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Complex Case Intervention
Rotational Atherectomy in Coronary Dissection
October 2010
ABSTRACT: Rotational atherectomy is contraindicated in the presence of coronary dissection. Clinical scenarios of coronary dissection in which rotational atherectomy offers the only option are rare but can occur. This case study presents a challenging circumstance of an extensive coronary dissection resulting from failed angioplasty of a resistant and undilatable lesion. Rotational atherectomy was used as a last resort when the patient became clinically unstable. Standard technique of rotational atherectomy and additional technical considerations for this uncommon but potentially devastating scenario are discussed.
J INVASIVE CARDIOL 2010;22:E204–E207
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Editor’s Note: While rotational atherectomy is contraindicated in the presence of extensive dissection (due to fear of flaps wrapping around the rota burr), rare clinical scenarios may dictate its use in the acute setting, as illustrated in this case. Extreme care should be taken to start with the smallest burr (1.25 mm) and with gentle advancement in treating these recalcitrant lesions.
— Samin K. Sharma, MD
Mount Sinai Medical Center, New York, New York
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The package insert for the Rotablator® Rotational Atherectomy System (Boston Scientific, Natick, Massachusetts) lists coronary artery dissection as a contraindication for the use of rotational atherectomy. Because coronary dissection is a potential complication of rotational atherectomy, it can likely propagate existing dissection sites. In the presence of coronary dissection, the package insert suggests conservative management for approximately 4 weeks to permit the dissection to heal prior to treatment with rotational atherectomy. Non-flow-limiting dissection can often be conservatively managed with resolution over time;1 serious complications including abrupt vessel closure due to dissection beyond 24 hours are rare.2,3
In the presence of flow-limiting dissection and patient instability, a concomitant resistant and non-dilatable coronary lesion can be a very difficult clinical and technical conundrum. In this case study, an initial attempt to dilate a resistant stenosis in the middle right coronary artery (RCA) resulted in an extensive but non-flow-limiting coronary dissection. Because the patient was asymptomatic and hemodynamically stable, the strategy was to plan for rotational atherectomy after resolution of the dissection in about 4 weeks as recommended. Unexpectedly, the patient developed recurrent chest pain 3 weeks later; repeat angiography showed impending vessel closure at the site of the dissection with TIMI-1 distal flow. Rotational atherectomy in the setting of extensive coronary dissection was reported in one study4 in which the cause of dissection was also by aggressive high pressure pre-dilatation of a resistant lesion. The authors were able to successfully dilate the lesion after careful rotational atherectomy using one burr. In the current study, a series of upsizing burrs had to be used due to the stubbornly resistant nature of the lesion. This case study highlights the treatment of a very resistant coronary lesion associated with significant iatrogenic dissection and the compulsory technique to gauge rotational atherectomy in this challenging setting. Case Report. A 62-year old male with a history of coronary artery bypass grafting 15 years prior, who had been lost to follow-up, presented with progressive exertional symptoms and a new cardiomyopathy. Echocardiography demonstrated a left ventricular ejection fraction (LVEF) of 20% and significant mitral regurgitation. Cardiac catheterization showed an occluded left anterior descending (LAD) artery with a patent left internal mammary artery (LIMA) to its distal portion. A patent sequential saphenous vein graft (SVG) is present supplying the diagonal branch and the obtuse marginal branch. The native left circumflex (LCX) artery, however, has a middle diffuse and long segment of 90% stenosis leading to a distal and ungrafted obtuse marginal branch. The RCA was not grafted and has a proximal 70–75% lesion with trace-to-mild angiographic calcification. Because of prohibitively high risk of a repeat open-heart operation with coronary artery bypass graft surgery (CABG) + mitral valve replacement (MVR), a decision was made with the patient to first proceed with percutaneous coronary intervention (PCI) of the