JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, VOL. 80, NO.

12, SUPPL B, 2022 B237

RESULTS The study included 10,003 patients (mean age 58.0 years;
22.96% female) with 1,879 having TO. The risks of TO significantly
increased with quintiles of Lp(a), non–HDL-C/HDL-C, and apoB/apoA-
1 (P for trend <0.001) but were only significantly higher in the fifth
quintiles of LDL-C, non–HDL-C, and apoB. TG had no association with
TO. Restricted cubic splines indicate significant positive linear re-
lations between the 2 ratios and TO (OR [95% CI] per 1-SD increase:
non–HDL-C/HDL-C: 1.135 [1.095-1.176], P < 0.001; apoB/apoA-1: 2.590
[2.049-3.274], P < 0.001). The areas under the receiver-operating
characteristic curves of the 2 ratios were significantly greater than
those of single lipid measures. Elevation in apoB/apoA-1 tertile
significantly increased TO risk at a given non–HDL-C/HDL-C tertile but
not vice versa.

Crude OR Adjusted OR
(95% CI) P Value (95% CI) P Value

Total cholesterol, mmol/L 1.050 (1.003, 1.099) 0.036 1.072 (1.023, 1.123) 0.004

TG, mmol/L 1.043 (0.998, 1.089) 0.060 1.016 (0.971, 1.065) 0.488

LDL-C, mmol/L 1.104 (1.047, 1.165) <0.001 1.119 (1.060, 1.182) <0.001

Non–HDL-C, mmol/L 1.110 (1.059, 1.163) <0.001 1.113 (1.061, 1.168) <0.001

Lp(a), mg/dL 1.003 (1.001, 1.005) <0.001 1.003 (1.002, 1.005) <0.001

apoB, g/L 1.603 (1.318, 1.949) <0.001 1.605 (1.313, 1.961) <0.001

Non–HDL-C/HDL-C 1.168 (1.129, 1.208) <0.001 1.135 (1.095, 1.176) <0.001

apoB/apoA-1 3.030 (2.419, 3.795) <0.001 2.590 (2.049, 3.274) <0.001

CONCLUSION apoB/apoA-1 confers better predictive power of TO

than non–HDL-C/HDL-C and single lipid measures in established CAD
patients.
CATEGORIES OTHER: Diabetes, Lipid Disorders, and Risk Factor
Management

TCT-576
Serum Cholesterol Levels Do Not Influence Lipid Core Burden
Index
Frans Mensink,1 Jan Los,1 Mohamed Reda,2
Jeroen Jaspers Focks,3 Rohit Oemrawsingh,4 Peter Damman,5
Marleen van Wely,6 Helmut Gehlmann,1 Niels van Royen,5
Robert-Jan Van Geuns5
1
Radboudumc, Nijmegen, the Netherlands; 2Assiut University
Hospitals, Assiut, Egypt; 3Slingeland Hospital, Doetinchem, the
Netherlands; 4Albert Schweitzer Hospital, Dordrecht, the Netherlands;
5
Radboud University Medical Center, Nijmegen, the Netherlands; and
the 6RadboudUMC, Nijmegen, Netherland

BACKGROUND High lipid content in the coronary artery vessel wall is

predictive of future major adverse cardiac events. The lipid core
burden index (LCBI) as measured by near-infrared spectroscopy
(NIRS) represents the amount of lipid in the vessel wall. It is often
assumed that high circulating low-density lipoprotein cholesterol
(LDL-C) increases the LCBI. However, to our knowledge, the actual
relationship between cholesterol levels and LCBI has not been entirely
elucidated.
METHODS We retrospectively analyzed cholesterol values and NIRS
data in chronic coronary syndrome (CCS) and acute coronary syn-
drome (ACS) patients who underwent coronary angiography with
B238 JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, VOL. 80, NO. 12, SUPPL B, 2022

