Breaking the Rules: Use of Rotational Atherectomy in STEMI

Introduction

Rotational atherectomy in a ST-elevation myocardial infarction (STEMI) is generally considered unconventional. Its use in acute coronary syndrome has shown promise¹, however, application of the device in the setting of STEMI has only been described in a handful of case reports.^2,3  The use of rotational atherectomy in a lesion with a visible thrombus is labeled a contraindication by its manufacturer (Rotablator, Boston Scientific) and the associated no-reflow phenomenon is a feared complication. Often in a STEMI, the interventionalist is faced with challenging circumstances that require uncustomary solutions. This case demonstrates the successful use of rotational atherectomy to facilitate dilation and revascularization of the culprit lesion in a patient with STEMI. 

Case report

An 83-year-old woman with a past medical history of hypertension and hyperlipidemia presented with an acute onset of substernal, non-radiating chest pressure that is described as eight out of ten in intensity and lasting five hours since its onset while she was at rest on her porch. The pain is described as non-pleuritic, and not worse with palpation or movement. There is no associated shortness of breath or diaphoresis. She denied tobacco, alcohol, or drug use, and does not have a family history of cardiovascular disease. Home medications include atenolol, simvastatin, lisinopril, amlodipine and hydralazine. She has no known drug allergies.

Upon paramedic arrival, her blood pressure was 120/72, pulse 70, respiratory rate 16, and oxygen saturation of 96 percent on room air. Her electrocardiogram (ECG) demonstrated normal sinus rhythm with premature atrial contractions, normal left axis, 1-2 mm ST-elevation in leads II, III and aVF, 1 mm ST-depression in aVL, Q waves in III and aVF, and delayed R-wave progression in the precordial leads.  Aspirin 162 mg and three doses of nitroglycerin 0.4 mg sublingual spray were administered. En route to the hospital, the patient continued to report chest pressure. In the emergency room, her blood pressure measured 103/62, pulse 86, respiratory rate 16, oxygen saturation 97% on room air, and body mass index was 26. ECG was unchanged from prior. An additional aspirin 162 mg, as well as heparin 4000 units IV, morphine IV, and normal saline IV were administered. The cardiac cath lab was activated. 

Initial labs demonstrated a troponin of 10.9 ng/ml, BNP 516, total cholesterol 93 mg/dL, LDL 47 mg/dL, HDL 36 mg/dL, triglycerides 55 ng/dL, white blood cell count 15.5 per uL, hemoglobin 12 GM/dL, platelets 167 per cmm, sodium 139 mEq/L, potassium 4.1 mEq/L, blood urea nitrogen 28 mg/dL, creatinine 1.2 mg/dL and glucose 124 mg/dL. There was no acute cardiopulmonary disease on chest x-ray.

Emergent cardiac catheterization was performed. Access was obtained through the right femoral artery and a 6 French (Fr) arterial sheath was inserted. Diagnostic coronary angiography demonstrated a heavily calcified lesion in the mid portion of the right coronary artery with 99% stenosis and TIMI-1 flow. The left coronary system demonstrated luminal irregularities with no angiographically significant stenosis. A 6 Fr, 100 cm Judkins R4 guide catheter was used to engage the ostium of the right coronary artery and a .014-inch Balance Middleweight (BMW) universal guide wire (Abbott Vascular) was advanced with difficulty across the complex right coronary artery lesion and positioned in the distal artery. A 1.5 x 15 mm Sprinter Rx balloon (Medtronic) was advanced; however, attempts to pass the lesion were unsuccessful. Additional medications including intravenous (IV) and intracoronary (IC) nitroglycerin, and eptifibatide IC bolus and IV infusion were given without relief.  A second BMW universal guide wire was used as a buddy wire and advanced across the lesion in the right coronary artery. A repeated attempt to advance the balloon across the lesion was unsuccessful. The patient remained hemodynamically stable, but continued to have severe chest pain with radiation to the interscapular region despite TIMI-1 flow. Aortic root angiography was performed and did not demonstrate any angiographic evidence of aortic dissection.  

After the previous failed attempts to dilate the lesion, the decision was made to implement rotational atherectomy. The guide wires and catheter were removed. The 6 Fr arterial sheath was exchanged for a 7 Fr system. The left femoral vein was accessed and a 5 Fr venous sheath was placed. A temporary pacer wire was advanced and positioned in the apex of the right ventricle under fluoroscopic guidance. 

