"The more marked the myocardial damage, the more serious the Covid-19"

“The more marked the myocardial damage, the more serious the Covid-19”

#marked #myocardial #damage #Covid19

LE DAILY: What do we know about the links between Sars-CoV-2 and myocarditis?

Dr. DELMAS: Patients with heart and/or coronary insufficiency have a higher risk of contracting Covid-19 and a worse prognosis than subjects without that history. For example, a person with heart failure doubles their risk of in-hospital mortality.

In total, 7 to 40% of patients treated for Covid-19 have myocardial damage, depending on the thresholds chosen for troponin (marker of myocardial cell necrosis) and NTproBNP (marker of overload of the heart chambers), as well as depending on the association, or not, of changes in the electrocardiogram (ECG) and/or echocardiography. However, from the moment this attack exists, hospital mortality multiplies from 3 to 8.

In addition, all the studies point in the same direction: the more marked the associated myocardial damage, the more severe the Covid-19 infection, with in-hospital mortality of up to 34%. Myocardial damage depends on viral load, immune response, and comorbidities (diabetes, high blood pressure, obesity, etc.).

What are the mechanisms involved?

In a patient with cardiac involvement prior to Covid-19 infection, the adaptive capabilities of cardiac output are lower. In fact, heart failure is increased by the fact that Covid-19 infection is accompanied by hypoxemia. Another mechanism can also come into play during the acute phase: the appearance of hemostasis and coagulation disorders. They are likely to cause macrovascular or microvascular coronary occlusions, which will result in suffering when the heart is put under increased strain. Finally, Covid-19 can cause diffuse inflammatory edema in the myocardium, causing cardiac contraction disorders (edematous myocarditis, endotheliitis) or more classic cellular inflammatory necrosis (myocarditis, more rarely found than the edematous form).

What is the role of the inflammatory storm?

Finally, the infection can take the form of a multisystem inflammatory syndrome, similar to Kawasaki syndrome or toxic shock, with mucosal, digestive, cutaneous, lymph node involvement… This syndrome is secondary to the inflammatory storm induced by Sars – CoV-2, which occurs within two weeks of Covid-19 infection and persists even after the virus is gone. Young people, mostly males (with a peak between the ages of four and nine), are the most affected. The picture can be very severe to the point of requiring circulatory, ventilatory or renal assistance. But we have learned to manage it with anti-inflammatories (including some directed specifically against interleukins), corticosteroids and immunoglobulins, resulting in very low mortality despite this very noisy scenario.

Should patients be followed long-term?

When we do systematic MRIs, we find cardiac abnormalities in 20 to 45% of patients who presented Covid-19, although the initial infection was not very marked, without the need for hospitalization. In particular, fibrosis and moderate impairment of contractile function are seen, suggestive of an early heart attack, thus raising the question of follow-up in these patients. The American and European scientific societies of cardiology have issued recommendations for remote monitoring of these patients, since fibrosis can cause arrhythmias and heart failure. To date, the usual treatments for heart failure (angiotensin-converting enzyme inhibitors, beta-blockers) are administered empirically.

What is the impact of the vaccine on the risk of developing myocarditis?

Whether due to the Covid-19 infection or the vaccine, it is difficult to be sure of the cause and effect link with the occurrence of myocarditis. When it occurs between D1 and D9, the link is possible, but it becomes weak from D10 to D21 and very uncertain beyond that. Young men are more affected during a second injection with the Moderna vaccine. Thus, it was recommended to reserve the Pfizer vaccine for those under 30 years of age for the second injection. Increasing the time between the two injections, among this young population, is another line of thought.

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