Achieving HbA1c <7.0% was associated with significant coronary plaque regression in non-obese T2DM patients (PAV change -1.27 vs +0.45, p=0.001) but not in obese patients.
Does achieving HbA1c <7.0% improve coronary plaque progression in obese versus non-obese type 2 diabetic patients with CAD?
Achieving HbA1c <7.0% is associated with coronary plaque regression in non-obese but not obese patients with type 2 diabetes and CAD, suggesting obese patients may require additional risk factor modification.
Tasa de eventos absoluta: 0% vs 0%
Abstract Background Obesity is a frequent comorbidity in patients with type 2 diabetes mellitus (T2DM). Given the higher prevalence of atherogenic cytokines in obese individuals, T2DM exhibiting obesity may be a high-risk subset requiring appropriate anti-atherosclerotic management. Current guidelines recommend achieving HbA1c 7.0% for the prevention of macrovascular complications; however, but the response in obese individuals to this target remains yet to be fully elucidated. The OPTIMAL study was a randomized controlled trial which employed intravascular imaging to compare the efficacy of continuous glucose monitoring-guided and HbA1c-guided glycemic control on coronary artery disease (CAD) in statin-treated type 2 diabetic patients with coronary artery disease. The current study investigates coronary plaque progression in response to achieving HbA1c 7.0% in obese and non-obese patients with type 2 diabetes mellitus (T2DM) through an OPTIMAL study sub-analysis. Purpose To compare plaque progression in T2DM patients with and without obesity in relation to achieving HbA1c 7.0%. Methods This study analyzed a total of 78 statin-treated type 2 diabetic patients with CAD. Serial IVUS imaging measured percent atheroma volume (PAV) at non-culprit segments at baseline and 48 weeks. Clinical characteristics and IVUS-derived measures were compared in obese (BMI≥25kg/m2, n=31) and non-obese patients (BMI25kg/m2, n=47) according to achieved HbA1c 7.0%, respectively. Results The proportion of patients who achieved HbA1c7.0% at 48 weeks was similar between obese and non-obese subjects (51.0% vs. 51.6%, p=0.99). In non-obese patients, there were no significant differences in clinical characteristics between two groups (Table 1). On serial IVUS imaging analysis, non-obese patients achieving HbA1c 7.0% showed greater regression of PAV (-1.27 ± 1.76 vs. +0.45 ± 1.34, p=0.001), even after clinical risk factor adjustment -1.25 (-2.51, -0.00), p=0.04. (Figure 1). In obese patients, those who achieved HbA1c7.0% were more likely to be male (93.7% vs. 60.0%, p=0.04) (Table 2), whereas other clinical characteristics and risk factor control did not differ between the two groups. There was no significant difference in change in PAV between obese patients with and without achieved HbA1c 7.0% (-0.24 ± 1.43 vs. +0.13 ± 0.75, p=0.40). Multivariate linear regression analysis revealed that achieved HbA1c 7.0% was not necessarily associated with change in PAV in obese subjects -0.55 (-1.49, +0.39), p=0.24. Conclusions Coronary atheroma in non-obese type 2 diabetic patients favorably responded to achieving HbA1c 7.0%. However, this favorable benefit was not observed in obese type 2 diabetic patients. These findings highlight clinical importance of multiple risk factor control especially in obese type 2 diabetic patients for further modifying their coronary atherosclerosis.Table 1 and Figure 1 non-obese patients Table 2 and Figure 2 obese patients
Salib et al. (Sat,) reported a other. Achieving HbA1c <7.0% was associated with significant coronary plaque regression in non-obese T2DM patients (PAV change -1.27 vs +0.45, p=0.001) but not in obese patients.