Introduction: Gut microbiota are shown to participate in the formation of a pro-atherogenic compound called trimethylamine-N-oxide (TMAO). TMAO levels were shown to directly influence the propensity of macrophages to accumulate cholesterol and form foam cells in atherosclerotic lesions, and have been reported the association with adverse cardiovascular events. However, the relationship between change in TMAO levels and coronary plaque progression is unclear.
Hypothesis: The change in TMAO levels between acute and chronic phases of acute myocardial infarction (AMI) relates with the progression of coronary plaque complexity.
Methods: We enrolled 82 AMI patients, and plasma TMAO levels were measured on admission (the acute phase) and 10 months later (the chronic phase). ΔTMAO levels were defined as the change in TMAO levels between the acute and chronic phases. SYNTAX score was assessed after all interventions to the residual stenosis in the acute phase and was reevaluated in the chronic phase to quantify the progression in coronary plaque complexity.
Results: The mean ± standard deviation of age was 62 ± 12 years, and 72 (88%) were male. The median of TMAO levels was 5.7 μM (interquartile ranges [IQRs]: 3.2 to 9.6 μM) in the acute phase and 6.8 μM (IQRs: 3.9 to 14.1 μM) in the chronic phase. SYNTAX score changed from 10.8 ± 6.7 to 13.1 ± 8.2 and increased in 40 patients (49%). In patients with increased SYNTAX score, Δlog TMAO was significantly higher than those without (0.312 ± 0.436 vs -0.044 ± 0.468, p<0.001). By the multivariate logistic regression analysis adjusted for age, sex, hypertension and diabetes mellitus, the increase in TMAO levels was independently associated with the increase in SYNTAX score (odds ratio for 0.1 increase in Δlog TMAO levels: 1.28, 95% CI: 1.13 - 1.48, p<0.001).
Conclusions: The increase in TMAO levels was significantly and independently associated with the progression in coronary plaque complexity assessed by SYNTAX score in patients with AMI.