Author + information
- Myong Hwa Yamamoto, MD,
- Akiko Maehara, MD∗ (, )
- Keyvan Karimi Galougahi, MD, PhD,
- Gary S. Mintz, MD,
- Yasir Parviz, MD,
- Sung Sik Kim, MD,
- Kohei Koyama, MD, PhD,
- Kisaki Amemiya, MD,
- Song-Yi Kim, MD,
- Masaru Ishida, MD,
- Monica Losquadro, MS, PA-C,
- Ajay J. Kirtane, MD, SM,
- Elizabeth Haag, RN,
- Fernando A. Sosa, MS,
- Gregg W. Stone, MD,
- Jeffery W. Moses, MD,
- Masahiko Ochiai, MD, PhD,
- Richard A. Shlofmitz, MD and
- Ziad A. Ali, MD, DPhil
- ↵∗Cardiovascular Research Foundation, 1700 Broadway, 9th Floor, New York, New York 10019
Rotational atherectomy (RA) and orbital atherectomy (OA) are designed to ablate calcified plaque, but differences in their mechanisms of action in vivo are not well described (1,2), despite the importance of atherectomy in treating complex coronary artery disease.
This was a retrospective observational study comparing the effects of OA (n = 30) versus RA (n = 30) on severely calcified lesions (maximum calcium angle by OCT >270°) followed by stenting from March 2014 to August 2016 at 3 centers (NewYork-Presbyterian Hospital, New York, New York: n = 6 [RA], n = 6 [OA]; Showa University Northern Yokohama Hospital, Yokohama, Japan: n = 24 [RA]; St. Francis Hospital, Roslyn, New York: n = 24 [OA]). OCT images were acquired with the ILUMIEN OPTIS system (St. Jude Medical, St. Paul, Minnesota) and the Dragonfly Duo or Dragonfly OPTIS imaging catheter (Abbott Vascular, Santa Clara, California) or the Lunawave optical frequency domain imaging system and FastView coronary catheter (Terumo, Tokyo, Japan). OCT was performed pre-intervention (if possible), post-atherectomy (RA or OA), and post-stenting.
Calcium cross-sectional area (CSA) at the maximum calcium ablation site was identified by comparing pre- and post-atherectomy images and measured by manual segmentation. Calcium angle and lumen CSA were measured every 1 mm throughout the calcified plaque in the post-atherectomy image. Calcium modification was identified as a round, concave, polished lumen surface (Figure 1). Noncalcified plaque modification was a round shape of the noncalcified plaque surface post-atherectomy. Stent malapposition (distance between stent strut and lumen surface >0.2 mm), asymmetry index (1 – minimum/maximum stent diameter irrespective of location), and eccentricity index (minimum/maximum stent diameter at same location) were evaluated. Calcium fracture was defined as discontinuity of the luminal surface in the calcified plaque.
Median patient age was 69 (interquartile range [IQR]: 62 to 75) years, 65% were men, and 18% were on hemodialysis; lesions were in the left anterior descending artery in 72%, with angiographic severe calcification in 58% (no difference between OA and RA). Pre-procedural OCT imaging was performed in 33 lesions (18 OA; 15 RA). At the maximum calcium modification site, calcium CSA pre-atherectomy (OA 3.6 [IQR: 3.1 to 5.0] mm2 vs. RA 4.5 [IQR: 3.0 to 6.5] mm2; p = 0.33), post-atherectomy (OA 2.9 [IQR: 2.4 to 4.6] mm2 vs. RA 3.8 [IQR: 2.7 to 5.9] mm2; p = 0.33), and the decrease in calcium CSA from pre- to post-atherectomy (OA 0.56 [IQR: 0.38 to 0.76] mm2 vs. RA 0.60 [IQR: 0.45 to 0.79] mm2; p = 0.49) were not different between devices.