ungrafted lesions in the LCX and RCA lesions. The need for ICD and/or MVR alone would be assessed in clinical follow up after the PCI. Intravenous heparin and eptifibatide were administered for the interventional procedures. The LCX lesion was successfully treated with 2 sequential Promus™ everolimus-eluting stents (Boston Scientific) with excellent angiographic result. Treatment of the proximal RCA lesion (Figure 1A) began with predilatation using a 3.0 x 12 mm Apex™ balloon (Boston Scientific) showing a significant waist (Figure 1B). A smaller semi-noncompliant balloon, a 2.5 x 8mm Quantum Maverick™ (Boston Scientific), was inflated to 20 atm (2.61 mm in diameter per inflation chart) as an attempt to dilate the resistant lesion while avoiding undue vessel trauma by deliberate undersizing the balloon. Despite high pressure inflation of the semi-noncompliant balloon, a persistent waist from the resistant lesion remained (Figure 1C). Repeat angiography showed an extensive dissection beginning at the site of the lesion extending to the middle RCA and the proximal portion of the acute marginal branch without flow limitation or dye staining (Figure 1D). The patient developed transient chest pain which responded promptly to administration of intracoronary nitroglycerin. The final angiogram of the RCA is shown (Figure 2). The patient’s heart rate and blood pressure were completely stable during the procedure. The patient was observed in the hospital for 2 days and was discharged when there were no recurrent symptoms with ambulation. The plan was to let the coronary dissection heal prior to a staged rotational atherectomy in approximately 4 weeks, while optimal medical therapy was administered including dual antiplatelet and antianginal agents. One week prior to the scheduled staged procedure, the patient returned to the hospital with chest pain and a non-ST elevation myocardial infarction. Repeat angiography showed a persistent dissection in the proximal to middle RCA with impending abrupt vessel closure and TIMI-1 distal flow (Figure 3). The beginning of the dissection was noted to be immediately distal to or at the site of the original lesion in the proximal RCA. An intra-aortic balloon pump and a temporary pacemaker were inserted. Intravenous heparin and eptifibatide were administered. Rotaglide™ lubricant was used. A 7 Fr JR4 guiding catheter was used for support. Because the luminal channel was visible to the operator, a gentle approach with a 0.014″ Choice PT wire (Boston Scientific) to cross the lesion and dissection was initiated. The guidewire transit was without any difficulty and remained in the true lumen of the entire vessel (Figure 4). The guidewire was exchanged for a 0.009″ Rotablator® Floppy wire (Boston Scientific) over a balloon catheter. After releasing wire tension from the burr advancement, rotational atherectomy began using a 1.25 mm burr with gentle forward motion to avoid excessive burr-contact with the dissected segment or forward lurching of the burr. The platform speed was 180,000 rpm and the rotational atherectomy was performed with less than 5,000 rpm rate drop at less than 5 sec of per run. After successful atherectomy, subsequent balloon dilatation with a 2.5 x 8 mm Quantum Maverick at 20 atm failed to show adequate plaque modification and a significant balloon-waist persisted (Figure 5A). The burr was upsized to 1.5 mm and rotational atherectomy using the same technique was performed. The ensuing balloon dilatation again showed a significant residual lesion (Figure 5B). Gradual upsizing of the burr continued to 1.75 mm. Using the same atherectomy technique, the burr passed through the site of the resistant lesion as with the other burrs without excessive atherectomy to the dissected segment. Balloon dilatation with the same balloon at the same inflation pressure finally showed full expansion without residual waist (Figure 5C). There was no abrupt closure or dissection extension of the vessel after the atherectomy; the patient was hemodynamically stable. After further pretreatment with a 2.75 x 20 mm Apex balloon, the resistant lesion along with the dissection were covered with a 2.75 x 32 mm Taxus® Liberte™ (Boston Scientific) paclitaxel-eluting stent. Post-dilatation was performed using a 3.0 x 20 mm Quantum Maverick balloon at 21 atm with an excellent final angiographic result (Figure 6). The patient was stable, asymptomatic and discharged home in a few days. Discussion. Due to the patient’s severe left ventricular dysfunction, severe mitral regurgitation and residual non-bypassed coronary