Retrospective record review on timing of COVID-19 vaccination and cardiac surgery.

BACKGROUND: Novel clinical challenges are faced by cardiac surgeons under the coronavirus disease 2019 (COVID-19) pandemic. Amidst the uncertainties faced due to the socioeconomic and public health impact, there is little evidence surrounding COVID-19 vaccination in patients undergoing cardiac surgery. Timing of vaccination and postvaccination adverse effects are required parameters to discuss with cardiac surgical patients. METHODS: This is a single-center, retrospective observational study. All patients who underwent adult cardiac surgery at the Prince of Wales Hospital, Hong Kong from January 2021 to December 2021 were included. Postoperative clinical outcomes, COVID-19 vaccination status, and vaccination-related adverse effects were collected. RESULTS: A total of 426 patients; 117 (27%) underwent isolated coronary artery bypass grafting, 111 (26%) underwent valvular surgery, and 97 (23%) underwent aortic surgery. Patients received either Sinovac CoronaVac or Pfizer BNT162b2 vaccine. Overall vaccination rate with at least 1 dose was 52% (n = 212), 15% (n = 63) received the first dose before surgery, 36% (n = 149) received the first dose vaccination after surgery. Rate of completion with second and third doses of vaccination were 22% (n = 89) and 4.9% (n = 20), respectively. The mean timing of first dose of vaccine after surgery was 216 ± 84 days from operation. Three (1.4%) patients recorded vaccination-related complications. CONCLUSIONS: COVID-19 vaccination is safe in patients who received major cardiac surgery, with low adverse effects recorded and no vaccine-related mortality observed. A time frame of 3-6 months after cardiac surgery receiving COVID-19 vaccination is reasonable and could serve as a guidance for future COVID-19 vaccination booster programs.

A human pluripotent stem cell-based model of SARS-CoV-2 infection reveals an ACE2-independent inflammatory activation of vascular endothelial cells through TLR4.

To date, the direct causative mechanism of SARS-CoV-2-induced endotheliitis remains unclear. Here, we report that human ECs barely express surface ACE2, and ECs express less intracellular ACE2 than non-ECs of the lungs. We ectopically expressed ACE2 in hESC-ECs to model SARS-CoV-2 infection. ACE2-deficient ECs are resistant to the infection but are more activated than ACE2-expressing ones. The virus directly induces endothelial activation by increasing monocyte adhesion, NO production, and enhanced phosphorylation of p38 mitogen-associated protein kinase (MAPK), NF-κB, and eNOS in ACE2-expressing and -deficient ECs. ACE2-deficient ECs respond to SARS-CoV-2 through TLR4 as treatment with its antagonist inhibits p38 MAPK/NF-κB/ interleukin-1ß (IL-1ß) activation after viral exposure. Genome-wide, single-cell RNA-seq analyses further confirm activation of the TLR4/MAPK14/RELA/IL-1ß axis in circulating ECs of mild and severe COVID-19 patients. Circulating ECs could serve as biomarkers for indicating patients with endotheliitis. Together, our findings support a direct role for SARS-CoV-2 in mediating endothelial inflammation in an ACE2-dependent or -independent manner.