Abstract: A 53-year-old man with stable angina had a staged percutaneous coronary intervention to a critical focal stenosis of the mid-segment of the right coronary artery (RCA). Two hours after successful RCA stent implantation, the patient re-presented with inferior ST elevation secondary to acute dissection originating at the distal edge of the stent, causing subtotal occlusion of the distal RCA. The patient had TIMI-2 flow in the posterolateral branch and occlusion of the posterior descending artery. This case describes the procedural challenges the operators were faced with and successful use of the “rescue STAR” technique as a last resort.
J INVASIVE CARDIOL 2015;27(1):E13-E15
Key words: drug-eluting stent, coronary dissection, management, acute coronary syndrome, ST elevation
A 53-year-old male with a background of hypertension, dyslipidemia, ex-smoker, and non-critical bilateral carotid artery stenosis underwent elective angiography for a staged revascularization of a significant mid-right coronary artery (RCA) lesion (Figure 1). He initially presented 3 months ago with stable angina and a positive exercise treadmill test. Invasive coronary angiogram (CA) at that time demonstrated a true bifurcation lesion involving the mid-left circumflex artery (LCX) and the obtuse marginal (OM) branch and a severe lesion in the mid-RCA. On that occasion, the LCX bifurcation was treated using a 2-stent culotte strategy with the Nobori stent (Terumo Corporation).
The patient’s current angiogram revealed good result of the previous LCX-OM bifurcation stenting. As documented previously, there was a focal severe stenosis (type A) in the mid-RCA (Figure 1A). The lesion was predilated with a 3 x 12 mm non-compliant balloon at 14 atm. Subsequently, we implanted a 3 x 12 mm amphilimus-eluting stent (Cre8; CID/Alvimedica). Immediately after stent implantation, the angiogram demonstrated diffuse spasm including the exit site of the stent (Figure 1B). The spasm was relieved with administration of intracoronary nitrates, but a mild stenosis persisted at the distal edge of the stent (Videos 1 and 2). Due to optimal distal flow and benign angiographic appearance of the lesion (Figures 1C and 1D), a decision was made for conservative management. Two hours later, the patient complained of central chest pain. Electrocardiogram (ECG) showed ST-segment elevation in the inferior leads; hence, an emergency CA was performed, which demonstrated extensive, spiral RCA dissection (originating from the distal stent edge) extending to the posterior descending artery (PDA) compromising distal flow (Figure 2A and Video 3). The distal RCA was subtotally occluded and TIMI-2 flow was seen in the posterolateral branch (PLA), whereas the PDA was occluded (Figure 2A). In view of the angiographic appearances and ongoing ST elevation, emergency percutaneous coronary intervention was performed. The first coronary Balance Middleweight wire (Abbott Vascular) was placed successfully in the true lumen of the PLA (verified by entry in small subbranches).The second wire was positioned in the mid-PDA; during the procedure, it was discovered that the wire was subintimal (Figure 2B). Initially, balloon dilatations with a semicompliant balloon were performed on the PLA wire, which was known to be in the true lumen; however, this did not result in improvement in distal flow. Subsequently, gentle balloon inflations were performed on the PDA wire in an attempt to achieve continuity between false and true lumen; however this was also unsuccessful. Eventually, using a knuckle wire, a rescue subintimal tracking and reentry (STAR) technique was performed with reentry in the true lumen in the mid-distal portion of the PDA (Figure 2C). Subsequent multiple balloon inflations on both wires, including kissing-balloon inflations at the PLA/PDA bifurcation, led to restoration of TIMI-3 flow in all branches (Figure 2D), myocardial blush grade 3, and resolution of ST-segment elevation. The final result showed extensive dissection, with TIMI-3 flow and absence of residual staining (Figure 2D and Video 4); hence, the decision was made to avoid stenting.
Postprocedural in-hospital stay was uncomplicated and the patient made a good recovery. Peak troponin (12-hour post ST-elevation myocardial infarction presentation) was 2264 ng/L (upper limit of normal, 38 ng/L), whereas repeat transthoracic echocardiogram revealed good left ventricular function with no obvious regional wall-motion abnormalities. The patient was discharged on dual-antiplatelet therapy (aspirin 100 mg and clopidogrel 75 mg daily) on top of an ACE inhibitor, a statin, and other antihypertensives.
