COVID-19 causes lighter heart damage during second vs first wave of infections

20 Dec 2021
COVID-19 causes lighter heart damage during second vs first wave of infections

In fatal cases of the coronavirus disease 2019 (COVID-19), cardiac inflammation, cardiomyocyte injury, and microvascular thrombogenicity are substantially lower in the second vs first wave of infections, a new study has found.

This pattern could reflect improvements in COVID-19 care and may be due to the increasing use of steroids in the management of COVID-19.

Researchers looked at autopsied hearts of 15 and 10 COVID-19 patients who had died during the first and second waves of the pandemic, respectively. Immunohistochemistry; leukocyte, lymphocyte, and macrophage infiltration patterns; cardiomyocyte necrosis; procoagulant factors; and microvascular thrombosis were all quantified and compared against 18 hearts of non-COVID-19 controls.

All COVID-19 patients had heightened cardiac inflammation, characterized by greater extravasation of CD45+ leukocytes, CD68+ macrophages, and CD3+ T lymphocytes in the myocardium. Semi-quantitative analysis showed that while CD68+ macrophages were comparable between infection waves, amounts of CD45+ (p=0.018) and CD3+ (p=0.019) cells were significantly higher in first-wave hearts.

Similarly, all wave 1 patients showed injury in dispersed small cardiomyocyte clusters or individual cells, as visualized by complement factor C3d immunostaining. Meanwhile, only four wave 2 patients had such a hallmark (p=0.001). Intravascular thrombi were also more common in wave 1 hearts (47 percent vs 0 percent; p=0.011).

In addition, microvascular deposits of N(ε)-Carboxymethyllysine, an advanced glycation end product, and Factor VII, a procoagulant factor, were significantly lower in hearts from the second wave of COVID-19.

“In this pathology study we show that cardiac inflammation, cardiomyocyte injury, and microvascular thrombogenicity in our cohort of deceased COVID-19 patients were markedly decreased in second wave compared to first wave patients,” the researchers said.

“It is noteworthy that whatever caused the decreased cardiac pathology in wave 2 patients did not affect the extent of damage to the lungs in our patients,” they added.

Int J Cardiol 2021;doi:10.1016/j.ijcard.2021.11.079