Percutaneous coronary intervention (PCI) is increasingly attempted in patients who are of advanced age or have comorbidities that may coincide with excessive coronary artery calcification. Calcified coronary lesions are associated with worse overall outcome [1
]. Therefore, calcium modification is paramount for proper stent deployment to avoid underexpansion and/or malapposition and to mitigate the risk of accelerated neoatherosclerosis, stent thrombosis and the need for reintervention [3
]. Different concepts exist for the modification of coronary calcifications, but formal recommendations are lacking [7
]. Orbital atherectomy (OA) with the Diamondback 360 system (Cardiovascular Systems, Inc., St Paul, MN, USA) features a relatively new approach to calcium modification that was originally introduced to treat calcium in peripheral arterial lesions [8
The orbital atherectomy device (OAD) received U.S. Food and Drug Administration approval in 2013 following the first-in-human ORBIT I [9
] and pivotal ORBIT II [10
] trials, which showed the safety and efficacy of treating de novo heavily calcified coronary lesions. Approvals in Asia and the Middle East followed in 2018 and 2019, respectively, and a CE mark was granted in January 2021. On 2 February 2021, the first patient with calcified coronary artery disease to be treated with an OAD in Europe underwent the procedure at the Erasmus University Medical Center. Herein, we report our initial series of consecutive patients with calcified coronary artery disease who underwent intended invasive imaging-guided, OA-facilitated PCI.
This initial single-center experience with OA to modify calcified coronary lesions confirmed appropriate device and procedural success with a favourable clinical outcome at 30 days of follow-up. OA refines coronary calcium through sanding and fracturing of both superficial and deeper medial calcium. The creation of microparticles < 2 µm and the absence of vessel obstruction during therapy may reduce the risk of a no-reflow phenomenon.
Despite a lack of experience in handling the device, coronary lesions in this series appeared more complex than those reported in the pivotal ORBIT I and II registries. Of all lesions, 95% were type B2/C, while the proportion was 44% and 83% in ORBIT I and II, respectively. All calcified lesions were assessed by invasive intracoronary imaging, revealing a mean arc of 278 degrees, with a maximum of 360 degrees and a mean length of 35 mm, values that not only correlate with severe calcification [7
] but are also predictors for stent underexpansion [16
]. In comparison, in the ORBIT II trial the maximum arc was 295 degrees with a mean calcium length of 29 mm.
A wide armamentarium exists to modify calcified coronary lesions, from plain old balloons to more sophisticated equipment like lasers, lithotripsy, rotational atherectomy (RA) and OA. The goal of these devices is to modify and/or fracture the calcium in order to adequately place a stent. While RA has been available since the late 1980s, OA was not launched in the USA until 2013 and in Europe not until 2021. There are some marked differences between RA and OA. Superficial sanding has become the main mechanism of action of RA, as healthy tissue is able to deflect away from the burr while the calcified plaque cannot do so, resulting in ablation of calcium. This results in smoothening of the luminal surface, without the need for luminal gain. The concept of plaque modification to facilitate balloon angioplasty and stent expansion instead of plaque debulking followed the STRATAS and CARAT trials, which showed more angiographic and clinical complications and more target lesion revascularisations with the use of larger burr sizes (burr/artery ratio > 0.7) [17
]. Because the OAD orbits through the lumen, there is less guidewire bias and potentially more luminal gain as compared to RA. Apart from superficial sanding OAD may fracture more deeply located calcium in the tunica media. Indeed, we observed a sanding effect in 27 of 30 vessels and medial calcium fractures in 19 of 30 vessels. Intravascular lithotripsy (IVL) is another calcium modification technique that can fracture deeper medial calcification, through generation of sonic pressure waves. The safety and efficacy of this technique were proven in the DISRUPT CAD I, II and III trials [19
]. Both RA and OA can be combined with IVL for the treatment of calcified lesions, and both combinations have been described in the literature with good results. From a mechanistic point of view, there seem to be more reasons for combining RA with IVL than for OA with IVL. With RA, deeper medial calcium is not modified but can be treated in addition with IVL. However, due to the orbital nature of the OAD, deeper medial calcium is also modified, which would decrease the need for IVL. In our registry, there was no need for additional treatment with IVL. A particular effect of OA was also seen on calcified nodules that were all abolished, which might be due to less guidewire bias compared to RA. The profound calcium modification resulted in 96% procedural success and < 50% residual stenosis post-stenting in all but one lesion. Coronary perforation and the no-reflow phenomenon did not occur in our series. Our findings echo those of the ORBIT I and II studies, which reported low rates of coronary perforation (2% and 0.9%, respectively) and absence of the no-reflow phenomenon. In a recent retrospective study [22
], coronary perforation was reported to be higher with OA than with RA, which might be due to the orbital nature of the OAD. The particles that arise from superficial sanding are small (< 2 μm) and, combined with the continuous antegrade flow, this leads to less distal embolisation and microvascular obstruction. As a result, there is a lower risk of no-reflow compared to RA, which is characterised by larger microparticles (5–10 μm) and burr-induced flow obstruction during therapy delivery.
In the ORBIT I and II trials, the rate of MACE at 30 days was 6% and 10.4%, respectively. In comparison, we found no major clinical events in our series, although minor cardiac damage was seen in 5 of 19 patients and major cardiac damage was seen in 13 of 19 patients in whom serial biomarkers were available. The randomised ECLIPSE trial (NCT03108456) compares the clinical outcome in patients with severely calcified coronary artery disease treated with an OA-based strategy with those undergoing conventional angioplasty. A total of 2000 patients will be randomised in 114 centres in the United States. The primary endpoint is target vessel failure, defined as a composite of cardiac death, target vessel-related myocardial infarction or ischaemia-driven target vessel revascularisation. A European prospective trial will explore in depth the effect of OA on severely calcified coronary lesions. One hundred patients in six centres in the Netherlands, Germany and Italy will undergo OCT-guided treatment. The primary endpoint will be stent expansion as assessed by OCT-derived minimal stent area, while secondary endpoints will include the number of calcium fractures, final minimal stent area, minimal lumen area post-OA and post-stenting, incidence of dissections and haematomas post-OA.
The findings are based on early experience with OA at a single centre in the Netherlands with possible selection bias. Nevertheless, the coronary lesions were complex and heavily calcified. Moreover, the high device and procedural success in addition to the low complication rate underscored the safe and steep learning curve during the adoption of the OAD technology in our practice. Imaging data were site reported but reported by experienced imagers who were blinded as regards the procedure and the clinical outcome of the patients.