The management of coronary artery dissections after percutaneous coronary intervention has been a matter of debate since the dawn of coronary stents. In the early 90s, in a prospective study of 149 coronary artery stenoses (129 patients) treated with plain old balloon angioplasty (POBA),1 non-occlusive dissections (49 lesions; 32.9%) were predictive of reduced binary restenosis at follow-up (12% vs 44% in dissected and non-dissected vessels, respectively), which was likely the effect of more aggressive balloon dilatation. Sixty matched patients who were treated with bare-metal stent implantation for the treatment of residual dissection after POBA exhibited similar angiographic restenosis rates at 6-month follow-up (25%). Another study in the mid 90s that included 42 patients with complete or impending vessel closure secondary to large-vessel wall dissections following POBA suggested that coronary stenting (successful in 93%) was an effective treatment measure with acceptable rates of subacute stent thrombosis (2/39; 5%). In that study, despite stenting, 4 patients left with large residual dissections had excellent angiographic and clinical outcomes at 6-month follow-up.2
Most recently, in a large retrospective study from four Italian centers (2418 included patients; 4630 lesions) by Biondi-Zoccai et al,3 the estimated incidence of final coronary dissection after drug-eluting stent (DES) implantation was 1.7% (77 lesions). It should be highlighted that these reflect residual dissections that could not be sealed and those that the operators decided to manage conservatively. Some initial dissections were eventually treated by the investigators successfully and not included; therefore, the results of this study should not be viewed as the “natural history” of dissections after DES implantation. Dissections were more proximal to the DES in 31.7% and distal in 61% of cases. Normal distal flow was noted in the majority of cases (80.2%), whereas type-F dissections (leading to impaired distal flow) occurred in only 6.5% of all dissections. Dissections were more frequent in longer and complex lesions in the left anterior descending artery, and were associated with increased rates of in-hospital (11.9% vs 5.2%; P=.02) and 1-month major adverse cardiovascular events (13.4% vs 6.0%; P=.01), with similar 6-month trends.
Stent thrombosis rates were also greater in patients with dissections (6.3% vs 1.3%; P=.01). Of interest, even non-obstructive dissections with TIMI-3 flow conferred a significantly worse prognosis (major adverse cardiovascular event rate, 12.2% vs 5.2%; P=.04) when comparing lesions with absence of dissection post PCI, contradicting the results from the aforementioned earlier studies. Surprisingly, residual dissections witnessed after a failed attempt to deploy an additional stent (38% of final dissections) were not associated with worse outcomes than those that were intentionally left untreated.
In another study where intravascular ultrasound was utilized to detect coronary dissections post PCI,4 the outcome of 124 lesions treated with either stent (65%) or POBA with residual non-obstructive dissections were compared with those of 124 lesions also treated with stent (65%) or POBA but without residual dissection. Angiographic and clinical results were comparable in the two groups. In the group with post-PCI residual dissection, minimum lumen area was a predictor of restenosis occurrence (P=.01). These results, however, contrast the ones presented by Lemos et al,5 where residual proximal edge dissections post sirolimus stent implantation were identified in 83% of restenotic (>50% diameter stenosis) lesions.
It seems that we are still far from finding the “holy grail” in the treatment of coronary artery dissections after PCI. In cases where distal flow is not compromised, the decision between immediate stenting and conservative management should, in our opinion, favor stenting, which provides safety to the procedure.
- Cappelletti A, Margonato A, Rosano G, et al. Short- and long-term evolution of unstented non-occlusive coronary dissection after coronary angioplasty. J Am Coll Cardiol. 1999;34(5):1484-1488.
- Alfonso F, Hernandez R, Goicolea J, et al. Coronary stenting for acute coronary dissection after coronary angioplasty: implications of residual dissection. J Am Coll Cardiol. 1994;24(4):989-995.
- Biondi-Zoccai GG, Agostoni P, Sangiorgi GM, et al. Incidence, predictors, and outcomes of coronary dissections left untreated after drug-eluting stent implantation. Eur Heart J. 2006;27(5):540-546. Epub 2005 Nov 11.
- Nishida T, Colombo A, Briguori C, et al. Outcome of non-obstructive residual dissections detected by intravascular ultrasound following percutaneous coronary intervention. Am J Cardiol. 2002;89(11):1257-1262.
- Lemos PA, Saia F, Ligthart JM, et al. Coronary restenosis after sirolimus-eluting stent implantation: morphological description and mechanistic analysis from a consecutive series of cases. Circulation. 2003;108(3):257-260. Epub 2003 Jul 14.
*Joint first authors.
1San Raffaele Scientific Institute, Interventional Cardiology Unit, Milan, Italy; and the 2Imperial College London, National Heart and Lung Institute, London, United Kingdom.
Funding: Dr Panoulas is the recipient of an interventional fellowship grant by Abbott Vascular United Kingdom & Ireland.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted May 5, 2014, and accepted May 22, 2014.
Address for correspondence: Dr Vasileios Panoulas, MD, MRCP, PhD, Clinical Lecturer in Cardiology, Imperial College London, National Heart and Lung Institute, Sir Alexander Fleming Building, South Kensington Campus, SW7 2AZ, London, UK. Email: firstname.lastname@example.org