artery disease, a second open-heart operation with combined mitral valve replacement and coronary bypass would carry a prohibitive risk and was not a viable option. An upfront strategy of rotational atherectomy was not chosen due to the baseline severe left ventricular dysfunction and the lack of significant angiographic coronary calcification. Transient regional myocardial dysfunction has been described with rotational coronary atherectomy,5 and may not be well tolerated in patients with little myocardial reserve. Intravascular ultrasound could have added information regarding the degree of calcification. Unless a substantial amount of coronary calcium was present (which was not appreciated by angiography), however, rotational atherectomy would not be first choice as stated. The chosen approach of balloon pre-treatment prior to stent placement was well justified. Unfortunately, extensive coronary dissection associated with the non-dilatable lesion in the proximal RCA occurred, which presented a difficult technical scenario. After the coronary dissection occurred, the initial careful observation approach was also justified. Because the dissection was not associated with flow impairment nor dye staining, it represented as type B in the NHLBI Coronary Dissection Classification.6 Huber et al6 compared NHLBI dissection types (B vs. C–F) showing a significantly lower event rates in the type B patient group. Another study by Cappelletti et al7 demonstrated that in the presence of TIMI 3 flow, coronary dissection is associated with a favorable outcome with spontaneous healing of the dissection in the majority of cases and has less restenosis compared to bare-metal stents. With the contraindication of rotational atherectomy in coronary dissection and the concomitant non-flow-limiting type B dissection, it was hoped that rotational atherectomy could be performed after appropriate healing has occurred. When the patient presented prematurely, repeat angiogram showed that TIMI 3 flow was no longer present and imminent abrupt vessel closure was at hand. Rather than healing, the patient’s coronary dissection had unexpectedly progressed to NHLBI type F and carried a significantly poor prognosis. Because the lesion had failed high-pressure balloon dilatation with a semi-noncompliant balloon, rotational atherectomy was the only remaining option. Excimer laser debulking could have been another option, but it was not available in the laboratory. Minimally-required rotational atherectomy was deemed essential to avoid propagation of the dissection or vessel closure. This would entail the use of the smallest burr, shortest burr time and gentlest burr advancement possible to achieve adequate plaque modification for complete balloon expansion. The standard rotablator technique was employed with a burr speed of 180,000 rpm, a speed drop of less than 5,000 rpm and short burr time (4 In this case study, the coronary dissection was caused by balloon rupture with a resistant lesion, and the authors felt the need to rotablate at the index procedure due to transient vessel closure. The rotational atherectomy technique, however, was not clearly defined; only a 1.5 mm burr was used at the onset at the speed of 100,000 rpm. In this rare technical subset, we encourage the use of the smallest possible burr at the standard recommended high-speed atherectomy technique. Speed dependent platelet activation is inhibited by the administration of glycoprotein IIb/IIIa inhibitor.8 Low-speed rotational atherectomy is less efficient, requires more manual dexterity, may generate larger particles9 and has no clear benefits. Significant deceleration must be avoided because of the potential to cause larger particulate debris, excessive heat generation,10 the risk of slow flow or no-reflow and may be more likely to seize and propagate the dissection flap. The technique described in the current study can help to reduce risks in this difficult and precarious technical situation. In summary, the routine use of rotational atherectomy in the presence of coronary dissection is strongly discouraged, as it remains a contraindication in this clinical setting. As a last resort, this study demonstrates technical strategies that may potentially be helpful in this challenging scenario.
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From the Division of Cardiology, Hawaii Region Kaiser Permanente, Honolulu, Hawaii.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted February 1, 2010, provisional acceptance given February 22, 2010, final version accepted March 1, 2010.
