<p>The aim of this study was to evaluate the relationship between N,N,N trimethyl-L-alanyl-L-proline betaine (TMAP) levels and myocardial infarction (MI).&#xa0;Causal relationship was estimated based on TMAP levels and MI data from genome-wide association studies (GWAS). The main analysis method of bidirectional two-sample Mendelian randomization (TSMR) was inverse variance weighting (IVW), with four other supplementary methods used.&#xa0;The IVW method yielded results indicating a negative correlation between TMAP levels and MI (IVW, odds ratio [OR] = 0.976, 95% confidence interval [CI]: 0.960–0.992, <i>P</i> = 0.004). In contrast, the inverse analysis did not provide evidence that MI affects TMAP levels (<i>P</i> &gt; 0.05).&#xa0;This study provided evidence for the causal effect of TMAP levels on MI. It was not the case in the opposite situation. It is plausible that TMAP may serve as a protective factor in MI.</p> Graphical Abstract <p></p>

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Role of N,N,N Trimethyl-L-alanyl-L-proline Betaine Levels in the Process of Myocardial Infarction

  • Ziyang Wu,
  • Dong Wang,
  • Chengchun Tang

摘要

The aim of this study was to evaluate the relationship between N,N,N trimethyl-L-alanyl-L-proline betaine (TMAP) levels and myocardial infarction (MI). Causal relationship was estimated based on TMAP levels and MI data from genome-wide association studies (GWAS). The main analysis method of bidirectional two-sample Mendelian randomization (TSMR) was inverse variance weighting (IVW), with four other supplementary methods used. The IVW method yielded results indicating a negative correlation between TMAP levels and MI (IVW, odds ratio [OR] = 0.976, 95% confidence interval [CI]: 0.960–0.992, P = 0.004). In contrast, the inverse analysis did not provide evidence that MI affects TMAP levels (P > 0.05). This study provided evidence for the causal effect of TMAP levels on MI. It was not the case in the opposite situation. It is plausible that TMAP may serve as a protective factor in MI.

Graphical Abstract