For the rotational atherectomy, an activated clotting time (ACT) was obtained. An additional 4000 units of IV heparin was given to achieve an ACT goal of ≥ 250 seconds. The Judkins R4 guide catheter was used to engage the right coronary artery under fluoroscopic guidance. A floppy RotaWire (Boston Scientific) was used to cross the lesion in the right coronary artery with extreme difficulty. Two runs of rotational atherectomy were performed using a 1.5 mm burr at 150,000 rpm for 15-20 seconds. Coronary angiography demonstrated an opened lumen with TIMI-3 flow. The patient became transiently hypotensive, and responded to dopamine IV and temporary pacing. Repeat angiography did not demonstrate any slow or no reflow. The RotaWire was exchanged over a 3.0 x 12 mm balloon to a Wiggle wire (Abbott Vascular). The balloon was used to dilate the lesion to 12 atms for 20 seconds without difficulty. The lesion was stented with a 4.0 x 18 mm Vision bare metal stent (Abbott Vascular).  Coronary angiography demonstrated no residual stenosis, with continued TIMI-3 flow. The patient was started on aspirin and clopidogrel therapy, and dopamine was titrated off. The patient’s chest pain also resolved.

Transthoracic echocardiogram demonstrated mildly decreased left ventricular systolic function with an ejection fraction of 50-55%, concentric left ventricular hypertrophy, mild mitral valve regurgitation, moderate tricuspid regurgitation, and a dilated right atrium and right ventricle.

Discussion

This case demonstrates successful implementation of percutaneous rotational atherectomy in a patient with a STEMI with ongoing chest pain and a complex calcified culprit lesion. Rotational atherectomy is traditionally avoided in the STEMI patient given the concern for slow or no reflow.⁴ In fact, its use in the setting of a possible thrombus is cautioned against by the manufacturer of the current rotational atherectomy device on the market. However, off-label use is becoming increasingly common.⁵

Previous studies have demonstrated high angiographic success despite increasing lesion complexity.⁶ As the populations ages, coronary lesions are expected to be progressively complex⁷ and may require unconventional solutions. Rotational atherectomy may be considered an alternative option in STEMI when standard balloon angioplasty and intervention are ineffective. Advances in pharmacology and procedural technique contribute to the success of previously shunned interventions. Atherectomy drug cocktails⁸ and glycoprotein IIb/IIIa inhibitor therapy⁹, as well as procedural modifications such as short burr runs¹⁰ and low rotational speed¹¹ contribute to atherectomy success. Herein, we demonstrate efficacious application of rotational atherectomy to achieve angiographic success and symptom relief with the use of rotational atherectomy in a patient with a complex, heavily calcified lesion presenting with a STEMI and ongoing chest pain.

Conclusion

Complex coronary lesions in STEMI patients often require creative, and at times, unconventional, solutions. When standard interventions fail, rotational atherectomy may serve as an alternate option in this challenging patient population.

Disclosure: The authors report no conflicts of interest regarding the content herein. 

This article received a double-blind peer review from members of the Cath Lab Digest Editorial Board.

The authors can be contacted via Ailin Barseghian, MD, at barsegha@uci.edu

References

1. Doshi SN, Kini A, Kim MC, et al. A comparative study of rotational atherectomy in acute and stable coronary syndromes in the modern era. Am J Cardiol. 2003; 92: 1404-1408. 
2. Ho PC. Rotational coronary atherectomy in acute ST-segment elevation myocardial infarction. J Interven Cardiol. 2005; 18: 315-318.
3. Hussain F, Golian M. Desperate times, desperate measures: rotablating dissections in acute myocardial infarction. J Invasive Cardiol. 2011; 23(9): E226-E228.
4. van Gaal WJ, Banning AP. Percutaneous coronary intervention and the no-reflow phenomenon. Expert Rev Cardiovasc Ther. 2007; 5(4): 715-731.
5. Sakakura K, Ako J, Wada H, et al. Comparison of frequency of complications with on-label versus off-label use of rotational atherectomy. Am J Cardiol. 2012; 110: 498-501.
6. Cavusoglu E, Kini AS, Marmur JD, Sharma SK. Current status of rotational atherectomy. Catheter Cardiovasc Interv. 2004; 62: 485-498. 
7. Cohen HA, Williams DO, Homes DR Jr, et al. Impact of age on procedural and 1-year outcomes in percutaneous transluminal coronary angioplasty: a report from the NHLBI dynamic registry. Am Heart J. 2003: 146(3): 513-519.
8. Matsuo H, Watanabe S, Watanabe T, et al. Prevention of no-reflow/slow-flow phenomenon during rotational atherectomy – a prospective randomized study comparing intracoronary continuous infusion of verapamil and nicorandil. Am Heart J. 2007; 154: 994.e1-994.e6.
9. 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. 
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.
11. Reisman M, Shuman BJ, Dillard D, et al. Analysis of low-speed rotational atherectomy for the reduction of platelet aggregation. Cathet Cardiovasc Diagn. 1998; 45: 208-214.