This study confirmed that AR could worsen myocardial abnormalities in T2DM patients. The research also focused on the atrioventricular interaction in patients with T2DM and AR. The following main findings were obtained: (1) patients with T2DM with and without AR exhibited normal LV function but impaired LA reservoir and conduit function when compared with the normal controls. (2) Deteriorating AR may aggravate LA and LV dysfunction and impair active LA function. (3) The enlargement and dysfunction of LA were synchronous with LV dysfunction. (4) The degree of AR was an independent determinant of εs and εe. The LVEDV was an independent determinant of εs, and LVESV was an independent determinant of εa.
LA and LV dysfunction in patients with T2DM
Our study found that patients with T2DM with normal cardiac volume exhibited a notable decrease in total LAEF, passive LAEF, εs, and εe; this finding suggests that the LA dysfunction in T2DM primarily occurs during the reservoir and conduit phase, whereas LV dysfunction mainly presents as a reduction in GLPS. These findings suggest that LA function is a powerful parameter for evaluating LV diastolic dysfunction, a characteristic of diabetes-associated heart diseases [19]. Previous investigations have shown the negative effect of T2DM on LA [13, 20, 21]. Because T2DM is a systemic-mediated disease, sustained hyperglycemia induces interstitial fibrosis, inflammation, and oxidative stress in LV and LA [22–24]. In addition, the conduction system disorders and imbalance in the autonomic nervous system induced by T2DM can contribute to paroxysmal atrial fibrillation, further impairing LA function [13]. Therefore, LA phasic function holds additional value in diagnosing myocardial injury in the diabetic population.
Assessment of LA and LV dysfunction in T2DM (AR +) patients with varied degrees of regurgitation
Our observations suggest that AR could potentially worsen the dysfunction of LA and LV. In patients with T2DM with mild AR, there was noticeable enlargement of the LA and LV, accompanied by a decline in the active LAEF and LVEF. The εa was maintained in the mild AR stage but decreased remarkably in the moderate and severe AR stages. In addition, as the degree of regurgitation increased, LA phasic function and LV compliance gradually decreased. Notably, εs and εa were found to be independently influenced by the degree of regurgitation.
Furthermore, AR is defined as a condition in which the LV experiences volume overload due to blood backflow during diastole [25]. Consequently, AR could result in increased LV preload, LV filling pressure, and subsequent increases in LA pressure and volume [26]. In T2DM-superimposed AR, the patients had worse left-heart volume and strain parameters. We speculated that they had a synergistic effect on the mechanism, leading to heart damage and rapid failure of the compensatory mechanism in the left heart [27]. Our study findings are consistent with those in a report by Zhang et al. stating that LA myocardial impairment in patients with T2DM with mitral regurgitation progressed without compensation [14, 28]. Therefore, the occurrence and progression of AR should be considered in managing patients with T2DM. Once mild AR occurs in patients with T2DM, timely intervention is needed to avoid irreversible heart damage caused by AR progression[29]. Patients who receive an early and timely diagnosis can plan surgery at the optimal time, thereby reducing the risk of long-term negative effects on cardiac function and malignant outcomes[30, 31].
The left atrioventricular interaction in patients with T2DM and AR
Several studies have highlighted the importance of LA workload and transport on LV function in patients with T2DM or AR respectively[32, 33]. Steele et al. have reported atrioventricular interaction in adolescents and young adults who were obese and with T2DM [20]. Similarly, Jenner et al. found an association between LA phasic function and LV diastolic dysfunction in patients with AR [34]. Our study findings indicated that LVEDV and LVMI were independent determinants of the εs observed in patients with T2DM with AR. Moreover, our study also suggests an independent association between LA strain and LV diastolic function. In the absence of valvular heart disease, the LA and LV functions and filling pressures are tightly coupled during diastole since they are directly connected [35]. The after-load LA depends on the LV end-diastolic pressure and LV wall stiffness; the function of the LA reservoir period ensures that the LV can be filled quickly under short-term and low-load conditions [11, 36]. Atrioventricular dysfunction is a common problem associated with T2DM, and its pathological mechanism becomes even more complicated when AR is present. Previous reports have suggested that a reduction in LVEF to < 50% is no longer a suitable surgical indication for patients with complicated AR, which was also the focus of the present study [37]. Our study showed a positive correlation between LA strain and LVEF. Therefore, assessing atrioventricular interaction seems to be a better method to quantify myocardial function and assist patients in finding the best treatment plan.
Limitations
Our study had several limitations. First, although the sample size was adequate to support our conclusion, this was a single-center study; therefore, a larger cohort or multicenter study is needed in the future. Second, long-term follow-up data were unavailable, so further research is needed to investigate the predictive effect of LA strain parameters on cardiovascular events. Lastly, as our study was retrospective, a prospective cohort study should be conducted to refine the occurrence, development, and treatment-related clinical and cardiac function parameters of patients with T2DM with AR.