Cardiovascular disease (CVD) is one of the greatest disease burdens and takes the lives of many each year. There are many risk factors both modifiable and non-modifiable which contribute to the onset and progression of the disease. Trimethylamine N-oxide (TMAO) in recent years has been found to have a correlation with CVD onset. Those with increased levels of the metabolite have a markedly increased risk of future development of cardiometabolic disorders.This literature review aimed to critique past studies undertaken to find a consensus of the significance of the interrelationship between TMAO and cardiovascular risk. A definite link between TMAO levels and a CVD outcome was found. The majority of the literature stated the relationship with evidence; however, there is still some uncertainty as to why and how the correlation occurs. Further study needs to be done to further dissect and understand the relationship between TMAO and CVD risk.

Introduction: In patients with left ventricular (LV) nonischemic cardiomyopathy and monomorphic ventricular tachycardia (VT), midmyocardial and epicardial substrates are often involved but endocardial structures may also be affected. Delayed enhancement – magnetic resonance imaging (DE–MRI) was used to characterize the substrates of predominantly epicardial VT to improve identification of target sites for ablation. Methods and Results: 12 patients with LV nonischemic cardiomyopathy and monomorphic VT (prior myocarditis in 9) had a predominantly epicardial (n = 8) or epicardial-only DE-MRI substrate (n = 4). Modest-sized endocardial involvement in predominantly epicardial substrates was identified by DE-MRI in 8 patients. Mapping of 22 VTs was performed in 12 patients using an endo-epicardial approach in 6 patients and an endocardial-only approach in 6 patients. Endocardial VT reentry circuit exit sites as defined by entrainment and pace mapping criteria corresponded to endocardial breakthroughs from predominantly epicardial DE-MRI substrates in 7 patients. The endocardial VT exits were located at the ventricular base near the mitral annulus in 6 patients. Successful endocardial ablation of at least one VT was accomplished in 5 patients. Epicardial ablation as a part of an endo-epicardial approach or as epicardial-only ablation was performed in 6 patients and was successful in 4 patients. Conclusion: Endocardial breakthroughs from predominantly epicardial DE-MRI substrates are often located near the ventricular base in the perivalvular region and correlate with endocardial VT reentry circuit exit sites amenable to ablation.