Usefulness of OCT during coronary intervention

Transcription

1 Usefulness of OCT during coronary intervention Takashi Akasaka, M.D. Department of Cardiovascular Medicine Wakayama, Japan

2 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) < Acute coronary syndrome 1.75 (1.13, 2.67) Age (10-year increment) 1.25 (1.05, 1.50) TLR Acute coronary syndrome 2.46 (1.68, 3.53) < Diabetes 1.45 (1.02, 2.04) 0.03 Urban et al, One-Year Follow-Up of the e-cypher Registry. Circulation 113: , 2006

3 Assessment of vascular responses following coronary stenting by OCT between ACS and stable AP.

4 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 inch OCT catheter (ImageWire ; LightLab Imaging, Westford, MA, USA)

5 Stent profiles and OCT findings in UAP and SAP UAP (n=22) SAP (n=17) p SES diameter, mm 3.1± ± SES length, mm 21±4.8 22± Max. inflation pressure, atm 19±2.1 19± Postdilatation, n (%) 12 (55) 10 (59) 0.79 OCT minimum lumen site minimum stent area, mm 2 6.7± ± stent eccentricity 0.86± ±

6 ACS; 69 y.o. M #6 Cypher 3.5 x 18 mm Pre PCI Post PCI

7 ACS; 69 y.o. M #6 Cypher 3.5 x 18 mm

8 Inadequate stent findings

9 Stent malapposition Tissue protrusion 1mm Inconsistent strut distribution 1mm Stent edge dissection 1mm 1mm

10 Inadequate stent findings in UAP and SAP 100 (%) P=0.03 P< P= P= UAP SAP Stent edge dissection UAP SAP Inconsistent strut distribution UAP SAP Stent malapposition UAP SAP Tissue protrusion

11 Three vessel OCT examinations in a patient with posterior AMI 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).

12 Three vessel OCT examinations in a patient with posterior AMI Also OCT revealed TCFA (9-13) and plaque rupture( 11,12,13) in the non-culprit lesions of RCA.

13 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± (42) 15(35) 1 (4) 0 (0) 0 (0) 194± (48) 2 (8) <

14 Vascular responses following coronary intervention in patients with stable AP assessed by OCT.

15 Pre PCI CAG Post PCI

16 CAG before PCI

17 CAG after PCI

18 IVUS Pre PCI Post PCI

19 OCT Pre PCI Post PCI

20 Directionary coronary atherctomy : DCA

21 Directionary coronary atherctomy : DCA pre DCA post DCA

22 OCT findings Eberhard Grube, MD, Siegburg Heart Center

23 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

24 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

25 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 mm mm 2 44% 2.5 mm 2 84% 0.3 mm 2 9% 0.1 mm 2 3% 0.1 mm 2 4%

26 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

27 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.