicated with fulminant myocarditis, ECMO combined with IABP was used.

Q: There appears to be apical/periapical dysfunction in a Takostubo’s pattern, but distal segments are not well-visualized.


Takotsuko may be caused by catalamine surge, which can lead the contraction of cardiac microvascular. What’s more, the lack of cholinergic nerve in the apex of the heart leads to more severe injury.

COVID pneumonia can causes myocardial injury in many ways: 

1.  Directly infect hear cells, causing myocardial injury

2.  Combined with ACE2 to cause myocardial injury. 

3. Hypoxemia

4. Immune disorder

Now, some COVID19 patients’ heart show apical/periapical dysfunction in a Takostubo’s pattern.  We hypothesize that the causes of similar symptoms of cardiomyopathy in the heart may be as follows: 

1. The diagnosis as COVID pneumonia can be a stress event for patients ,which leads to Takotsuko cardiomyopathy. 

2.  It may be related to the myocardial injury because of the combination of the virus and ACE2, but it still needs to be confirmed by relevant studies.

Q: What’s the role D-dimer?


Because of the damage of alveoli and capillaries in the COVID-19 patients, we can see the formation of pulmonary microthrombus of the autopsy results of the patients. At the same time, microthrombus formation has also been observed in the blood vessels of critically ill patients, so the d-dimer is generally high in all patients. The results of our retrospective study showed that elevation of the D-dimer level was more significant in the non-survivors, and was an independent risk factor of death. If these patients have no contraindications for anticoagulants, we would recommend the routine use of low molecular weight heparin as an anticoagulant for critically ill patients. For critical COVID-19 patients who need to be bedridden for a long time or who are on a non-invasive/invasive mechanical ventilation ventilator, anticoagulants should be routinely used to prevent thrombosis in the lower extremities and pulmonary thrombosis.

Q: Shouldn’t we correlate the heart rate with the patient’s ejection fraction?


Yes, heart rate increased significantly with the aggravation of heart failure in patients. Heart rate was easily affected by a variety of factors such as fever, anoxia, or shock. It could not be regarded as an independent evaluation standard for cardiac insufficiency in COVID-19 patients. LVEF is an assessment of the systolic function of the whole body of the heart.  Generally, it is no time limit. However, the decline of the function is not inversely proportional to the increase of the heart rate, though there is inverse trend. Undoubtedly, correlate the heart rate with the patient’s ejection fraction can reflect the changing trend of corresponding index more sensitively, but we didn’t do that according to the routine.

Q: For patients needing ECMO, what percentage are Arterio-venos vs. veno-venous ECMO? Thanks.


Most patients had VV ECMO, since viral pneumonia and ARDS is the major presentation of COVID-19. HFrEF is not a common cardiovascular complication in COVID-19 patients. From a single ICU observation of 6 patients with ECMO, 5 had VV and one with VA mode.

Q: The reason of increased D-dimmer?


The coagulation function in patients with SARS-CoV-2 is significantly deranged compared with healthy people, but monitoring D-dimer and FDP values may be helpful for the early identification of severe cases.

Q: When you do echo, the heart function is still ok. The COVID-19 patient changes too fast. In this situation, when you have the laptest, the elevated pro-BMP, the echo examine are at the same period. Could it explain?


In severe COVID-19 patients, although cTnI is often elevated, while the heart function is not severely impaired. Such as severe COVID-19 patients received ecmo, we usually apply VV-ECMO, but not VA-ECMO, because the blood pressure could be maintained.