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Three quarters of mild to moderate Covid illnesses show heart damage

Posted By Jo Nova On August 1, 2020 @ 2:58 pm In Global Warming,Health,Microbiology | Comments Disabled

No wonder the Chinese lockdown a million people with every outbreak. Two thirds of these cases were not hospitalized.

These studies are small and need confirmation, but the medical specialists are asking if it is possible that Covid infections create new cases of heart failure which may trigger problems long after infection?

A startling number of COVID-19 patients suffer lasting heart damage

Fermin Koop, ZME Science

A study from the University Hospital Frankfurt looked at the cardiovascular MRIs of 100 people who had recovered from the coronavirus and compared them with heart images of people who hadn’t been infected.

Most of the patients hadn’t been hospitalized and recovered at home, with symptoms ranging from none to moderate. Two months after recovering from COVID-19, the patients were more likely to have troubling cardiac signs than people in the control group. Up to 78% of them had structural changes to the heart, while 76% had evidence of a biomarker signaling cardiac injury typically found after a heart attack, and 60% had signs of inflammation.

The Puntmann study was based in Germany, and the average age of cases was 49. Troponin is a marker used in standard hospital blood tests to find out if people have had heart attacks.

We don’t know how long it takes this inflammation and damage to return to normal, or if some damage is permanent.

Compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and raised native T1 and T2. A total of 78 patients recently recovered from COVID-19 (78%) had abnormal CMR [Cardiac Magnetic Resonance] findings, including raised myocardial native T1 (n = 73), raised myocardial native T2 (n = 60), myocardial late gadolinium enhancement (n = 32), and pericardial enhancement (n = 22).

These findings don’t tell us what’s happening in the roughly 45% of cases which are asymptomatic. Nor do they apply to severe ICU cases or the under 18s.

Another study by Lindner et al looked at 39 autopsies of Covid cases and found 60% had viral RNA in their heart tissue. Most of these patients, who were older, had died of pulmonary failure. In 40% there was no sign of the virus infiltrating the heart. But the heart inflammation wasn’t associated with the presence of the virus. In cases where there was virus, it wasn’t in the heart muscle cells but in the immune cells of the heart. I think all we can say from Lindner is that we really need to understand this disease better. Is it more an immune system disease than a vascular one?

 Our findings from in situ hybridization revealed the most likely localization of SARS-CoV-2 not to be in the cardiomyocytes but in interstitial cells or macrophages invading the myocardial tissue.

Yancy and Fonarow write in JAMA that they hope doctors will check for ongoing heart inflammation, and that these findings need to be confirmed. They ask whether heart failure might be the next chapter in the Covid crisis:

When added to the postmortem pathological findings from Linder et al,4 we see the plot thickening and we are inclined to raise a new and very evident concern that cardiomyopathy and heart failure related to COVID-19 may potentially evolve as the natural history of this infection becomes clearer.

We wish not to generate additional anxiety but rather to incite other investigators to carefully examine existing and prospectively collect new data in other populations to confirm or refute these findings. We hope these findings represent that of a select cohort of patients. Yet, if this high rate of risk is confirmed, the pathologic basis for progressive left ventricular dysfunction is validated, and especially if longitudinal assessment reveals new-onset heart failure in the recovery phase of COVID-19, then the crisis of COVID-19 will not abate but will instead shift to a new de novo incidence of heart failure and other chronic cardiovascular complications.

 My simple rule for new likely bioweapon releases is (and always was), just cut it off at the border until we learn how nasty it is. We can always and easily restart the flights, but we can’t undo the damage or rewind the clock if it runs wild. Will Western nations adopt this policy in the long run (like most of China’s neighbouring countries already do)?

REFERENCES

Clyde W. Yancy, MD, MSc1,2Gregg C. Fonarow, MD3,4 (2020) Coronavirus Disease 2019 (COVID-19) and the Heart—Is Heart Failure the Next Chapter?, JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3575

Lindner  D, Fitzek  A, Bräuninger  H,  et al. (2020) Association of cardiac infection with SARS-CoV-2 in confirmed COVID-19 autopsy cases.   JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3551

Puntmann  VO, Carerj  ML, Wieters  I,  et al.  (2020)  Outcomes of cardiovascular magnetic resonance in patients recently recovered from coronavirus disease 2019 (COVID-19).   JAMA Cardiol. Published online July 27, 2020. doi:10.1001/jamacardio.2020.3557

 

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