Regarding cardiac involvement in COVID, we may not witness cardiogenic shocks (only seldom) and sure, many patients don't require high-dose vasoactives even under deep sedation

Then there was that bogus athlete myocarditis paper
But it doesn't mean there's no cardiac involvement

The heart is just a vessel, it has endothelium
The pericardium is in close contact with pleurae, so inflammation by proximity is possible (& a staple of bodily serous envelopes!)

Hence, a low-grade, subclinical myopericarditis is possible
And we know heart rhythm alterations are frequent during and after COVID. We saw them

And then there's the unsettling "severe-COVID sinus bradycardia":

In which you have a rapidly deteriorating patient, whose heart rhythm stays suspiciously static (zero variability), about 40-45 bpm, with little response to atropine

Like if the heart was denervated

We currently think that this CoV doesn't have a significant tropism for cardiomyocites, but inflammation can happen anyway:

either by proximity to pleuro-pericardial structures (which predictably react to the intense lung inflammation)

or by an interaction between endothelitis and viral neurotropism, which can end in conduction system disorders or neural dysregulation (cardiac dysautonomia)

The heart conduction system is mostly subendocardial (subendothelial). This proximity is a risk factor if there's endothelial cardiac involvement https://www.ahajournals.org/doi/full/10.1161/01.RES.82.6.629