Incidence of Bradycardia and Outcomes of Patients Who Underwent Orbital Atherectomy Without a Temporary Pacemaker

Abstract: Objective. We analyzed the incidence of bradycardia and the safety of patients with severely calcified coronary lesions who underwent orbital atherectomy without the insertion of a temporary pacemaker. Background. The presence of severely calcified coronary lesions can increase the complexity of percutaneous coronary intervention due to the difficulty in advancing and optimally expanding the stent. High-pressure inflations to predilate calcified lesions may cause angiographic complications like perforation and dissection. Suboptimal stent expansion is associated with stent thrombosis and restenosis. Orbital atherectomy safely and effectively modifies calcified plaque to facilitate optimal stent expansion. The incidence of bradycardia in orbital atherectomy is unknown. Methods. Fifty consecutive patients underwent orbital atherectomy from February 2014 to September 2016 at our institution, none of whom underwent insertion of a temporary pacemaker. The final analysis included 47 patients in this retrospective study as 3 patients were excluded because of permanent pacemaker implantation. The primary endpoint was significant bradycardia, defined as bradycardia requiring emergent pacemaker placement or a heart rate <50 bpm at the end of atherectomy. Results. The primary endpoint occurred in 4% of all patients, all driven by patients who experienced a heart rate decreasing to <50 bpm. The major adverse cardiac and cerebral event rate was 6%, driven by death (2%) and myocardial infarction (4%). No patient experienced target-vessel revascularization, stroke, or stent thrombosis. Angiographic complications included perforation in 2%, slow-flow in 4%, and flow-limiting dissection in 0%. Conclusion. Significant bradycardia was uncommon during orbital atherectomy. Performing orbital atherectomy without a temporary pacemaker appears to be safe. 

J INVASIVE CARDIOL 2017;29(2):59-62

Key words: orbital atherectomy, calcification, percutaneous coronary intervention, bradycardia

Coronary artery calcification (CAC) represents an advanced form of atherosclerosis.¹ The complexity of percutaneous coronary intervention (PCI) is higher when CAC is present due to the difficulty in advancing stents and achieving optimal stent expansion, which may explain the lower rates of procedural success and higher rates of angiographic and ischemic complications.^2,3 

Rotational atherectomy has been used for almost 30 years to treat severe CAC.⁴ Although the ROTAXUS (Rotational Atherectomy Prior to Taxus Stent Treatment for Complex Native Coronary Artery Disease) trial demonstrated greater strategic success and short-term lumen gain with rotational atherectomy, surveillance angiography at 9 months revealed an increase in late lumen loss and no difference in major adverse cardiac events.⁵ Heart block and bradycardia are well-recognized complications of rotational atherectomy, especially with right coronary artery lesions. A temporary pacemaker can be placed prophylactically to prevent severe bradycardia during atherectomy. 

The ORBIT II trial, which was a prospective, multicenter, single-arm trial that enrolled 443 patients with severely calcified lesions to undergo pre-stent lesion preparation using orbital atherectomy, demonstrated the safety and efficacy of this system at 30 days, as well as at 1-year, 2-year, and 3-year follow-up.^6-9 After Food and Drug Administration approval in 2013, orbital atherectomy supplanted rotational atherectomy as the treatment of choice for the modification of severely calcified plaque at our institution, because it is operator-friendly, has good clinical data, and offers mechanistic advantages. The incidence of bradycardia with orbital atherectomy is unknown, and the instructions for use state that a temporary pacing lead may be necessary when treating lesions in the right coronary and circumflex arteries due to the possible occurrence of electrophysiological alternations.¹⁰ This retrospective study evaluated the incidence of significant bradycardia and the feasibility and safety of performing orbital atherectomy without a temporary pacemaker. 

Methods

Study population. A total of 50 patients underwent orbital atherectomy (Cardiovascular Systems, Inc [CSI]) at the UCLA Medical Center in Los Angeles, California from February 2015 to September 2016. The final analysis included 47 patients, because 3 patients with a history of permanent pacemaker implantation were excluded from this study. Patients were included in this analysis if they had heavily calcified coronary lesions, a reference vessel diameter ≥2.5 mm and ≤5.0 mm, and a stenosis of ≥70% or fractional flow reserve assessment ≤0.80 for intermediate coronary artery stenosis. Severe CAC was defined by visualization of radioopacities on fluoroscopy involving both sides of the arterial wall or intravascular ultrasound (IVUS) revealing ≥270° of CAC. The Institutional Review Board approved the review of the data. 

Device description, procedural technique, and medical treatment. The mechanism of action of orbital atherectomy is differential sanding, in which an eccentrically mounted 1.25 mm crown coated with 30 micron diamonds modifies calcified plaque while the healthy elastic tissue flexes away, minimizing damage to the vessel. The crown rotates and expands laterally due to centrifugal force, resulting in 360° crown contact of the calcified vessel in an elliptical motion. The 0.012˝ stainless-steel ViperWire (CSI), which has a silicone coating, was advanced across the lesion in the majority of cases. If the ViperWire could not traverse the lesion easily, a workhorse wire was used followed by switching out with a ViperWire through an exchange catheter. The ViperSlide lubricant (CSI) reduces friction between the drive shaft and the ViperWire, allowing the device to advance easily. 

