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June 26, 2022
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CV complications of COVID-19 vary widely; patients with HF at high risk

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PHILADELPHIA — The CV complications of COVID-19 are wide-ranging, and the consequences can be especially serious in patients with HF, a speaker said at the Heart in Diabetes CME conference.

The presentation by Lee R. Goldberg, MD, MPH, FACC, section chief of advanced cardiac failure and heart transplant, vice chair for medicine informatics and professor of medicine at the University of Pennsylvania, covered a number of topics related to cardiac complications of COVID-19.

COVID-19
Source: Adobe Stock

COVID-19 in preexisting HF

Patients with preexisting HF can have it exacerbated after getting COVID-19, Goldberg said. COVID-19 can also confer acute MI and acute pulmonary emboli, he said, noting that “the symptom that we’ve focused on a lot is the impact of COVID-19 on the development of myocarditis and of heart failure secondary to cardiac inflammation.”

Lee Goldberg

Many patients with HF are already at elevated risk for complications from COVID-19 because they may have reduced immunity, frail and “have reduced hemodynamic ability to cope with more severe infections, including ones involving the lungs,” Goldberg said, noting they may also have comorbidities associated with worse COVID-19 outcomes including diabetes, obesity, renal disease and elevated levels of pulmonary fluid.

HF can also manifest in patients who did not previously have it before contracting COVID-19, Goldberg said. This can be through myocarditis, MI or right ventricular failure in the form of pulmonary hypertension or pulmonary emboli, he said.

Myocarditis controversy

COVID-19-induced myocarditis “has been one of the more frightening things about the pandemic, and something that has caused controversy,” Goldberg said. “There is variable guidance for how we should manage this.”

Because of all the conflicting information, the American College of Cardiology published an expert consensus decision pathway on management of COVID-19-induced myocarditis, he said. The document captured the symptoms that should be flagged and the techniques for confirming the diagnosis.

“There was a lot of controversy with young male athletes who were getting inflammation of the heart and being told they could not play,” Goldberg said. “The concern was that inflammation of the heart lowers the threshold significantly for sudden cardiac death.” As a result, the ACC document included guidance on when it was appropriate for an athlete to return to play.

One study has estimated that in people aged younger than 20 years, the incidence of myocarditis with COVID-19 is 450 per 1 million, “but there is incomplete assessment of a lot of these folks,” Goldberg said. “The good news is that fulminant myocarditis is very rare in the general population.”

Mechanisms affecting the heart

Mechanisms of cardiac injury from COVID-19 include systemic inflammatory response syndrome, oxygen supply-demand ischemia, ACE-2-mediated direct damage and cardiac microvascular injury, he said.

In most cases of COVID-19-induced myocarditis, SARS-CoV-2 remains outside the cardiac cells, “which suggests that COVID-19 itself may not be very cardiotropic. This becomes important when we start talking about vaccines and myocarditis,” Goldberg said. “Vaccines may trigger myocarditis because it’s not the virus itself, it’s the immune response to the virus that triggers the myocardial inflammation. Maybe that’s the pathway we need to focus on.”

Severity of COVID-19 does not predict cardiac involvement, nor does preexisting CV risk factors, he said.

Using standard HF medications to treat COVID-19-induced myocarditis is common, and some patients may need mechanical circulatory support, he said.

Nonsteroidal anti-inflammatory drugs, colchicine and prednisone are used if pericardial involvement is suspected, while IV corticosteroids may be used if COVID-19-induced myocarditis and the patient is hemodynamically compromised or has MIS-A, and empiric corticosteroids can be used in patients with shock, Goldberg said.

Myocarditis after COVID-19 vaccination is rare and when it appears, tends to occur in young men, usually after the second dose. It should be diagnosed similarly to how COVID-19-induced myocarditis is, “but the outcomes seem to be very, very good,” Goldberg said.

Anticoagulation should be considered if a thrombotic cause is suspected, he said.

Considerations in transplant patients

Mortality among patients with heart transplant who contract COVID-19 is around 25%, but corticosteroids seem to help this population and those who are vaccinated usually do better, he said. He added that mortality for patients on ventricular assist devices with COVID-19 is also high, around 15%.

If possible, patients with advanced HF should be vaccinated against COVID-19 before their heart transplant, because response is not as good in the first year after transplant, Goldberg said. If vaccination is done after transplant, there should be three doses at first followed by one booster later, as this strategy increases response, he said. The monoclonal antibodies tixagevimab and cilgavimab can be administered every 6 months to this population, he added.

For patients with heart transplant who get COVID-19, the best treatments appear to be monoclonal antibodies, remdesivir (Veklury, Gilead Sciences) and dexamethasone, Goldberg said.

“COVID-19 is associated with a variety of cardiovascular complications and the unifying mechanism appears to be inflammation,” Goldberg said. “That can persist up to 12 months, even with therapy. Myocarditis is mild in most cases but can be fulminant, but the vast majority recover. Thrombotic complications are common and lead to stroke and MI. Heart transplant patients are extremely high risk for COVID-19 complications and mortality, and that’s why prophylaxis even with monoclonal antibodies and pre-transplant vaccination is critical to protect that population.”

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