Address for correspondence: Paul C. Ho, MD, MSc, FACC, FSCAI, Chief, Division of Cardiology, Hawaii Region Kaiser Permanente, 3288 Moanalua Road, Honolulu, HI 96819. E-mail: paul.c.ho@kp.org
In the presence of flow-limiting dissection and patient instability, a concomitant resistant and non-dilatable coronary lesion can be a very difficult clinical and technical conundrum. In this case study, an initial attempt to dilate a resistant stenosis in the middle right coronary artery (RCA) resulted in an extensive but non-flow-limiting coronary dissection. Because the patient was asymptomatic and hemodynamically stable, the strategy was to plan for rotational atherectomy after resolution of the dissection in about 4 weeks as recommended. Unexpectedly, the patient developed recurrent chest pain 3 weeks later; repeat angiography showed impending vessel closure at the site of the dissection with TIMI-1 distal flow. Rotational atherectomy in the setting of extensive coronary dissection was reported in one study4 in which the cause of dissection was also by aggressive high pressure pre-dilatation of a resistant lesion. The authors were able to successfully dilate the lesion after careful rotational atherectomy using one burr. In the current study, a series of upsizing burrs had to be used due to the stubbornly resistant nature of the lesion. This case study highlights the treatment of a very resistant coronary lesion associated with significant iatrogenic dissection and the compulsory technique to gauge rotational atherectomy in this challenging setting. Case Report. A 62-year old male with a history of coronary artery bypass grafting 15 years prior, who had been lost to follow-up, presented with progressive exertional symptoms and a new cardiomyopathy. Echocardiography demonstrated a left ventricular ejection fraction (LVEF) of 20% and significant mitral regurgitation. Cardiac catheterization showed an occluded left anterior descending (LAD) artery with a patent left internal mammary artery (LIMA) to its distal portion. A patent sequential saphenous vein graft (SVG) is present supplying the diagonal branch and the obtuse marginal branch. The native left circumflex (LCX) artery, however, has a middle diffuse and long segment of 90% stenosis leading to a distal and ungrafted obtuse marginal branch. The RCA was not grafted and has a proximal 70–75% lesion with trace-to-mild angiographic calcification. Because of prohibitively high risk of a repeat open-heart operation with coronary artery bypass graft surgery (CABG) + mitral valve replacement (MVR), a decision was made with the patient to first proceed with percutaneous coronary intervention (PCI) of the ungrafted lesions in the LCX and RCA lesions. The need for ICD and/or MVR alone would be assessed in clinical follow up after the PCI. Intravenous heparin and eptifibatide were administered for the interventional procedures. The LCX lesion was successfully treated with 2 sequential Promus™ everolimus-eluting stents (Boston Scientific) with excellent angiographic result. Treatment of the proximal RCA lesion (Figure 1A) began with predilatation using a 3.0 x 12 mm Apex™ balloon (Boston Scientific) showing a significant waist (Figure 1B). A smaller semi-noncompliant balloon, a 2.5 x 8mm Quantum Maverick™ (Boston Scientific), was inflated to 20 atm (2.61 mm in diameter per inflation chart) as an attempt to dilate the resistant lesion while avoiding undue vessel trauma by deliberate undersizing the balloon. Despite high pressure inflation of the semi-noncompliant balloon, a persistent waist from the resistant lesion remained (Figure 1C). Repeat angiography showed an extensive dissection beginning at the site of the lesion extending to the middle RCA and the proximal portion of the acute marginal branch without flow limitation or dye staining (Figure 1D). The patient developed transient chest pain which responded promptly to administration of intracoronary nitroglycerin. The final angiogram of the RCA is shown (Figure 2). The patient’s heart rate and blood pressure were completely stable during the procedure. The patient was observed in the hospital for 2 days and was discharged when there were no recurrent symptoms with ambulation. The plan was to let the coronary dissection heal prior to a staged rotational atherectomy in approximately 4 weeks, while optimal medical therapy was administered including dual antiplatelet and antianginal agents. One week prior to the scheduled staged procedure, the patient returned to the hospital with chest