1. Should we Use OCT in STEMI Patients?
Marco A. Costa, MD, PhD, FACC, FSCAI
Professor of Medicine, Director of Invasive Services
Director Center for Research and Innovation

2. Conflict of Interest: Consultant: St Jude Medical
Marco A. Costa, MD, PhD
Conflict of Interest:
Consultant: St Jude Medical

3. Brief overview of Pathology of ACS
Basics of Optical Coherence Tomography
OCT Plaque Imaging
Review of Clinical OCT Data (ACS, TCFA)
Clinical Cases

4. ATHEROSCLEROSIS A Generalized and Progressive Process
Athero- sclerotic plaque
Plaque rupture/ fissure
Fatty streak
Fibrous plaque
Normal
Increasing Age
Thrombosis
Atherosclerosis
Note: Plavix® (clopidogrel) is not indicated for all the conditions listed on this slide.
Vascular disease is the common underlying disease process for MI, ischemia and vascular death.
Acute coronary syndrome (ACS) is a classic example of the progression of vascular disease to an ischemic event.
ACS (in common with ischemic stroke and critical leg ischemia) is typically caused by rupture or erosion of an atherosclerotic plaque followed by formation of a platelet-rich thrombus.
Atherosclerosis is an ongoing process affecting mainly large and medium-sized arteries, which can begin in childhood and progress throughout a person’s lifetime.
Stable atherosclerotic plaques may encroach on the lumen of the artery and cause chronic ischemia, resulting in (stable) angina pectoris or intermittent claudication, depending on the vascular bed affected.
Unstable atherosclerotic plaques may rupture, leading to the formation of a platelet-rich thrombus that partially or completely occludes the artery and causes acute ischemic symptoms.
Unstable angina MI
Sudden Death
Stable angina
Heart Failure

5. Characteristics of Unstable and Stable Plaque
Lack of inflammatory cells
Inflammatory cells
Thin fibrous cap
Thick fibrous cap
Few SMCs
More SMCs
Atherosclerotic plaques have 2 main components—a soft lipid-rich core and a hard collagen-rich fibrous cap.1
In stable plaques, a thick fibrous cap may represent >70% of plaque volume. It stabilizes the plaque and prevents it from undergoing rupture.1
In contrast, unstable plaques have a thin fibrous cap and are at greater risk for rupture. In unstable plaques, the lipid-rich core may represent the majority of the plaque volume.1
Falk reviewed the work of other investigators regarding severity of stenosis and its association with the risk of MI. Results showed that >86% of MIs resulted from lesions that were <70% stenosed.1 Most experts prior to Falk thought that patients had heart attacks because of blockages that increased in size until they eventually blocked the blood vessel and caused a heart attack.
Based on the findings by Falk, we now know the primary cause of heart attacks is the rupture of unstable plaques that are <70% stenosed and are clinically silent. Approximately 200 patients from 4 studies were used to generate these results, which have been confirmed in other studies.
Intact endothelium
Eroded endothelium
Activated macrophages
Foam cells
Libby P. Circulation. 1995;91:
References
1 Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995;92:
2 Libby P. Molecular bases of the acute coronary syndromes. Circulation. 1995;91:

6. Brief overview of Pathology of ACS
Basics of Optical Coherence Tomography
OCT Plaque Imaging
Review of Clinical OCT Data (ACS, TCFA)
Clinical Cases
OCT Evaluation of DES in STEMI

7. OCT: 1st Translational Imaging Modality
A Cardiologist View of the Pathology Data
OCT: 1st Translational Imaging Modality
OCT creates images similar to ultrasound but uses light
Adopted from Bouma, B., Tearney, G. Handbook of Optical Coherence Tomography

8. Blood, not a minor detail

9. Brief overview of Pathology of ACS
Basics of Optical Coherence Tomography
OCT Plaque Imaging
Review of Clinical OCT Data (ACS, TCFA)
Clinical Cases
OCT Evaluation of DES in STEMI

10. OCT – histology data collection ROI mapping / measurement
Pressure-fixed cadaver hearts
Arteries
Histology sections
ROI mapping / measurement
Number completed 28
137
307
293
Chenyang Xu, Joseph M. Schmitt, Stephane G. Carlier, Renu Virmani. Characterization of atherosclerosis plaques by measuring both backscattering and attenuation coefficients in optical coherence tomography. Journal of Biomedical Optics 13 (3), 2008, p

11. We can use OCT to assess plaques OCT – Histology correlation
Fibrotic plaque
Predominantly calcified plaque
Lipid rich plaque

12. Macrophage quantification
(Circulation. 2003;107: )
Normal standard deviation(NDS) of signal intensity
~High NSD correlated with macrophage conc.
28w APOE-/-
0.5mm
62.5 by 62.5 um window for mouse

13. Macrophages Under OCT
Mac-3
OCT HE

14. Clinical Validation vs Others
OCT
(n=30) AS
(n=30)
IVUS
(n=30)
Finding p
Fibrous cap disruption
73% *†
47%
40%
0.021
Fibrous cap erosion
23% *† 3% 0%
0.003
100% †
Thrombus
100% ‡
33%
< 0.001
* OCT vs AS, p< †OCT vs IVUS, p< ‡ AS vs IVUS, p<0.01.
OCT was able to visualize intracoronary findings better than IVUS/Angioscopy
Kubo, et al. J Am Coll Card 2007; 50: 933

15. 3D view
En face view
Red:
TCFA
Green: 65µm<Fibrous cap <150µm
Fly-through view
Blue:
fibrous cap >150µm

16. How we use OCT Clinically Total Graft Occlusion

17. Thrombectomy

18. Post thrombectomy

19. Post thrombectomy
Distal MLA
Thrombus site
Proximal lipid rich plaque

20. Post Stent Implantation

21. Malapposition

22. Post dilatation of distal stent

23. Not all STEMI have Ruptured Plaque

24. Not all STEMI have Ruptured Plaque

25. Non Obstructire Thin-Cap Fibroatheroma

26. Should we Use OCT in STEMI Patients?
YES, we should always use OCT unless….
Understanding of the mechanism/cause of vessel occlusion
Better definition of the culprit segment
Optimal stent deployment (sizing, dissection, geographical miss)
….are not relevant to your PCI practice