After either OA or RA, calcium and noncalcified plaque modification was colocalized at the site of the OCT imaging catheter. Among all analyzed slices, noncalcified plaque modification post-atherectomy (OA: 1,067 slices; RA: 1,389 slices) was more frequent in the OA group vs. the RA group (16.9% [IQR: 8.4% to 23.8%] vs. 10.0% [IQR: 6.4% to 14.0%] of slices per lesion; p = 0.01). Among slices with any OCT-defined calcium (OA: 912 slices; RA: 1,046 slices), there was a trend toward more post-atherectomy calcium modification after OA versus RA (63.6% [IQR: 43.6% to 71.3%] vs. 51.8% [IQR: 39.9% to 63.3%] of slices per lesion; p = 0.09), particularly at sites with a post-atherectomy lumen CSA >4 mm2 (53.0% [IQR: 43.5% to 76.9%] vs. 35.0% [IQR: 0% to 52.2%] of slices per lesion; p = 0.001), but not ≤4 mm2 (71.4% [IQR: 51.7% to 85.7%] vs. 66.7% [IQR: 50.0% to 85.8%] of slices per lesion; p = 0.81). Calcium modification was greater in slices with a smaller lumen CSA and a larger angle of calcium in both devices (Figure 1).
Comparing OA versus RA, minimum stent CSA (5.3 [IQR: 3.8 to 6.2] mm2 vs. 5.0 [IQR: 4.6 to 6.1] mm2; p = 0.86), stent expansion (67.4% [IQR: 55.0% to 80.5%] vs. 66.7% [IQR: 61.8% to 88.9%]; p = 0.61), asymmetry (0.35 [IQR: 0.26 to 0.41] vs. 0.34 [IQR: 0.24 to 0.34]; p = 0.49), and eccentricity (0.75 [IQR: 0.66 to 0.79] vs. 0.76 [IQR: 0.70 to 0.80]; p = 0.29) were similar. Although malapposition was frequent in both groups (OA: 96.7% vs. RA: 90%; p = 0.61), maximum malapposition CSA was limited (1.5 [IQR: 0.9 to 2.3] mm2 vs. 1.1 [IQR: 0.8 to 1.8] mm2; p = 0.31). Overall, calcium fracture behind stent was frequent (82%), with similar prevalence and length (OA: 4.5 [IQR: 1.9 to 7.9] mm vs. RA: 3.0 [IQR: 1.9 to 5.2] mm; p = 0.38). There was no coronary perforation.
Potentially due to the lack of randomization, patients undergoing OA had vessels with larger diameter (OA: 2.67 [IQR: 2.50 to 3.05] mm vs. RA: 2.49 [IQR: 2.30 to 2.92] mm; p = 0.10) and less severe narrowing (OA: 57.7% [IQR: 49.1% to 66.7%] vs. RA: 66.3% [IQR: 63.5% to 72.6%]; p = 0.004) in pre-procedural quantitative coronary analysis, thus a bias in device selection cannot be excluded.
With both RA and OA, guidewire bias contributes to and directs plaque modification. Compared with RA, OA creates more calcium modification in lesions with larger lumen area as well as more noncalcified plaque modification; the effect in lesions with smaller lumen area is similar between devices. Importantly, final stent expansion was similar after plaque modification with either device.
Please note: Dr. Maehara has received research grant support from Boston Scientific and Abbott Vascular; served as a consultant for Boston Scientific and OCT Medical Imaging; and received speaker fees Abbott Vascular. Dr. Mintz has served as a consultant for and received honoraria from Boston Scientific and ACIST Medical Systems; and received fellowship/grant support from Volcano, Boston Scientific, and InfraReDx. Dr. Kirtane has received institutional research grant support from Medtronic, Boston Scientific, Abbott Vascular, Abiomed, Cardiovascular Systems Inc., CathWorks, Siemens, Philips, ReCor Medical, and Spectranetics. Dr. Stone owns equity in SpectraWave. Dr. Ochiai has served on the Speakers Bureau for Boston Scientific. Mr. Sosa is an employee of Abbott Vascular. Dr. Shlofmitz has served as a speaker for Cardiovascular Systems Inc. Dr. Ali has received institutional research grant support from Abbott Vascular and Cardiovascular Systems Inc.; and served as a consultant for Abbott Vascular, St. Jude Medical, Cardiovascular Systems Inc., and ACIST Medical Systems. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation