Abstract Background Acute coronary syndrome (ACS) is a phenotypic feature of CAD associated with worse cardiovascular outcomes. Pathophysiologically, ACS more likely harbor activated inflammatory disease substrate which promotes the formation of vulnerable plaques within entire coronary trees. This distinct feature suggests the need to identify inflammatory driver associated with plaque vulnerability in the setting of ACS. Circulating lipoprotein (a) Lp(a) is a proatherogenic lipoprotein which elevates future risks of atherosclerotic cardiovascular disease. Given that Lp(a) harbors pro-inflammatory properties, Lp(a) may be an important contributor to pancoronary formation of vulnerable plaques in ACS patients. Near-infrared spectroscopy (NIRS) imaging enables to quantitatively evaluate the degree of lipidic plaque material which reflects the degree of plaque vulnerability. Purpose The current study employed NIRS imaging to elucidate the association of circulating Lp(a) with NIRS-derived lipid-rich plaque materials in ACS and stable CAD patients, respectively. Methods The current study analyzed 391 patients with CAD who received NIRS/IVUS-guided PCI in the REASSURE-NIRS registry. Lp(a) level was measured at the index of PCI with enzymatic methods (Sekisui Medical, Tokyo, Japan) using an automated analyzer (Hitachi Labospect 008; Hitachi-Hitec, Tokyo, Japan). In stable CAD (n=255) and ACS (n=136) patients, subjects were stratified according to Lp(a) level ≧30 mg/dL, respectively. Then, maxLCBI4mm at non-culprit lesions (stable CAD: n=442, ACS: n=213) was compared. Results The proportion of patients exhibiting Lp(a) level ≧30 mg/dL was 26.7% and 25.7% in stable CAD and ACS patients, respectively. 90.2 and 34.1% of stable CAD patients received a statin and high-intensity statin, respectively (Table 1). On NIRS imaging analysis, maxLCBI4mm and the proportion of maxLCBI4mm400 did not differ between two groups (Figure 1). Multivariate analysis showed that maxLCBI4mm was associated with BMI but not with Lp(a) level ≧30mg/dL. In ACS patients, those with Lp(a) level ≧30 mg/dL were more likely to be female (Table 2). Statin was more frequently used in those with Lp(a) level ≧30 mg/dL, but this comparison did not meet statistical significance (Table 2). NIRS imaging analysis demonstrated a higher maxLCBI4mm in those with Lp(a) level ≧30 mg/dL (Figure 2). Furthermore, a greater frequency of non-culprit lesions exhibiting maxLCBI4mm400 was observed in those with Lp(a) level ≧30 mg/dL (Figure 2). On multivariate analysis, Lp(a) level ≧30 mg/dL was an independent factor associated with maxLCBI4mm400 (OR=1.869, 95%CI=1.003-1.869, p=0.049). Conclusion Accumulation of lipidic materials within vessel wall was observed in association with Lp(a) level ≧30 mg/dL in patients with ACS but not stable CAD. These observations highlight the importance of circulating Lp(a) to predict pancoronary vulnerability in ACS patients.Table 1 Figure 1 Table 2 Figure 2
Iwai et al. (Sat,) studied this question.