This study investigated the association between lesion-specific FAI and MACE in patients with T2DM. Over a monitoring duration of three years, the lesion-specific FAI emerged as an independent prognostic marker for MACE in T2DM subjects. Additionally, incorporating lesion-specific FAI with CACS enhances the predictive accuracy for MACE among this demographic. To our knowledge, our study is at the forefront of unraveling the significance of lesion-specific FAI in foretelling the risk of MACE in patients with T2DM.
PCAT, ectopic adipose tissue around coronary artery, is increasingly recognized for its significant influence in escalating cardiovascular disease risk. As an dynamic endocrine and paracrine organ, the inflammatory reaction of PCAT is usually aggravated, marked by an intensified release of pro-inflammatory mediators in patients with T2DM[17]. These mediators readily permeate the coronary artery walls, undermining endothelial function and expediting atherogenesis[18]—paving the way to complications such as coronary artery constriction, myocardial ischemia, and infarction. Such perturbations in the inflammatory milieu and adipose equilibrium within PCAT are detectable via imaging, revealing a heightened CT attenuation signal[7]. Through this study, we have corroborated the association between altered PCAT attenuation and the progression of T2DM, highlighting its implications for patient prognosis.
RCA-FAI has been regarded as a valuable marker for early detection of inflammation in coronary artery[7]. It serves a dual role, not only mirroring the progression of cardiovascular disease in patients but also providing prognostic information regarding potential future cardiac events in those with coronary heart disease[16][19]. Previous studies have established that RCA-FAI was markedly elevated in patients with T2DM as opposed to those without, and this holds true irrespective of the degree of arterial stenosis or the vulnerability of plaque formations[6]. Further investigation focusing on individuals with T2DM has highlighted that the effectiveness of RCA-FAI in identifying coronary artery disease was more representative than the Left anterior descending (LAD) and Left circumflex (LCX) arteries, making it a better diagnostic tool for coronary artery disease in T2DM patients[20]. Additionally, RCA-FAI has been identified as an independent prognostic factor for the onset of microvascular complications in T2DM patients[21]. Despite these findings showed that RCA-FAI seems to better reflect the overall inflammatory state of T2DM patients, our study did not corroborate a statistical discrepancy in RCA-FAI between T2DM patients who suffered from MACE and those without. This discrepancy may be attributable to a lower presence of criminal plaque in the RCA of patients with T2DM who experienced MACE in this study, compared to T2DM patients who did not encounter such events.
To date, the use of PCAT-FAI as a prognostic tool for MACE in patients with T2DM has not been extensively explored. The study of Ichikawa et al. showed that high FAI of LAD-PCAT can significantly predict cardiovascular events in patients with T2DM, whereas RCA-PCAT attenuation cannot[22]. Although vascular-based measurements provide a broad perspective on disease state and risk at an individual patient level, lesion-specific measurements may be of particular concern when trying to identify plaque at risk of rupture. Therefore, our study was different from the previous research on PCAT around three coronary arteries, but focused on PCAT around lesion, which may potentially lead to unconscionable MACE in patients with T2DM. This approach provides a more direct insight into the early inflammatory state of possible adverse lesions, which is helpful to better predict the outcome of lesion development. Our study confirmed that the FAI around criminal plaque could effectively predict MACE within three years in patients with T2DM and offered a non-invasive imaging marker to predict adverse cardiovascular outcomes.
Previous studies have demonstrated that CACS holds independent predictive value for MACE in patients with coronary heart disease[23][24]. This is mainly attributed to the fact that CACS reflects the severity of arterial atherosclerosis and is closely correlated with the overall burden of plaque. Diabetic patients have high incidences of coronary artery calcification, and the degree of coronary artery calcification is more extensive and severe than that of non-diabetic people[25]. However, diabetes can lead to cardiac vascular intima and media calcification, the media calcification does not protrude into the lumen and narrow the vascular lumen, but the CACS also counts such calcification lesion into the total CACS. Therefore, the high CACS of patients with T2DM does not necessarily mean that the coronary artery disease is severe, which has limitation for the prediction of MACE[26]. In our study, combining lesion-specific FAI with CACS enhanced the predictive efficacy of MACE in T2DM patients, allowing for early identification of high-risk patients prone to developing MACE before it happened. Our research indicated that lesion-specific FAI, as a novel imaging biomarker, can refine the risk stratification for predicting cardiovascular events in T2DM patients.
Our study, despite its contributions, is not without limitations. Initially, the fact that it is a single-center retrospective inquiry means that the sample size is inherently limited, which may impinge upon the generalizability of our findings. Secondly, recognizing that FAI values can vary across different segments of coronary arteries, it is imperative that future investigations delve into the nuanced relationships between segment-specific FAI and the incidence of cardiovascular events. Lastly, our study focus on measuring lesion-specific FAI exclusively at the outset. The variable treatment regimens that patients underwent throughout the follow-up period could exert an influence on the eventual occurrence of MACE, carrying the potential to skew the outcomes of our research. Hence, it is essential to account for these varying therapeutic approaches when interpreting the results.
The findings of our study lead us to several pertinent conclusions. First and foremost, we observed a strong association between elevated lesion-specific FAI and the occurrence of MACE among T2DM patients, extending also to those with severe coronary artery calcification over a three-year span. Second, integrating lesion-specific FAI with CACS markedly improved the prediction of MACE within the T2DM patient cohort. This combined approach shows promise for the more accurate identification of patients at high risk, thereby enabling more proactive and targeted interventions and treatments for those individuals.