pain and a non-ST elevation myocardial infarction. Repeat angiography showed a persistent dissection in the proximal to middle RCA with impending abrupt vessel closure and TIMI-1 distal flow (Figure 3). The beginning of the dissection was noted to be immediately distal to or at the site of the original lesion in the proximal RCA. An intra-aortic balloon pump and a temporary pacemaker were inserted. Intravenous heparin and eptifibatide were administered. Rotaglide™ lubricant was used. A 7 Fr JR4 guiding catheter was used for support. Because the luminal channel was visible to the operator, a gentle approach with a 0.014″ Choice PT wire (Boston Scientific) to cross the lesion and dissection was initiated. The guidewire transit was without any difficulty and remained in the true lumen of the entire vessel (Figure 4). The guidewire was exchanged for a 0.009″ Rotablator® Floppy wire (Boston Scientific) over a balloon catheter. After releasing wire tension from the burr advancement, rotational atherectomy began using a 1.25 mm burr with gentle forward motion to avoid excessive burr-contact with the dissected segment or forward lurching of the burr. The platform speed was 180,000 rpm and the rotational atherectomy was performed with less than 5,000 rpm rate drop at less than 5 sec of per run. After successful atherectomy, subsequent balloon dilatation with a 2.5 x 8 mm Quantum Maverick at 20 atm failed to show adequate plaque modification and a significant balloon-waist persisted (Figure 5A). The burr was upsized to 1.5 mm and rotational atherectomy using the same technique was performed. The ensuing balloon dilatation again showed a significant residual lesion (Figure 5B). Gradual upsizing of the burr continued to 1.75 mm. Using the same atherectomy technique, the burr passed through the site of the resistant lesion as with the other burrs without excessive atherectomy to the dissected segment. Balloon dilatation with the same balloon at the same inflation pressure finally showed full expansion without residual waist (Figure 5C). There was no abrupt closure or dissection extension of the vessel after the atherectomy; the patient was hemodynamically stable. After further pretreatment with a 2.75 x 20 mm Apex balloon, the resistant lesion along with the dissection were covered with a 2.75 x 32 mm Taxus® Liberte™ (Boston Scientific) paclitaxel-eluting stent. Post-dilatation was performed using a 3.0 x 20 mm Quantum Maverick balloon at 21 atm with an excellent final angiographic result (Figure 6). The patient was stable, asymptomatic and discharged home in a few days. Discussion. Due to the patient’s severe left ventricular dysfunction, severe mitral regurgitation and residual non-bypassed coronary artery disease, a second open-heart operation with combined mitral valve replacement and coronary bypass would carry a prohibitive risk and was not a viable option. An upfront strategy of rotational atherectomy was not chosen due to the baseline severe left ventricular dysfunction and the lack of significant angiographic coronary calcification. Transient regional myocardial dysfunction has been described with rotational coronary atherectomy,5 and may not be well tolerated in patients with little myocardial reserve. Intravascular ultrasound could have added information regarding the degree of calcification. Unless a substantial amount of coronary calcium was present (which was not appreciated by angiography), however, rotational atherectomy would not be first choice as stated. The chosen approach of balloon pre-treatment prior to stent placement was well justified. Unfortunately, extensive coronary dissection associated with the non-dilatable lesion in the proximal RCA occurred, which presented a difficult technical scenario. After the coronary dissection occurred, the initial careful observation approach was also justified. Because the dissection was not associated with flow impairment nor dye staining, it represented as type B in the NHLBI Coronary Dissection Classification.6 Huber et al6 compared NHLBI dissection types (B vs. C–F) showing a significantly lower event rates in the type B patient group. Another study by Cappelletti et al7 demonstrated that in the presence of TIMI 3 flow, coronary dissection is associated with a favorable outcome with spontaneous healing of the dissection in the majority of cases and has less restenosis compared to bare-metal stents. With the contraindication of rotational atherectomy in coronary dissection and the concomitant non-flow-limiting type B