Periprocedural Left Main Coronary Artery Dissection — Successful Conservative Management

Periprocedural Left Main Coronary Artery Dissection — Successful Conservative Management
Periprocedural Left Main Coronary Artery Dissection — Successful Conservative Management
Periprocedural Left Main Coronary Artery Dissection — Successful Conservative Management
Periprocedural Left Main Coronary Artery Dissection — Successful Conservative Management

Ravindranath Khandenahally Shankarappa, MD, DM, Arunkumar Panneerselvam, MD,
Manjunath Cholenahally Nanjappa, MD, DM

From the Department of Cardiology, Sri Jayadeva Institute of Cardiology, Bangalore, India.

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

Manuscript submitted December 3, 2008, and accepted February 4, 2009.

Address for correspondence: Prof. Ravindranath Khandenahally Shankarappa, MD, DM, Sri Jayadeva Institute of Cardiology, Jaya Nagar, 9th Block, BG Road, Bangalore 560069, India. E-mail: [email protected]



A retrograde left main coronary artery (LMCA) dissection during left anterior descending (LAD) artery angioplasty, though infrequent, is associated with potentially life-threatening complications including sudden cardiac arrest.1 The options for treatment are dictated by the patient’s stability, the nature of the dissection and the ability to restore coronary circulation with further interventions. In asymptomatic individuals with hemodynamic stability and thrombolysis in myocardial infarction (TIMI) grade 3 flow, a strategy of “watchful waiting” may be appropriate. Here, we present a case of LMCA dissection that was treated successfully with a similar approach.

Case Report. A 65-year-old diabetic and hypertensive male presented with intermittent anginal-type chest pain of 1 day’s duration. He was admitted and treated intensively as a case of Troponin-T negative unstable angina, Braunwald Class III B.2 His coronary angiogram showed a long, calcified, eccentric 90% stenosis in the proximal LAD (Figure 1A), with a normal LMCA and left circumflex coronary artery (LCX). The right coronary artery (RCA) was nondominant with 80% stenosis proximally. The patient was already on aspirin therapy and was preloaded with 300 mgs of clopidogrel.

Percutaneous transluminal coronary angioplasty (PTCA) was performed by using a 7 Fr JL4 guiding catheter and the lesion was crossed with a Hi-torque 0.014 inch floppy guidewire (Abbott Vascular, Santa Clara, California). After dilating the lesion with a 2.0 x 10 mm Sprinter balloon (Medtronic, Inc., Minneapolis, Minnesota) at 14 atm, contrast injection revealed dissection of the proximal LAD, which retrogradely extended up to the LMCA ostium (Figure 1B). There was no evidence of antegrade extension of the dissection in the LAD and TIMI 3 flow was maintained. The balloon used for dilatation was withdrawn into the guiding catheter and no further dilatations were performed. Another guidewire was kept within the guiding catheter, ready to be placed in the LCX. An intra-aortic balloon pump (IABP) was kept on standby and the surgical team was alerted. We kept the option open of stenting the LMCA across the LAD with overlapping stents. Despite the extensive dissection of the LMCA, the patient was asymptomatic, hemodynamically stable and the electrocardiogram showed no signs of ischemia. Hence, a “watchful waiting” strategy was adopted. The patient was monitored intensively on the table for any hemodynamic deterioration, without any further contrast injection. After 20 minutes of observation, contrast injection revealed that the extraluminal cap of contrast in the LMCA had almost disappeared (Figure 2A) and there was TIMI 3 flow in the left coronary system (LCA). A 2.75 x 33 mm Cypher™ stent (Cordis Corp., Miami Lakes, Florida) was deployed at 12 atm across the proximal LAD without including the LMCA. A final postdilatation was performed within the stented segment with a 2.75 x 10 mm balloon at 18 atm. Control angiography performed after stenting showed complete resolution of the coronary dissection and TIMI 3 flow (Figure 2B). At 3-month follow up, the patient was asymptomatic and his stress test was negative for inducible ischemia at 12 METS.

Discussion. Acute dissection of the LMCA during PTCA is an uncommon complication, with an incidence of about 0.05%.3 Such retrograde dissections during PTCA are more common in the RCA than the LCA. The tunica media of the LCA has more spiral smooth muscle cells arranged in concentric layers with abundant elastic fibers making the LCA more resistant to retrograde dissection.

The etiologies of coronary dissection complicating PTCA have been emphasized due to the use of rigid wires, forceful manipulations of guiding catheters, balloon catheters and vigorous contrast medium injections.1 Other factors that predispose patients to dissection include calcification, age > 60 years, hypertension and inflammation. All of the above-mentioned predisposing factors were present in our patient, and the dissection was probably induced by direct intimal injury from balloon dilatation.

Propagation of dissection is enhanced by contrast injection4 and shearing forces of blood flow during systole and diastole.1 In our patient vigorous contrast injection was avoided to prevent extension of the dissection.

LMCA dissection can be potentially life-threatening, and its management depends on the patient’s condition, progression of the dissection and the underlying coronary anatomy.5 When possible, dissections should be treated with stent deployment distal to the dissection and proximal to the ostium, thus sealing off the entry port.6 However, if the above procedure fails or cannot be attempted without significant risk of further compromising the coronary circulation, surgery is indicated. Since our patient was asymptomatic and hemodynamically stable with TIMI grade 3 flow, we opted for a “watchful waiting” strategy. After 20 minutes of observation, the extraluminal cap of contrast in the LMCA almost disappeared. This is probably due to the entry port of dissection being sealed of spontaneously.

The question at this point was, should the LMCA be stented? We decided to stent the LAD lesion and then decide about LMCA stenting. After deployment of the LAD stent, there was no evidence of extraluminal contrast stasis. Because of the patient’s lack of chest pain and signs of ischemia on the ECG and the absence of further contrast stasis, the LMCA was neither stented nor bypass grafted.

Conclusion. Prompt recognition and rapid management are required when acute LMCA dissection occurs. In an asymptomatic, hemodynamically stable patient with TIMI 3 flow in whom the entry port of the dissection is sealed off, LMCA dissection can be managed conservatively without stenting or bypass grafting.

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