Acute Coronary Syndromes Insights from intravascular imaging Robert
Acute Coronary Syndromes. Insights from intravascular imaging. Robert L Wilensky, MD Professor of Medicine Perelman School of Medicine, University of Pennsylvania
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Unstable angina resulting in sudden death
Intravascular imaging modalities Fenning & Wilensky Curr Athero Rep 2014; 16: 397
VH-IVUS: • Axial resolution: approx 250 μm • Lateral resolution: 250 μm. • Advanced processing using spectral analysis of backscatter signals van Velzen JE et al. Heart 2009; 95: 1990
Greater plaque burden is associated with future coronary events. • Non-culprit lesions in ACS associated with recurrent events are more likely to have a plaque burden >70% by VH-IVUS N Engl J Med 2011; 364: 226. • Patients with stable or unstable CAD and a plaque burden >70% are more likely to have future cardiac events JACC Cardiovasc Intervent 2011; 4: 894 • Large plaque burden identifies plaques that develop progressive lumen narrowing by IVUS Circulation 2012; 126: 172.
PROSPECT: Event rates for non-culprit lesions at a median follow-up of 3. 4 years. 49% of events caused by non-TCFAs Stone GW et al. N Engl J Med 2011; 364: 226
VIVA IVUS study: Plaque burden is associated with MACE from non-culprit lesions Calvert PA et al. JACC: Cardiovasc Imag 2011; 4: 894
Near infrared spectroscopy IVUS: • Designed to quantify lipid core • Emits infrared light and collects absorbable spectra over a range of wave lengths.
Higher lipid content is associated with coronary events. • Culprit lesions in ACS are more likely to have a high lipid core than non-culprit lesions (84. 4% vs 52. 8%) Circ Cardiovasc Intervent 2012; 5: 55. • Non-culprit lesions in ACS have a higher lipid core than patients with stable angina Circ Cardiovasc Intervent 2012; 5: 55 • Culprit lesions in STEMI have higher lipid core burden index compared to non-culprit lesions Arterioscler Thromb Vasc Biol 2016; 36: 1010 • Increased LCBI predicts future CV events. Eur Heart J 2017: doi: 10. 1093 d
Lipid burden in culprit segments is greater than in non-culprit segments Sensitivity- 64% Specificity- 85% Madder RD et al. Arterioscler Thromb Vasc Biol. 2016; 36: 1010
Receiver-operating characteristic curves for the discrimination of STEMI culprit segments by NIRS and IVUS. p<0. 001 vs non-culprit segments Madder RD et al. Arterioscler Thromb Vasc Biol. 2016; 36: 1010
Time-to-event for all-cause mortality or non-fatal ACS Median LCBI 43 Oemrawsingh RM et al JACC 2014; 64: 2510
ATHEROREMO/IBIS 3 -NIRS: Lipid core burden index predicts adverse CV outcomes Schuurman et al. Eur Heart J 2018; 39: 295
OCT: • Axial resolution: 10 -20 μm • Measures echo time delay and intensity of reflected or back-scattered light.
OCT images of culprit lesions Plaque rupture Plaque erosion Calcified nodule L Wang et al EHJ CV Imag 2015; 16: 1381
Culprit plaque subtypes causing STEMI Gualiumi G et al JACC Cardiovasc Intv 2014; 958
Thinner fibrous caps are associated with coronary events. • Thinner fibrous caps are more common in MI and ACS patients compared to stable angina patients Circulation 2005; 111: 1551. • Thinner fibrous caps in MI than stable angina culprit lesions (111 ± 65 vs 181 ± 70 μm) Am J Cardiol 2010; 105: 318. • ACS patients at rest have rupture of thinner caps than those that rupture with exertion (50 vs 90 μm) Circulation 2008; 118: 2368.
Distribution of fibrous cap thickness OCT in ACS patients who had plaque rupture. 33% with >70μm cap thickness Tanaka, A. et al. Circulation 2008; 118: 2368
Non-culprit plaque characteristics in patients with ACS caused by plaque erosion vs plaque rupture Sugiyama et al, JAMA Cardio 2018
OCTAVIA: Eroded versus ruptured plaques at the culprit site of STEMI by OCT 140 patients with STEMI Intact fibrous cap: Less lipid rich areas 75% vs 100% in ruptured fibrous cap Intact fibrous cap: higher patency of infarct related artery Intact fibrous cap: lower CPK Saia et al JACC Cardiovasc Imag. 2015; 8: 566
49 year old woman with acute chest pain: SCAD
Characterization of SCAD Entry door type False lumen type Nishiguchi et al EHJ Acute CV care 2016; 5: 263
Comparison of in-vivo and ex-vivo results in ACS patients Wang Kajander Patients studied Saia Guailiumi Higuma Jia STEMI Nishiguchi Yonestu ACS van der Wall Farb Hisaki STEMI SCD ACS Necropsy Plaque rupture 58% 49% 65% 49% 63% 53% 49% 35% 60% 56% Plaque erosion 39% 44% 33% 25% 27% 38% 47% 28% 40% 44% Calcified nodule 8% 7% 0% X 8% 10% X X 0% 0% 0% X X 1. 4% 1. 6% 1% X 4% X X SCAD
Summary l Intravascular imaging has demonstrated that high-risk lesions possess greater plaque burden, larger lipid pools and thinner fibrous caps. l Intravascular imaging has led insights into pathophysiologic mechanisms of ACS: plaque rupture, plaque erosion, calcified nodules and SCAD. l TCFAs and plaque ruptures are also observed in patients with stable disease. l Lesions can be dynamic, making future prediction of clinical events difficult.
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