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Background/Objectives: This study aimed to investigate the association between colorectal cancer (CRC) and the risk of breakthrough respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in vaccinated patients with CRC. Methods: This retrospective cohort study used the TriNetX research network to identify vaccinated patients with CRC. Patients were matched using propensity score matching (PSM) and divided into patients with CRC and control (without history of CRC) groups. The primary outcome was the risk of breakthrough SARS-CoV-2 in vaccinated patients. The secondary outcome was a composite of all-cause emergency department (ED) visits, hospitalization, and death during the follow-up period after the diagnosis of COVID-19. Results: A total of 15,416 vaccinated patients with CRC were identified and propensity matched with 15,416 vaccinated patients without CRC. Patients with CRC had a significantly increased risk for breakthrough infections compared to patients without CRC (aOR = 1.78; [95% CI: 1.47-2.15]). Patients with CRC were at increased risk of breakthrough SARS-CoV-2 infections after two doses (aOR = 1.71; [95% CI: 1.42-2.06]) and three doses (aOR = 1.36; [95% CI: 1.09-1.69]) of SARS-CoV-2 vaccine. Vaccinated patients with CRC were at a lower risk of COVID-19 infection than unvaccinated CRC patients (aOR = 0.342; [95% CI: 0.289-0.404]). The overall composite outcome (all-cause ED visits, all-cause hospitalization, and all-cause death) was 51.6% for breakthrough infections, which was greater than 44.3% for propensity score-matched patients without CRC (aOR = 1.79; [95% CI: 1.29-2.47]). Conclusions: This cohort study showed significantly increased risks for breakthrough SARS-CoV-2 infection in vaccinated patients with CRC. Breakthrough SARS-CoV-2 infections in patients with CRC were associated with significant and substantial risks for hospitalizations.
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Right ventricular (RV) dysfunction can lead to complications after acute inferior myocardial infarction (MI). However, it is unclear how RV failure after MI contributes to left-sided dysfunction. The aim of the present study was to investigate the consequences of right coronary artery (RCA) ligation in mice. RCA ligation was performed in C57BL/6JRj mice ( n = 38). The cardiac phenotypes were characterized using high-resolution echocardiography performed up to 4 wk post-RCA ligation. Infarct size was measured using 2,3,5-triphenyltetrazolium chloride staining 24 h post-RCA ligation, and the extent of the fibrotic area was determined 4 wk after MI. RV dysfunction was confirmed 24 h post-RCA ligation by a decrease in the tricuspid annular plane systolic excursion ( P < 0.001) and RV longitudinal strain analysis ( P < 0.001). Infarct size measured ex vivo represented 45.1 ± 9.1% of the RV free wall. RCA permanent ligation increased the RV-to-left ventricular (LV) area ratio ( P < 0.01). Septum hypertrophy ( P < 0.01) was associated with diastolic septal flattening. During the 4-wk post-RCA ligation, LV ejection fraction was preserved, yet it was associated with impaired LV diastolic parameters ( E/ E', global strain rate during early diastole). Histological staining after 4 wk confirmed the remodeling process with a thin and fibrotic RV. This study validates that RCA ligation in mice is feasible and induces RV heart failure associated with the development of LV diastolic dysfunction. Our model offers a new opportunity to study mechanisms and treatments of RV/LV dysfunction after MI. NEW & NOTEWORTHY Right ventricular (RV) dysfunction frequently causes complications after acute inferior myocardial infarction. How RV failure contributes to left-sided dysfunction is elusive because of the lack of models to study molecular mechanisms. Here, we created a new model of myocardial infarction by permanently tying the right coronary artery in mice. This model offers a new opportunity to unravel mechanisms underlying RV/left ventricular dysfunction and evaluate drug therapy.
