Author + information
- Received August 6, 2015
- Revision received October 8, 2015
- Accepted November 3, 2015
- Published online November 1, 2016.
- Giovanni J. Ughi, PhDa,
- Hao Wang, PhDa,
- Edouard Gerbaud, MDa,
- Joseph A. Gardecki, PhDa,
- Ali M. Fard, PhDa,
- Ehsan Hamidi, PhDa,
- Paulino Vacas-Jacques, PhDa,
- Mireille Rosenberg, PhDa,
- Farouc A. Jaffer, MD, PhDa,b,∗∗ ( and )
- Guillermo J. Tearney, MD, PhDa,c,d,∗ ()
- aWellman Center for Photomedicine, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts
- bCardiovascular Research Center and Cardiology Division, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts
- cDepartment of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
- dHarvard-MIT Health Sciences and Technology, Boston, Massachusetts
- ↵∗Reprint requests and correspondence:
Dr. Guillermo J. Tearney, Massachusetts General Hospital, Wellman Center for Photomedicine, 40 Blossom Street, BHX-604A, Boston, Massachusetts 02114.
- ↵∗∗Dr. Farouc Jaffer, Massachusetts General Hospital, Cardiovascular Research Center, Simches Research Building, Room 3206, 55 Fruit Street, Boston, Massachusetts 02114.
Objectives The authors present the clinical imaging of human coronary arteries in vivo using a multimodality optical coherence tomography (OCT) and near-infrared autofluorescence (NIRAF) intravascular imaging system and catheter.
Background Although intravascular OCT is capable of providing microstructural images of coronary atherosclerotic lesions, it is limited in its capability to ascertain the compositional/molecular features of plaque. A recent study in cadaver coronary plaque showed that endogenous NIRAF is elevated in necrotic core lesions. The combination of these 2 technologies in 1 device may therefore provide synergistic data to aid in the diagnosis of coronary pathology in vivo.
Methods We developed a dual-modality intravascular imaging system and 2.6-F catheter that can simultaneously acquire OCT and NIRAF data from the same location on the artery wall. This technology was used to obtain volumetric OCT-NIRAF images from 12 patients with coronary artery disease undergoing percutaneous coronary intervention. Images were acquired during a brief, nonocclusive 3- to 4-ml/s contrast purge at a speed of 100 frames/s and a pullback rate of 20 or 40 mm/s. OCT-NIRAF data were analyzed to determine the distribution of the NIRAF signal with respect to OCT-delineated plaque morphological features.
Results High-quality intracoronary OCT and NIRAF image data (>50-mm pullback length) were successfully acquired without complication in all patients (17 coronary arteries). The maximum NIRAF signal intensity of each plaque was compared with OCT-defined type, showing a statistically significant difference between plaque types (1-way analysis of variance, p < 0.0001). Interestingly, coronary arterial NIRAF intensity was elevated only focally in plaques with a high-risk morphological phenotype (p < 0.05), including OCT fibroatheroma, plaque rupture, and fibroatheroma associated with in-stent restenosis.
Conclusions This OCT-NIRAF study demonstrates that dual-modality microstructural and fluorescence intracoronary imaging can be safely and effectively conducted in human patients. Our findings show that NIRAF is associated with a high-risk morphological plaque phenotype. The focal distribution of NIRAF in these lesions furthermore suggests that this endogenous imaging biomarker may provide complementary information to that obtained by structural imaging alone.
Massachusetts General Hospital has a patent licensing arrangement with Terumo and Canon Corporations. Dr. Tearney (Terumo, Canon), Dr. Gardecki (Canon), and Dr. Jaffer (Canon) have the right to receive royalties as part of these licensing arrangements. The authors have received financial support from Canon USA (support of new technology advancement in OCT-NIRAF), NIH grant R01HL093717 (to Dr. Tearney for the development of the imaging system and imaging of the first 2 patients), NIH grant R01HL HL122388 (to Dr. Jaffer), AHA Grant-in-Aid 13GRNT1760040 (to Dr. Jaffer), and Bullock-Wellman Fellowship Award, Harvard Medical School (to Dr. Ughi). Dr. Jaffer has received research grants from Merck, Kowa, and Siemens; served as a consultant for Abbott Vascular and Boston Scientific; and has received nonfinancial support from Boston Scientific. Dr. Tearney has received royalties from MIT; has received sponsored research from Canon; and has received catheter components from Terumo. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Jaffer and Tearney are joint senior authors.
- Received August 6, 2015.
- Revision received October 8, 2015.
- Accepted November 3, 2015.
- American College of Cardiology Foundation