Atherosclerotic cardiovascular disease (ASCVD) is the primary cause of death globally, with nine million deaths directly attributable to ischemic heart diseases in 2020. Since the last few decades, great effort has been put toward primary and secondary prevention strategies through identification and treatment of major cardiovascular risk factors, including hypertension, diabetes, dyslipidemia, smoking, and a sedentary lifestyle. Once labelled “the forgotten organ”, the gut microbiota has recently been rediscovered and has been found to play key functions in the incidence of ASCVD both directly by contributing to the development of atherosclerosis and indirectly by playing a part in the occurrence of fundamental cardiovascular risk factors. Essential gut metabolites, such as trimethylamine N-oxide (TMAO), secondary bile acids, lipopolysaccharides (LPS), and short-chain fatty acids (SCFAs), have been associated with the extent of ischemic heart diseases. This paper reviews the latest data on the impact of the gut microbiome in the incidence of ASCVD.

Background: Recent studies have suggested an increased risk of acute myocardial infarction (AMI) following daylight saving time (DST) transitions in cohorts of American and European patients. We aim to validate this finding in a Canadian population. Methods: We performed a retrospective cohort study of patients admitted to the Hôpital du Sacré-Coeur de Montréal with a diagnosis of AMI requiring a coronary angiogram from 28 February 2016 to 3 December 2022. The transition period was defined as two weeks following DST, while the control periods were two weeks before and two weeks after the transition period. Patients aged 18 years or older were included. The primary endpoint was the incidence rate ratio (IRR) of AMI following DST transitions while the secondary endpoint was infarct size by biomarkers. A subgroup analysis compared the pre-COVID-19 period (2016–2019) to the post-COVID-19 period (2020–2022). Results: A total of 1058 patients were included (362 in the transition group and 696 in the control group). The baseline clinical characteristics were comparable between both groups. The rate of AMI per day following the DST transitions was 1.85 compared to 1.78 during control periods. The DST transitions were not associated with an increase in AMI (IRR = 1.04, 95% CI 0.91–1.18, p = 0.56) nor with infarct size. In the subgroup analysis, DST was associated with a significant increase in the incidence of AMI only in the pre-COVID-19 period, with a rate of 2.04 AMI per day in the transition group compared to 1.71 in the control group (IRR = 1.19, 95% CI 1.01–1.41, p = 0.041). In contrast, there was a significant increase in the size of AMI following DST in the post-COVID-19 period subgroup, with a creatine phosphokinase-MB (CK-MB) concentration of 137 ± 229 µg/L compared to 93 ± 142 µg/L (p = 0.013). Conclusions: In this Canadian cohort, there was a significant increase in the incidence of AMI in the pre-COVID-19 period, and infarct sizes were significantly larger following the DST transitions in the post-COVID-19 period. No significant associations emerged when pre- and post-COVID-19 periods were pooled.