Abstract Body (Do not enter title and authors here): Background:
Anti-atherosclerotic response to statin has been shown to differ in patients with ACS and stable CAD. Statin induced a greater reduction of subsequent cardiac events’ risks and more plaque regression in ACS patients. This observation suggests the property of statin to more favorably modulate other proatherogenic drivers in the setting of ACS. Angiopoietin-like protein 3 (ANGPTL3) is a glycoprotein associated with lipid metabolism and vascular inflammation. However, how statins modulate ANGPTL3 levels in patients with ACS and stable CAD remains unknown.
Hypothesis:
Statin therapy may modulate ANGPTL3 levels, especially in ACS patients.
Aim:
To investigate serial changes in ANGPTL3 after statin therapy in patients with ACS and stable CAD.
Methods:
The current study prospectively enrolled 108 statin naïve patients with CAD. Blood samples were collected at baseline, and 1 and 3 months after statin therapy. ANGPTL3 level was measured by using a commercially available human enzyme-linked immunosorbent assay (Immuno-Biological Laboratories, Gunma, Japan). Clinical characteristics and percent changes in ANGPTL3 were compared in patients with ACS and stable CAD.
Results:
Baseline ANGPTL3 levels were 420±177ng/mL and 398±171 ng/mL in ACS and stable CAD patients, respectively (p=0.532). In ACS patients, a higher ANGPTL3 level was observed in patients with STEMI compared to those with NSTEMI (449 vs. 328, p=0.001). Following the commencement of statins (high-intensity statin: 61 vs. 47%, p=0.203), LDL-C levels were significantly lowered at 1 month in both two groups (Table). There was no significant difference in on-treatment LDL-C level at 1 and 3 months between ACS and stable CAD (Table). Despite lowering LDL-C with statin, ANGPTL3 levels in stable CAD patients did not change during the course of the study (Figure). By contrast, ACS patients exhibited significant reduction of ANGPTL3 levels at 1 month after statin therapy (Figure). Of note, this greater reduction of ANGPTL3 was more evident in patients with STEMI (percent change in ANGPTL3 = -15.4%, p = 0.001 vs. baseline) rather than NSTEMI (percent change in ANGPTL3 = +4.8%, p = 0.569 vs. baseline).
Conclusion:
Greater reduction of ANGPTL3 levels after statin therapy was observed in ACS patients. This statin-mediated effect on ANGPTL3 may account for more favorable response in cardiovascular events and plaque regression in ACS patients receiving a statin.