dissection, it was hoped that rotational atherectomy could be performed after appropriate healing has occurred. When the patient presented prematurely, repeat angiogram showed that TIMI 3 flow was no longer present and imminent abrupt vessel closure was at hand. Rather than healing, the patient’s coronary dissection had unexpectedly progressed to NHLBI type F and carried a significantly poor prognosis. Because the lesion had failed high-pressure balloon dilatation with a semi-noncompliant balloon, rotational atherectomy was the only remaining option. Excimer laser debulking could have been another option, but it was not available in the laboratory. Minimally-required rotational atherectomy was deemed essential to avoid propagation of the dissection or vessel closure. This would entail the use of the smallest burr, shortest burr time and gentlest burr advancement possible to achieve adequate plaque modification for complete balloon expansion. The standard rotablator technique was employed with a burr speed of 180,000 rpm, a speed drop of less than 5,000 rpm and short burr time (4 In this case study, the coronary dissection was caused by balloon rupture with a resistant lesion, and the authors felt the need to rotablate at the index procedure due to transient vessel closure. The rotational atherectomy technique, however, was not clearly defined; only a 1.5 mm burr was used at the onset at the speed of 100,000 rpm. In this rare technical subset, we encourage the use of the smallest possible burr at the standard recommended high-speed atherectomy technique. Speed dependent platelet activation is inhibited by the administration of glycoprotein IIb/IIIa inhibitor.8 Low-speed rotational atherectomy is less efficient, requires more manual dexterity, may generate larger particles9 and has no clear benefits. Significant deceleration must be avoided because of the potential to cause larger particulate debris, excessive heat generation,10 the risk of slow flow or no-reflow and may be more likely to seize and propagate the dissection flap. The technique described in the current study can help to reduce risks in this difficult and precarious technical situation. In summary, the routine use of rotational atherectomy in the presence of coronary dissection is strongly discouraged, as it remains a contraindication in this clinical setting. As a last resort, this study demonstrates technical strategies that may potentially be helpful in this challenging scenario.
References
1. Lincoff AM, Topol EJ, Chapekis AT, et al. Intracoronary stenting compared with conventional therapy for abrupt vessel closure complicating coronary angioplasty: A matched case-control study. J Am Coll Cardiol 1993;21:866–875. 2. de Feyter PJ, van den Brand M, Laarman GJ, et al. Acute coronary artery occlusion during and after percutaneous transluminal coronary angioplasty. Frequency, prediction, clinical course, management, and follow-up. Circulation 1991;83:927–936. 3. Simpfendorfer C, Belardi J, Bellamy G, et al. Frequency, management and follow-up of patients with acute coronary occlusions after percutaneous transluminal coronary angioplasty. Am J Cardiol 1987;59:267–269. 4. Pedersen WR, Goldenberg IF, Johnson RK, Mooney MR. Successful rotational atherectomy in the setting of extensive coronary dissection: A case of failed balloon angioplasty in a nondilatable calcified lesion complicated by balloon rupture and extensive dissection. Cathet Cardiovasc Intervent 2003;59:329–332. 5. Williams MJ, Dow CJ, Newell JB, et al. Prevalence and timing of regional myocardial dysfunction after rotational coronary atherectomy. J Am Coll Cardiol 1996;28:861–869. 6. Huber MS, Mooney JF, Madison J, Mooney MR. Use of a morphologic classification to predict clinical outcome after dissection from coronary angioplasty. Am J Cardiol 1991;68:467–471. 7. Cappelletti A, Margonato A, Rosano G, et al. Unstented nonocclusive coronary dissection after coronary angioplasty. J Am Coll Cardiol 1999;34:1484–1488. 8. Williams MS, Coller BS, Vaananen HJ, et al. Activation of platelets in platelet-rich plasma by rotablation is speed-dependent and can be inhibited by abciximab (c7E3 Fab; ReoPro). Circulation 1998;98(8):742–748. 9. Reisman M, DeVore LJ, Ferguson M. Analysis of heat generation during high-speed rotational ablation: Technical implications. J Am Coll Cardiol 1996;27:292A. 10. Reisman M, Shuman BJ, Harms V. Analysis of heat generation during rotational atherectomy using different operational techniques. Cathet Cardiovasc Diagn 1998;44:453–455.
