Coronary perforation is a rare but potentially life-threatening complication of percutaneous coronary intervention (PCI). As an increasing number of complex PCI procedures are undertaken with aggressive anticoagulation and antiplatelet therapy, a high index of suspicion and a clear management algorithm are necessary to prevent an adverse outcome. We present the case of a life-threatening guidewire perforation successfully treated with catheter-based local thrombin injection. Such definitive percutaneous techniques may have an inherent advantage over inherently high-risk emergency cardiac surgery. Case Report. An 84-year-old female with a history of congestive heart failure and peripheral vascular disease presented with medically refractory angina and was referred for coronary angiography. Coronary angiography revealed severe triple-vessel disease (Figure 1). All vessels were heavily calcified. The patient refused coronary bypass surgery, and the decision was made to undertake multivessel PCI. After therapeutic anticoagulation was obtained with 5,000 Units of intravenous heparin, initial attention was paid to the left anterior descending artery (LAD), which was wired with a Pilot® 50 guidewire (Guidant Corp., Indianapolis, Indiana) through a 6 Fr XBLAD guiding catheter (Johnson & Johnson Corp., New Brunswick, New Jersey). Predilatation with a 2.0 mm balloon was followed by deployment of a 3.0 x 12 mm Taxus® drug-eluting stent (Boston Scientific, Natick, Massachusetts). After this was performed, the right coronary artery ostium was predilated with a 3.0 mm balloon, and a second 3.0 x 8 mm Taxus drug-eluting stent was placed. The patient tolerated the procedure well, and there was TIMI 3 flow in all vessels. Shortly after the procedure, however, the patient developed profound sinus bradycardia and hypotension. An immediate echocardiogram was performed at the bedside, showing a large concentric pericardial effusion with both right atrial and right ventricular collapse. The patient was taken emergently back to the cardiac catheterization laboratory where immediate pericardiocentesis revealed 600 cc of bloody fluid. Repeat angiography revealed extravasation of dye from a small diagonal branch of the LAD that had housed the wire tip (Figure 2). The patient was monitored by serial echocardiography and angiography. There was no reaccumulation of fluid, and the extravasation had substantially decreased in magnitude. The patient was transferred back to the holding area and remained clinically stable. However, approximately 2 hours later, she experienced another transient episode of bradycardia and hypotension, and emergent echocardiography revealed reaccumulation of pericardial fluid and tamponade physiology. The pericardial drain was flushed, and drained an additional 500 cc of bloody fluid. Repeat angiography revealed recurrence of the extravasation. Cardiac surgical intervention was considered, but was decided to be too high risk. Given the need to definitively address the bleeding, we re-entered the culprit diagonal branch with a coronary guidewire. A 1.5 x 9 mm over-the-wire Maverick™ balloon (Boston Scientific) was advanced to the diagonal artery, the wire was removed and the balloon was inflated to 4 atmospheres. Selective left coronary angiography and angiography performed through the wire lumen of the balloon catheter were used to confirm complete exclusion of the affected vessel. Two thousand units of thrombin, obtained from a femoral vascular closure device package, were injected through the wire lumen of the balloon. Total balloon inflation time was 5 minutes. Repeat angiography after balloon deflation showed no further extravasation (Figure 3). The patient was transferred to the intensive care unit. She remained hemodynamically stable throughout the course of treatment. There was no further reaccumulation of pericardial fluid, nor was there drainage from the pericardial drain. Troponin I peaked at 37, and the patient was discharged on postprocedure day 2. Discussion. We present a case of coronary perforation successfully treated with local thrombin injection, leading to a complete clinical recovery. In doing so, we have identified an important technique for rapid, definitive percutaneous management in small vessels that uses readily available materials. This approach has only been reported once before, and ours is the first description of its use in the setting of hemodynamic instability. Our case also underscores the value of early recognition of this complication. Coronary perforation is a rare but potentially serious complication of PCI, resulting in death for up to 10% of patients.1,2 The incidence has been described to be between 0.1–2.1%, but has varied with refinement in interventional techniques.1–7 A high index of suspicion, timely diagnosis, and often definitive treatment are required to minimize adverse outcomes from this complication. The Ellis Classification, described