Low-speed (80,000 rpm) atherectomy was initially performed in all patients. It was the discretion of the operator to perform high-speed (120,000 rpm) atherectomy if the reference vessel diameter was ≥3 mm. The duration of each pass was limited to ≤20 seconds. Upon completion of orbital atherectomy, standard PCI techniques were used through a 6 Fr guiding catheter. Drug-eluting stents were used unless the patient was unable to continue dual-antiplatelet therapy for at least 1 year.

Dual-antiplatelet therapy was initiated prior to PCI. Weight-based unfractionated heparin was administered intraarterially to maintain an activated clotting time >250 seconds. Atropine and phenylephrine were readily available for emergent administration. Dual-antiplatelet therapy was recommended for at least 1 month for bare-metal stent and 1 year for drug-eluting stent implantation. 

Study endpoints and clinical follow-up. The primary endpoint was significant bradycardia, defined as bradycardia requiring emergent temporary pacemaker placement or a heart rate <50 bpm at the end of atherectomy. Major adverse cardiac and cerebral events were defined as the composite of death, myocardial infarction, target-vessel revascularization, and stroke. Myocardial infarction was defined as ischemic symptoms with the development of new ST-segment elevation or elevation of cardiac biomarkers to at least twice the upper limit of normal. Target-vessel revascularization was defined as a repeat revascularization of the target vessel due to restenosis or thrombosis. The Academic Research Consortium definition of stent thrombosis was used.¹¹ Demographic, angiographic, and procedural data, as well as clinical outcomes, were collected from medical records and entered into a dedicated PCI database.

Statistical analysis. Continuous variables are presented as mean ± standard deviation. Categorical variables are presented as percentages. All data were analyzed with SPSS, version 20.0 (SPSS-PC). 

Results

Baseline demographic and procedural characteristics. The mean patient age was 62 ± 12 years, and 36% of patients had diabetes mellitus (Table 1). Unfractionated heparin was used in all cases (Table 2). High-speed atherectomy was used in 72% of patients. The mean number of runs per case was 3.3 ± 1.3. Orbital atherectomy was performed on the left anterior descending artery in 66%, right coronary artery in 30%, and unprotected left main coronary artery in 13%.

Clinical outcomes at 30 days. The primary endpoint occurred in 4%, all driven by patients who experienced a heart rate <50 bpm after atherectomy (Table 3). The heart rhythm was sinus bradycardia in both patients without atrioventricular conduction disturbance. However, both patients promptly responded to atropine with immediate restoration of electrical stability without clinical sequelae. No patients required emergent temporary pacemaker placement. The major adverse cardiac and cerebral event rate was 6%, driven by death (2%) and myocardial infarction (4%). No patient experienced target-vessel revascularization, stroke, or stent thrombosis. Perforation occurred in 2%, and 4% had slow-flow with resolution after administration of intracoronary nitroglycerin. Flow-limiting dissection did not occur.

Discussion

In our initial experience, significant bradycardia was uncommon during orbital atherectomy. Orbital atherectomy can be performed safely without the prophylactic placement of a temporary pacemaker as long as atropine is immediately available to treat significant bradycardia if it occurs. 

The exact mechanism of bradycardia with rotational atherectomy is unknown, but may be due to a vagal response or localized release of adenosine.¹² Orbital atherectomy may be associated with less bradycardia compared with rotational atherectomy because of the different mechanism of action. The eccentrically mounted crown rotates and orbits in an elliptical motion, allowing blood to continuously flow and particles to flush during atherectomy, which may decrease the incidence of bradycardia. Constant flushing of saline during ablation minimizes thermal injury, which may also decrease the incidence of bradycardia.

Orbital atherectomy without prophylactic placement of a temporary pacemaker should only be performed if the operator has heightened awareness and is anticipating bradycardia. The operator should be adequately and immediately prepared to treat bradycardia if it occurs.

When orbital atherectomy is activated, the nurse is asked to be on standby near the patient to administer atropine immediately if bradycardia occurs. The nurse also has phenylephrine immediately available to administer if the patient develops hypotension. Asking the patient to cough violently while bradycardic may help increase blood pressure to avoid hemodynamic collapse. 

Techniques that may minimize the incidence of bradycardia include slow advancement of the crown (1 mm/second) without aggressively pushing the advancer knob, retracting the crown if resistance is encountered, and restricting each pass to a short duration (≤20 seconds). All cases were started at low speed regardless of the size of the reference vessel diameter. Atherectomy was performed at high speed only if the reference vessel diameter was at least 3 mm and the calcified plaque was adequately modified at low speed. Evidence that low-speed atherectomy was sufficient included using the concept of “look, listen, and feel.” Atherectomy was escalated from low speed to high speed if the crown advanced easily at 1 mm/second while visualizing under fluoroscopy and high-pitched tone that was initially heard when the crown engaged the lesion decreased to a low-pitched tone at a lower volume, and the resistance encountered during the pass was lower. If the lesion length is long and diffuse, the initial pass does not necessarily need to completely traverse the calcified lesion. If the patient experiences any changes in clinical status like chest discomfort, ischemic electrocardiographic changes, bradycardia, hypotension, or slow-flow/no-reflow, the operator should wait until they resolve before atherectomy is performed again. 

