Coronary Artery Dissection and Perforation Complicating Percutaneous Coronary Intervention

Jason H. Rogers, MD; John M. Lasala, MD, PhD

Disclosures

J Invasive Cardiol. 2004;16(9) 

In This Article

Contemporary Incidence of Perforation in Setting of GP IIb/IIIa Inhibitors

The reports by Ellis and Ajluni and to some degree Gruberg were published before the widespread use of adjunctive glycoprotein IIb/IIIa inhibitors during percutaneous intervention. To evaluate the impact of these adjunctive antiplatelet regimens in concert with new atheroablative devices on the incidence and management of coronary perforation, Dippel et al examined 6,214 PCIs from 1995 to 1999,6 36 (0.58%) perforations occurred and were graded by the Ellis criteria outlined above. Those patients with perforation more often had congestive heart failure (22.2% vs. 11.1%, p = 0.028), but coronary lesion angiographic characteristics including calcification, eccentricity, angulation and ACC/AHA lesion class were not predictive of perforation. The use of atheroablative techniques resulted in a higher incidence of perforation (odds ratio of 16.3) and an increased severity of perforation type (odds ratio 28.9 for development of Type III perforation in atheroablative versus nonatheroablative techniques). Surprisingly, no association existed between abciximab use with either the incidence or the angiographic classification of coronary perforation. Concurrent with report by Ellis, Type I and Type II perforations were associated with low complication rates (Type I, 0% tamponade, urgent CABG and death; Type II, tamponade 5.3%, 0% death and urgent CABG). Conversely, patients with Type III perforations had significant morbidity and mortality (tamponade 42.9%, urgent CABG 50.0% and death 21.4%,). Type III cavity spilling perforations resulted in no tamponade, urgent CABG or death.

Dippel et al conclude that the therapeutic strategy employed to treat coronary perforation is best determined by the specific angiographic classification for perforation. An algorithm for the management of coronary perforation complicating PCI with adjunctive abciximab administration is proposed, but this has not been prospectively evaluated. It involves an approach similar to that outlined in the management section of this review. They also advise against the deployment of a noncovered stent at the site of the perforation, given that it may prevent the vessel's normal ability to vasoconstrict and seal the perforation. The clinical outcomes of the aforementioned studies as categorized by perforation type are summarized in Table 1 .

An algorithm outlining the management of coronary artery dissection and perforation as detailed below may be found in Figure 6.

Algorithm for the management of iatrogenic coronary artery dissection and perforation. Refer to text for complete details.

The management of coronary artery dissection in the current era consists primarily of stent deployment. Stenting remains the most important measure used for the treatment of coronary dissection, abrupt vessel closure and minimizing ischemic complications.[38] As mentioned previously, the operator should seek to contain and cover the distal extent of the dissection as soon as possible with a stent to prevent further extension. This is accomplished more readily if a guidewire resides within the true lumen at the time of dissection. If not, there are several techniques that are useful in rewiring the true lumen. If the dissection occurs at an ostial location, one must often disengage the guide in an attempt to rewire the true lumen from the aorta. If a wire is passed into the false lumen, it may be prudent to leave it in place, and bring down a second wire — the wire in the false lumen may deflect the tip of the second wire into the true lumen. In fact, any technique which alters the wire bias (such as an over-the-wire balloon or "wiggle wire") may aid in the wiring of a true lumen. If attempts to wire the true lumen are unsuccessful, and a sizeable territory of myocardium remains ischemic, urgent bypass surgery must be considered.

In the advent of a coronary perforation, conservative management should be attempted initially and is achieved with prolonged balloon inflation, and reversal of anticoagulation for severe perforations. A balloon (with a balloon to artery ratio ~1.0) should initially be positioned over the site of contrast extravasation and inflated for at least 10 minutes. If the patient is unable to tolerate ischemia during balloon inflation, a perfusion balloon should be used. Perfusion balloons allow distal vessel perfusion, thereby reducing ischemia during prolonged inflations.[39]

Emergent echocardiography should be performed at the first sign of perforation, and if clinical evidence of tamponade is apparent, immediate pericardiocentesis should be performed. Given the evidence that frank perforation with pericardial tamponade may occur in the first 24 hours after a threatened perforation that is apparently sealed in the catheterization laboratory, close clinical observation and repeat echocardiography within 12 to 24 hours is warranted or sooner if hemodynamic compromise is manifest.