possible percutaneous intervention. In total, 110 patients were CONCLUSION Higher levels of Lp(a) were associated with thinner
included for analysis (49 ACS, 58 CCS). Correlations were assessed in OCT fibrous caps in patients with obstructive coronary lesions before
additional subgroups: ACS vs CCS; stable statin use vs no statin use; statin therapy. After intensive statin therapy, Lp(a) levels significantly
high LDL-C vs low LDL-C; and high high-density lipoprotein choles- increased; however, the change in Lp(a) levels did not have an effect
terol (HDL-C) vs low HDL-C. Comparisons between mean maxLC- on FCT.
BI4mm and total LCBI in different subgroups were done. CATEGORIES IMAGING AND PHYSIOLOGY: Imaging: Intravascular
RESULTS Median LDL-C was 102.5 mg/dL (74.6-145.0). Median HDL-C
was 41.0 mg/dL (34.4-49.1). Mean maxLCBI4mm was 378.0 (165.1),
and median total LCBI was 64.0 (30.5-100.5). No significant correla-
tion was found between either maxLCBI4mm or LDL-C (Spearman’s VASCULAR ACCESS FOR PCI I
rho ¼ –0.074; P ¼ 0.44), or total LCBI and LDL-C (Spearman’s rho ¼
–0.061; P ¼ 0.53). For HDL-C, similar results were found (rho ¼ 0.006,
P ¼ 0.95 for maxLCBI4mm; rho ¼ 0.021, P ¼ 0.83 for total LCBI).
Subgroup analyses are presented in Table 1. In none of the different Abstract nos: 578-583
subgroups was any correlation between LDL-C and total LCBI or
maxLCBI4mm found. TCT-578
ACS (n [ 48) CCS (n [ 58) P Value Coronary Artery Catheterization Success Rates Comparing Left
LDL-C (IQR) 129.9 (88.9-159.3) 85.8 (68.8-115.6) <0.001 vs Right Radial Approach in Relation to Age
HDL-C (IQR) 41.0 (37.5-48.0) 40.6 (33.6-52.2) 0.76 Maximilian Will,1 Thomas Weiss,2 Michael Weber,3
MaxLCBI4mm (SD) 366.0 (171.9) 384.1 (160.3) 0.58
Shing Kwok,4 Josip A. Borovac,5 Markus Unterdechler,6
Simone Aufhauser,7 Jim Nolan,8 Julia Mascherbauer,7
Total LCBI (IQR) 61.5 (28.3-103.5) 71.5 (34.5-100.0) 0.56
Konstantin Schwarz9
No Statin (n [ 46) Statin (n [ 62) P Value 1
Department of Internal Medicine 3, Sankt Pölten University Hospital,
LDL-C (IQR) 145.8 (112.5-166.3) 83.5 (66.5-99.4) <0.001 Vienna, Austria; 2Medical School, Sigmund Freud University Vienna,
HDL-C (IQR) 42.2 (37.5-49.1) 40.2 (32.9-48.3) 0.18 Vienna, Austria; 3Karl Landsteiner University of Health Sciences,
Department of General Health Studies, Division Biostatistics and Data
MaxLCBI4mm (SD) 355.7 (165.1) 400.4 (159.1) 0.84
Science, Krems, Austria; 4Royal Stoke Hospital, UHNM, Stoke-on-Trent,
Total LCBI (IQR) 69.0 (28.2-99.8) 65.0 (33.0-101.3) 0.57
United Kingdom; 5University of Split School of Medicine, Split, Croatia;
6
CDL VaSiCS, LIT CPS Lab, Johannes Kepler University Linz, Linz,
CONCLUSION No correlation was found between baseline LDL-C or Austria; 7Department of Internal Medicine 3, Sankt Pölten University
HDL-C and LCBI in this patient group (coronary angiography and NIRS Hospital, St. Pölten, Austria; 8Royal Stoke Hospital, UHNM, Stoke on
for CCS or ACS) with suboptimal cholesterol levels. It is to be inves- Trent, United Kingdom; and the 9Department of Internal Medicine 3,
tigated if LDL-C reduction to minimum levels of current guidelines Sankt Pölten University Hospital, St. Pölten, Austria
influences plaque composition in low-risk lesions.
CATEGORIES IMAGING AND PHYSIOLOGY: Imaging: Intravascular BACKGROUND Old age is associated with the unfolding of intratho-
