Key result
Carvedilol and thyroid hormone co-administration in rats post-AMI attenuated adverse cardiac remodeling, reduced Bax expression, activated Akt, and decreased β1AR levels compared to MI alone.
Why the study?
Adverse cardiac remodeling post-AMI involves cellular death and survival signaling, prompting investigation into whether co-treatment with carvedilol and thyroid hormones sustains cellular homeostasis and affects apoptosis and survival proteins.
Does co-administration of carvedilol and thyroid hormones improve cardiac remodeling and survival signaling in a rat model of acute myocardial infarction?
Does co-administration of carvedilol and thyroid hormones improve cardiac remodeling and survival signaling in a rat model of acute myocardial infarction?
Answers are grounded in this paper and cite their sources.
Co-administration of carvedilol and thyroid hormones may offer cardioprotection against adverse remodeling post-AMI via modulation of apoptotic and survival signaling pathways.
Cellular death and survival signaling plays a key role in the progress of adverse cardiac remodeling after acute myocardial infarction (AMI). Therapeutic strategies, such as co-treatment with beta-blocker carvedilol and thyroid hormones (THs), give rise to new approaches that can sustain the cellular homeostasis after AMI. Therefore, we sought to investigate the effects of carvedilol and TH co-administration on apoptosis and survival proteins and on cardiac remodeling after AMI. Male Wistar rats were distributed in 5 groups as follows: sham-operated group (SHAM), infarcted group (MI), infarcted plus carvedilol group (MI+C), infarcted plus TH group (MI+TH), and infarcted plus carvedilol and TH co-treatment group (MI+C+TH). Echocardiographic analysis was performed, and hearts were collected for western blot evaluation. The MI group presented systolic posterior wall thickness loss, an increase in the wall tension index, and an increase in atrial natriuretic peptide tissue levels than the SHAM group. However, in the MI+C+TH group, these parameters were equally to the SHAM group. Moreover, whereas the MI group showed Bax protein expression elevated in relation to the SHAM group, the MI+C+TH group presented Bax reduction and also Akt activation compared with the MI group. In addition, the MI+TH group revealed beta-1 adrenergic receptor (β1AR) upregulation compared with the MI and MI+C groups, whereas the MI+C+TH group presented lower levels of β1AR in relation to the SHAM and MI+TH groups. In conclusion, we suggest that carvedilol and TH co-administration may mediate its cardioprotective effects against adverse cardiac remodeling post-AMI through the Bax reduction, Akt activation, and β1AR decrease.
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Ortiz et al. (2020) studied Acute myocardial infarction. Carvedilol and thyroid hormones co-administration vs. Sham, MI alone, MI+carvedilol, and MI+thyroid hormones was evaluated on Apoptosis and survival proteins and cardiac remodeling. Carvedilol and thyroid hormone co-administration in rats post-AMI attenuated adverse cardiac remodeling, reduced Bax expression, activated Akt, and decreased β1AR levels compared to MI alone.
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