Although hemodynamic collapse after coronary artery perforation is generally caused by the rapid development of cardiac tamponade from blood extravasation into the pericardial space, cardiogenic shock has been reported to occur from a localized subepicardial hematoma. This is felt to occur more commonly in patients with previous coronary artery bypass surgery, in whom epicardial-pericardial adhesions exist.[40]

Initial efforts to seal a perforation should be undertaken while the patient remains anticoagulated with heparin to prevent vessel thrombosis, although platelet IIb/IIIa receptor antagonists should be discontinued once perforation occurs. If reversal of anticoagulation is clinically warranted in the setting of a major perforation, the pharmacologic reversal of heparin should be performed. This is most commonly achieved through the intravenous administration of protamine sulfate. In the absence of prior NPH-insulin use, the incidence of adverse reactions to protamine (such as hypotension and bradycardia) are minimal. Platelet transfusion should be employed for reversal of abciximab antiplatelet effect. In the presence of normal renal function, infusions of small molecule glycoprotein IIb/IIIa inhibitors such as eptifibatide and tirofiban may be stopped with prompt reversal given their short half-lives.

There have been numerous reports describing the use of polytetrafluoethylene (PTFE)-covered stents to treat coronary perforations which fail to seal despite prolonged balloon inflations and reversal of anticoagulation.[41–43] In hemodynamically compromising perforations complicating coronary interventions, PTFE-covered stents can be used emergently with a high success rate and may be life-saving where other conventional treatment modalities are associated with high morbidity and mortality (Figure 7).

Coronary artery perforation sealed with covered Jomed stent. (A) Ellis Type III perforation in the obtuse marginal after stent deployment (arrow). (B) After deployment of PTFE-covered Jomed stent (dashed line), the perforation is sealed.

Coronary artery perforation sealed with covered Jomed stent. (A) Ellis Type III perforation in the obtuse marginal after stent deployment (arrow). (B) After deployment of PTFE-covered Jomed stent (dashed line), the perforation is sealed.

Briguori et al reported a high success rate using the PTFE-covered Jostent (Abbott Laboratories, Abbott Park, Ill.) in a series of patients (n = 12) with perforations during PCI compared to a matched control group (n = 17) treated with bare stent implantation.[44] The in-hospital MACE rate was significantly lower in the PTFE group, and PTFE-covered stent implantation resulted in decreased cardiac tamponade and need for bypass surgery. Because of the small size of the study and lack of routine angiographic follow-up, no firm conclusions could be drawn as to the incidence of restenosis or late stent thrombosis (2 of 7 in PTFE group had restenosis equaling 29% at 6 ± 2 months). There is to date no published report establishing the long-term patency rates of the PTFE-covered Jostent. The use of autologous vein-covered stents has been reported but remains impractical due to the prolonged time required for vein harvest and suturing of the vein graft to a stent prior to deployment.[45]

Although proximal or mid-vessel perforations are generally amenable to covered stent placement, distal perforations may occur, often as a result of guidewire trauma, which are not easily approached by covered stents. Hydrophilic-coated guidewires may confer an increased risk of perforation due to their low coefficient of friction and ease of distal migration.[46] Surgical ligation remains a therapeutic option, although other methods have been reported. Microcoils have been deployed distally to achieve thrombosis and thus closure of the perforation.[47–49] An obvious drawback of this approach is permanent loss of the vessel lumen beyond the site of microcoil placement and subsequent infarction. Therefore, this approach should be limited to life-threatening circumstances in which no other options are readily available, or for the treatment of very distal perforations where the amount of myocardium jeopardized is minimized.

Other approaches for distal vessel perforations reported include the injection of autologous clotted blood[50] injection of polyvinyl alcohol form[51] or Gelfoam[35] through the balloon catheter lumen. For the reasons outlined previously, this technique is best reserved for distal small vessel (< 1 mm) perforations not amenable to balloon inflations or covered stent deployment.

Should the above measures fail to seal a perforation, or should the clinical situation warrant, patients should be sent for emergency thoracotomy to repair the perforation. Unfortunately, emergency coronary artery bypass surgery carries a high morbidity and mortality. A French multicenter registry reported 17% in-hospital mortality and 25% myocardial infarction rates in patients who underwent emergency CABG within 24 hours of PCI.[52]

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