racic aorta. This may result in increased difficulties navigating cath-
TCT-577 eters from a right radial approach (RRA) compared with a left radial
approach (LRA).
Lipoprotein(a) and Intracoronary Imaging After Intensive Statin
Treatment METHODS We compared coronary angiography success rates of an
Shingo Minatoguchi,1 Keisuke Yasumura,1 Yuliya Vengrenyuk,1 RRA and an LRA according to different age groups.
Joseph Sweeny,2 Parasuram Krishnamoorthy,1 Javed Suleman,1 RESULTS A total of 21,259 coronary angiographies were evaluated.
Pedro Moreno,2 Jagat Narula,3 Samin Sharma,4 Annapoorna Kini5 With increasing age, the first-pass success rate from either radial ac-
1
Mount Sinai Hospitals Group, Inc., New York, New York, USA; 2Mount cess decreased significantly (P < 0.001). In patients <85 years of age,
Sinai Medical Center, New York, New York, USA; 3Mount Sinai Hospital there was no difference between LRA and RRA. However, in patients
Morningside, New York, New York, USA; 4The Mount Sinai Medical 85 years of age, LRA was associated with significantly higher success
Center, Scarsdale, New York, USA; and the 5Icahn School of Medicine, rates compared with RRA (90.1% vs 82.8%; P ¼ 0.003). Patients 85
Mount Sinai Medical Center, New York, New York, USA years of age received less contrast and had shorter fluoroscopy time
when LRA was used: 86.6  41.1 mL vs 99.6  48.7 mL (P < 0.001) and
BACKGROUND Lipoprotein(a) (Lp[a]) has been widely recognized as 4.5  4.1 minutes vs 6.2  5.7 minutes (P < 0.001) for LRA vs RRA,
an independent cardiovascular risk factor associated with increased respectively (mean  SD).
risk of myocardial infarction. Statin therapy results in a significant
increase of Lp(a) plasma levels; however, the effect of the Lp(a) on
plaque progression in stain-treated patients is not clear due to the lack
of imaging studies. This study assessed changes in Lp(a) levels and
plaque morphology using intravascular imaging in patients receiving
high-dose statin therapy.
METHODS Lp(a) was measured in patients with stable coronary artery
disease who underwent percutaneous coronary intervention for a
culprit lesion followed by OCT and IVUS/NIRS imaging of an
obstructive nonculprit lesion (YELLOW II study). All subjects received
40 mg of rosuvastatin for 8 to 12 weeks; the nonculprit lesion was then
reimaged and intervention performed (follow-up). We assessed the
effect of intensive statin therapy on Lp(a) plasma levels and the
relationship between Lp(a) and lesion morphology. Patients were
separated into 2 groups, high and low Lp(a), according to the Lp(a)
levels at baseline with a cutoff of 70 mg/dL.
RESULTS A total of 85 patients were included in the analysis with
mean Lp(a) values of 44.5  51.6 mg/dL, 20.2  17.4, and 118.8  50.3
mg/dL in the low and high Lp(a) groups, respectively. Twenty patients
demonstrated Lp(a) 70 mg/dL at baseline. OCT minimal fibrous cap
thickness (FCT) was significantly thinner in the high Lp(a) group: 84 
32 mm vs 103  44 mm (P ¼ 0.046). After statin treatment, Lp(a)
significantly increased up to 60.4  70.4 mg/dL (P < 0.001), leading to
an additional 6 patients in the high Lp(a) group; however, there was
no difference in FCT (103.0 m m vs 107.2 mm; P ¼ 0.64) in both groups at
follow-up. Furthermore, an increase in Lp(a) after stain therapy was
not an independent predictor of the changes in FCT on multivariate
analysis.