Usefulness of OCT during coronary intervention Takashi Akasaka, M.D. Department of Cardiovascular Medicine Wakayama, Japan
Predictors at 12 Months of Stent Thrombosis and Target Lesion Revascularization by Multiple Variable Regression Analysis Variable HR (95% CI) P Stent thrombosis Insulin-dependent diabetes 2.76 (1.71, 4.29) <0.0001 Acute coronary syndrome 1.75 (1.13, 2.67) 0.0105 Age (10-year increment) 1.25 (1.05, 1.50) 0.0122 TLR Acute coronary syndrome 2.46 (1.68, 3.53) <0.0001 Diabetes 1.45 (1.02, 2.04) 0.03 Urban et al, One-Year Follow-Up of the e-cypher Registry. Circulation 113:1434-1441, 2006
Assessment of vascular responses following coronary stenting by OCT between ACS and stable AP.
Subjects and Methods Study population Unstable angina pectoris (UAP; n=22) Stable angina pectoris (SAP; n=17) Antiplatelet and anticoagulation therapy Oral aspirin (100 mg) and ticlopidine (200mg) Intravenous heparin (10,000 U/d for 48hrs in UAP) Coronary intervention Sirolimus-eluting stent OCT image Acquisition a 0.016-inch OCT catheter (ImageWire ; LightLab Imaging, Westford, MA, USA)
Stent profiles and OCT findings in UAP and SAP UAP (n=22) SAP (n=17) p SES diameter, mm 3.1±0.4 3.0±0.8 0.61 SES length, mm 21±4.8 22±4.3 0.50 Max. inflation pressure, atm 19±2.1 19±1.9 0.99 Postdilatation, n (%) 12 (55) 10 (59) 0.79 OCT minimum lumen site minimum stent area, mm 2 6.7±1.7 6.6±1.9 0.86 stent eccentricity 0.86±0.05 0.84±0.07 0.13
ACS; 69 y.o. M #6 Cypher 3.5 x 18 mm Pre PCI Post PCI
ACS; 69 y.o. M #6 Cypher 3.5 x 18 mm
Inadequate stent findings
Stent malapposition Tissue protrusion 1mm Inconsistent strut distribution 1mm Stent edge dissection 1mm 1mm
Inadequate stent findings in UAP and SAP 100 (%) P=0.03 P<0.001 80 P=0.76 60 40 P=0.89 20 0 UAP SAP Stent edge dissection UAP SAP Inconsistent strut distribution UAP SAP Stent malapposition UAP SAP Tissue protrusion
Three vessel OCT examinations in a patient with posterior AMI 1 8 7 8 1 2 34 2 5 6 7 3 4 5 6 The culprit lesion was LCX (#11), and TCFA (1), plaque rupture (2,3) and intracoronary thrombus (2, 3, 4) were observed by OCT. Although the plaques in LAD (7, 8) were not observed, plaque rupture (5, 6) were detected by OCT in the non-culprit lesions of LCX (#13).
Three vessel OCT examinations in a patient with posterior AMI 9 10 9 10 11 1213 11 12 13 Also OCT revealed TCFA (9-13) and plaque rupture( 11,12,13) in the non-culprit lesions of RCA.
OCT analysis of the non-culprit plaques Non-culprit plaque AMI (n=43) SAP (n=25) p-value Plaque rupture (n, %) Plaque erosion (n, %) Intracoronary thrombus (n, %) Fibrous cap thickness (μm) Lipid arc > 90 (n, %) TCFA (n, %) 10 (24) 1 (2) 11(26) 109±55.5 18 (42) 15(35) 1 (4) 0 (0) 0 (0) 194±81.9 12 (48) 2 (8) 0.035 0.632 0.006 <0.001 0.623 0.012
Vascular responses following coronary intervention in patients with stable AP assessed by OCT.
Pre PCI CAG Post PCI
CAG before PCI
CAG after PCI
IVUS Pre PCI Post PCI
OCT Pre PCI Post PCI
Directionary coronary atherctomy : DCA
Directionary coronary atherctomy : DCA pre DCA post DCA
OCT findings Eberhard Grube, MD, Siegburg Heart Center
OCT assessment of non-culprit lesion Case. 47year-old male administrated statin. Baseline T.Chol. 200 mg/dl TG 79 mg/dl HDL-C 47 md/dl LDL-C 128 mg/dl
OCT assessment of non-culprit lesion Case. 47year-old male administrated statin. 9 month later T.Chol. 187 mg/dl TG HDL-C LDL-C 133 mg/dl 49 md/dl 98 mg/dl
OCT assessment of non-culprit lesion (47y.o. male) Baseline 9 month later T.Chol. 200 mg/dl TG 79 mg/dl HDL-C 47 mg/dl LDL-C 128 mg/dl T.Chol. 187 mg/dl TG 133 mg/dl HDL-C 49 mg/dl LDL-C 98 mg/dl Lumen Area 6.1 mm 2 EEL Area 12.3 mm 2 Plaque Area 6.2 mm 2 %plaque burden 50% FI Green Area 2.1 mm 2 68% FF Light green Area 0.4 mm 2 12% DC White Area 0.1 mm 2 2% NC Red area 0.6 mm 2 18% 8.0 mm 2 14.4 mm 2 6.4 mm 2 44% 2.5 mm 2 84% 0.3 mm 2 9% 0.1 mm 2 3% 0.1 mm 2 4%
Changes of plaque characteristics by statin Baseline Follow-up p Statin group Fibrous cap thickness (μm) 114±83 162±75 <0.01 Lipid arc (degrees) 132±37 116±23 <0.01 Non-statin group Fibrous cap thickness (μm) 117±78 129±54 ns Lipid arc (degrees) 129±37 128±28 ns
Conclusions OCT may allow us to identify vulnerable plaques before PCI by demonstrating the lipid-rich plaques, thin fibrous cap, rupture (or ulceration) of the fibrous cap, thrombus and macrophage accumulation. OCT can estimate the results of PCIs precisely, including mal-appositions, thin neo-intima formation, thrombus after DES. OCT can assess the pathophysiology of coronary artery atheroscrelosis in detail.