in 1994, is a commonly accepted method of grading the severity of coronary perforation (Table 1) and has been shown to correlate with clinical outcomes.4 Perforation caused by a guidewire tip is normally limited to Class I and II perforations.4 Due to their small nature, however, they can be difficult to recognize and hence place the patient at risk for late tamponade, sometimes after the patient has left medical observation. Often, these small perforations will heal spontaneously and require no more than observation. However, in this era of higher-risk PCI and aggressive anticoagulation and antiplatelet therapy, the operator must have options available to stop these bleeds rapidly. Management of coronary perforation centers around stopping the bleeding from the vessel into the pericardial space. Initial reversal of anticoagulation is universally recommended, though initial reports suggested that this step was not necessary in Class I perforations.4 Definitive management is typically through cardiac surgical techniques, but percutaneous techniques are becoming more common. Initial balloon dilatation can be performed just at, or proximal to, the site of extravasation. While a perfusion balloon will tamponade the site while still allowing distal blood flow, emphasis should be placed on quickly preventing life-threatening bleeding with tools that are readily available. Thus, any available appropriately-sized balloon can be used to temporize while plans for definitive management are being undertaken. Many Class I and II perforations will seal with prolonged balloon inflation alone, although a significant risk of late tamponade mandates close postprocedure monitoring.4 Another percutaneous option for definitive management of coronary perforation is to use covered stents which are covered on their abluminal side with either xenopericardial tissue or polytetraflouroethylene (PTFE). Such stents have been used successfully in coronary perforation, exclusion of coronary fistulae and exclusion of coronary artery aneurysms.8–10 However, for this technique to be used, the area of perforation must be clearly delineated and amenable to stenting. The target area must be of appropriate size and accessibility and free of significant side branches that could be excluded by the covered stent. This technique is thus often limited to the larger epicardial vessels where guidewire perforations are unlikely to occur. Embolization of the target vessel is another option for definitive percutaneous management, and one that was exercised in our case. Many different materials have been used. While coil embolization is an option, it usually requires a relatively large vessel and thus can lead to compromise in flow to a large area of myocardium.11 Options for smaller vessels are more limited. Gelfoam embolization has been reported in case reports.12 Autologous blood can be used with some success and is inherently attractive because of its ubiquitous availability.13 Injection of denatured alcohol, as is used for septal ablation techniques, can sclerose the affected vessel.14 However, this carries a significant risk if care is not taken to limit the injection to the involved area. In addition, its denaturing affect assures the destruction of myocardial tissue in the area, even if collateral circulation may be able to allow myocardial viability there. In our case, thrombin injection was used with success. The choice was guided by the fact that both the involved diagonal and its parent LAD were too small to allow traditional PCI and placement of a covered stent, and the patient was deemed too high-risk for surgical intervention as anything but a last resort. Thrombin also represented the most readily available substance for embolization of the artery (besides autologous blood). To our knowledge, this technique has been reported in a single report of two cases in the literature, and we present another case of successful use employing similar interventional techniques.15 Although it is possible that prolonged balloon inflation alone may have provided control of the bleeding from the perforation, we feel that the thrombin adds durability to the repair and guards against the development of late tamponade, which has been reported in similar patients. As interventional techniques are refined, PCI is achieving a complexity never before deemed possible. Hand-in-hand with such complexity is an increased risk of procedural complications, however. A high index of suspicion, early diagnosis and a clear management algorithm are vital to successfully managing patients with coronary perforation. We present a case of life-threatening coronary perforation successfully treated with catheter-based local thrombin injection. Definitive percutaneous techniques such as this should be exhausted in appropriate patients prior to consigning the patient to inherently high-risk emergency surgery.
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