Clinical judgment should be used to identify patients who are at risk for significant bradycardia and would benefit from the prophylactic placement of a temporary pacemaker. A temporary pacemaker may be indicated in patients with low resting heart rates, high-degree atrioventricular conduction disease, and long, diffuse, calcified lesions particularly involving the proximal right coronary artery or dominant left circumflex artery. However, if a temporary pacemaker is not prophylactically placed, a 5 Fr sheath, pacemaker generator, and temporary pacemaker wire should be readily available in case the patient develops significant bradycardia that is refractory to atropine. 

In an era where cost containment is emphasized, a strategy of performing orbital atherectomy without the prophylactic placement of a temporary pacemaker has cost-saving implications. This strategy also avoids the potential complications associated with venous access and the risk of right ventricular perforation from the pacemaker catheter. 

Study limitations. This was a small, non-randomized, retrospective analysis conducted at a single center. The follow-up was limited to only 30 days. Periprocedural myocardial infarction was likely underdiagnosed, as cardiac biomarkers were not routinely measured after PCI.

Conclusion

Bradycardia is an uncommon complication during orbital atherectomy. Performing orbital atherectomy without the prophylactic placement of a temporary pacemaker appears to be safe as long as atropine is immediately available to administer if bradycardia develops. Clinical judgment, optimal technique, heightened vigilance, anticipation, adequate preparation, and immediate response with atropine if bradycardia develops can minimize and sufficiently deal with this complication. Larger studies are needed to confirm our results.

References

1.     Vliegenthart R, Oudkerk M, Hofman A, et al. Coronary calcification improves cardiovascular risk prediction in the elderly. Circulation. 2005;112:572-577.

2.     Lee MS, Shah N. The impact and pathophysiologic consequences of coronary artery calcium deposition in percutaneous coronary interventions. J Invasive Cardiol. 2016;28:160-167.

3.     Lee MS, Yang T, Lasala J, Cox D. Impact of coronary artery calcification in percutaneous coronary intervention with paclitaxel-eluting stents: two-year clinical outcomes of paclitaxel-eluting stents in patients from the ARRIVE program. Catheter Cardiovasc Interv. 2016;88:891-897.

4.     Ritchie JL, Hansen DD, Intlekofer MJ, Hall M, Auth DC. Rotational approaches to atherectomy and thrombectomy. Z Kardiol. 1987;76(Suppl 6):59-65.

5.     Abdel-Wahab M, Richardt G, Joachim Buttner H, et al. High-speed rotational atherectomy before paclitaxel-eluting stent implantation in complex calcified coronary lesions: the randomized ROTAXUS (Rotational Atherectomy Prior to Taxus Stent Treatment for Complex Native Coronary Artery Disease) trial. JACC Cardiovasc Interv. 2013;6:10-19.

6.     Chambers JW, Feldman RL, Himmelstein SI, et al. Pivotal trial to evaluate the safety and efficacy of the orbital atherectomy system in treating de novo, severely calcified coronary lesions (ORBIT II). JACC Cardiovasc Interv. 2014;7:510-518.

7.     Généreux P, Lee AC, Kim CY, et al. Orbital atherectomy for treating de novo severely calcified coronary narrowing (1-year results from the pivotal ORBIT II trial). Am J Cardiol. 2015;115:1685-1690.

8.     Généreux P, Bettinger N, Redfors B, et al. Two-year outcomes after treatment of severely calcified coronary lesions with the orbital atherectomy system and the impact of stent types: insights from the ORBIT II trial. Catheter Cardiovasc Interv. 2016;88:369-377.

9.     Chambers JW. ORBIT II final 3-year data. Presented on May 5, 2016. SCAI 2016 Scientific Sessions, Orlando, Florida.

10.    https://mastercontrol.csi360.com/mastercontrol/Main/MASTERControl/vault/view_doc.cfm?ls_id=KKYZNN7JBRHLFEFNBU

11.     Cutlip DE, Windecker S, Mehran R, et al; Academic Research Consortium. Clinical end points in coronary stent trials: a case for standardized definitions. Circulation. 2007;115:2344-2351.

12.     Braden GA, Bailey RJ, Fitzgerald DM, Young T, Utley L, Applegate RJ. Mechanism of bradyarrhythmias associated with rotational atherectomy. J Am Coll Cardiol. 1996;27:168.

From the ¹Division of Interventional Cardiology, UCLA Medical Center, Los Angeles, California; and ²Division of Cardiology, St. Francis Hospital, Roslyn, New York.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Lee and Dr Shlofmitz report honoraria from CSI. Dr Nguyen reports no disclosures regarding the content herein.

Manuscript submitted October 26, 2016, final version accepted November 2, 2016.

Address for correspondence: Michael S. Lee, MD, 100 Medical Plaza, Suite 630, Los Angeles, CA  90095. Email: mslee@mednet.ucla.edu