Achieving LDL-C <1.8 mmol/L led to significant plaque regression in obese T2DM patients (PAV -1.06%, p=0.02), but not in non-obese patients.
Does achieving LDL-C <1.8 mmol/L improve coronary plaque regression in obese versus non-obese patients with T2DM and CAD?
Achieving an LDL-C target of <1.8 mmol/L is associated with significant coronary plaque regression in obese patients with T2DM and CAD, highlighting the need for aggressive lipid lowering in this subgroup.
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Abstract Background Obesity is a major risk factor for atherosclerotic cardiovascular disease (ASCVD), which promotes the formation and progression of coronary atherosclerosis. Given expected rise in obesity prevalence, effective anti-atherosclerotic strategies are essential for obese patients. Lowering LDL-C level is a guideline-recommended strategy to mitigate risk of ASCVD. However, whether obese patients favorably respond to lowering LDL-C levels has not yet been fully characterized. 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 atherosclerosis in statin-treated type 2 diabetic patients with CAD. The current study is a sub-analysis of the OPTIMAL study which evaluates coronary plaque progression in response to lowering LDL-C levels in obese and non-obese patients with type 2 diabetes mellitus (T2DM). Purpose To compare the effect of achieving LDL-C 1.8 mmol/L on coronary plaque progression in non-obese and obese subjects with T2DM. Methods This analysis included a total of 78 statin-treated type 2 diabetic patients with CAD. Serial IVUS imaging was conducted to measure percent atheroma volume (PAV) at non-culprit segments at both baseline and 48 weeks. Clinical characteristics and change in PAV were compared in obese (BMI≥25kg/m2, n=31) and non-obese patients (BMI25kg/m2, n=47) according to achieved LDL-C level 1.8mmol/L at 48-weeks, respectively. Results LDL-C target attainment was similar in obese and non-obese individuals (41.9% vs. 57.4%, p=0.23). In non-obese patients, clinical characteristics and NIRS/IVUS parameters did not differ between those with and without achieved LDL-C 1.8mmol/L (Table 1). Achieving LDL-C level 1.8mmol/L was not necessarily associated with a significant change in PAV -0.36% (-1.62, +0.90), p=0.57 (Figure 1). In obese patients, those achieving LDL-C 1.8 mmol/L were more likely to receive high-intensity statins (100% vs. 66%, p=0.03) and β-blockers (92% vs. 55%, p=0.04) with a lower frequency of metformin use (23% vs. 66%, p=0.03) (Table 2). On serial IVUS imaging analysis, following adjustment of clinical demographics and medication use, a greater regression of PAV was observed in association with achieving LDL-C 1.8 mmol/L -1.06% (-1.93, -0.18), p=0.02 (Figure 2). Conclusions Plaque regression in response to achieving LDL-C 1.8 mmol/L differed by obesity, with significant benefit observed in obese T2DM patients. These findings highlight the need for aggressive LDL-C lowering in obese individuals to further reduce their cardiovascular risk.Table 1 and Figure 1 non-obese patients Table 2 and Figure 2 obese patients
Salib et al. (Sat,) reported a other. Achieving LDL-C <1.8 mmol/L led to significant plaque regression in obese T2DM patients (PAV -1.06%, p=0.02), but not in non-obese patients.