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Delayed and Recurrent Cardiac Tamponade following Distal Coronary Perforation of Hydrphilic Guidewires during Coronary Interve
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J INVASIVE CARDIOL 2008;20:E150-E153
Vessel perforation is a rare but dire complication of percutaneous coronary interventions (PCI) and is associated with a high risk of pericardial tamponade. Recent increases in the use of atheroablative devices, the availability and use of stiff-tip and hydrophilic guidewires and aggressive periprocedural antiplatelet regimens (including glycoprotein IIb/IIIa antagonists), have increased both the potential risk and severity of this complication. We report two cases in which this complication was associated with an unusual loop-shaped tip configuration of distally placed hydrophilic guidewires in coronary arteries.
Case 1. An 80-year-old hypertensive and dyslipidemic patient was referred for cardiac catheterization following the onset of typical exertional chest pain experienced 5 weeks prior during a nondiagnostic stress-test and normal baseline echocardiography. Selective coronary angiography showed a left-dominant coronary system and single-vessel disease involving the left circumflex-first obtuse marginal bifurcation. Clopidogrel and aspirin were administered in loading doses prior to PCI and systemic heparin (70 UI/kg) was administered at the start of the procedure. Using the transfemoral approach, the left coronary artery was engaged with a 6 Fr EBU Launcher 4.0 catheter (Medtronic, Inc., Minneapolis, Minnesota). Balance Middleweight wires (Guidant Corp., Santa Clara, California) were inserted into each branch of the bifurcation. Direct stenting of the circumflex artery was performed using a Taxus® Express 2.5 x 16 mm stent (Boston Scientific Corp., Natick, Massachusetts) deployed at 9 atm. Following the failure of the Balance Middleweight wire to recross the stent struts into the marginal branch, a PT2® Moderate Support guidewire (Boston Scientific) was selected and advanced into the distal part of this branch (Figure 1).
The procedure was completed with a kissing inflation of two 2.5 mm Maverick 2 Monorail balloons (Boston Scientific) at 8 atm each, with a satisfactory angiographic result. Retrospective analysis of the angiogram, however, led to the suspicion that minimal dye extravasation had gone unnoticed during the procedure (Figure 2).
Five hours after the procedure, the patient experienced chest discomfort with nonspecific lateral T wave changes recorded in the lateral electrocardiogram (ECG). Coronary angiography was repeated, demonstrating patency of the stent. No contrast media extravasation was observed on this occasion and the patient was transferred back to the ward (Figure 3).
Forty-eight hours after the original procedure, the patient again complained of chest pain and rapidly developed cardiogenic shock (systolic blood pressure < 80 mmHg). The ECG showed diffuse ST-segment elevation (Figure 4). The patient was immediately transferred for angiography where severe diameter reduction mimicking vasospasm of all distal portions of the major coronary vessels was revealed (Figure 5). Since the vasoconstriction was unresponsive to vasodilator agents (molsidomine, cautious intracoronary nitrate infusion), emergency echocardiography was performed and revealed a substantial pericardial effusion with significant right heart and left atrial compromise. Immediate pericardiocentesis was undertaken and a pericardial drain positioned. The evacuation of 400 ml of minimally coagulated blood promptly reverted the clinical status of the patient with resolution of both shock and ST-segment elevation (Figure 6). Peak Troponin I of 25 ng/mL was documented on day 3 and the patient was discharged uneventfully on the fifth day post procedure.
Case 2. A 68-year-old male hypertensive, ex-smoker was referred to our institution following a positive stress test to investigate the recent onset of exertional chest pain. Multiple severe calcified lesions of the right coronary artery (RCA) were revealed by selective coronary angiography. After 4 days of clopidogrel loading and treatment with aspirin, the patient was readmitted for PCI. Via the right radial approach, the RCA ostium was cannulated with a 6 Fr 3DRC Launcher catheter (Medtronic) and unfractionated heparin was administered. Due to tortuous anatomy, a Balance Middleweight (Guidant) was exchanged for a hydrophilic Whisper guidewire (Guidant), which was advanced with difficulty to the distal portion of the first retroventricular wall branch (RVB). The ostium of this RVB was treated with implantation of a Cypher 2.5 x 13 mm stent (Cordis), after predilatation with two 1.5 and 2.0 mm diameter Maverick balloons (Boston Scientific). A second wire (Balance Middleweight) was positioned in the posterior descending artery (PDA) for the treatment of a type 3 distal RCA/ PDA bifurcation. Direct stenting was performed with a Cypher™ 3.0 x 13 mm stent (Cordis) and a kissing inflation with two 2.5 mm diameter Maverick 2 balloons (Boston Scientific) concluded the treatment of this lesion. The mid-RCA lesion was treated by direct implantation of a 3.5 x 12 mm Janus stent (Sorin Biomedica) with an optimal angiographic result. Again in this case, reanalysis of the angiograms showed an Ellis Type 2 perforation1 located in the distal part of the RVB in the same position in which Whisper guidewire looping had been observed (Figures 7 and 8).
Pericardiocentesis with evacuation of 510 ml of non coagulated blood quickly reverted his clinical status. For the following two days there was no further pericardial drainage show and the drain was removed. After echocardiographic confirmation of the absence of pericardial effusion, the patient was discharged on day 6 after the event, taking aspirin and clopidogrel, both 75 mg daily. Immediately on reaching his home, however, he collapsed again in a state of cardiogenic shock. His confirmed recurrent tamponade was on this occasion treated surgically with evacuation of a difficult-to-quantify volume of partially clotted blood and repair of the RVB with biologic glue. His peak troponin I was 4.92 ng/ml and he was discharged 2 weeks later without further complication.
Discussion
Most studies report the incidence of coronary artery perforation complicating PCI to be between 0.3–0.6%,1–3 with guidewire-related perforation accounting for 31–51% of these cases and device-related perforation responsible for the remainder.2,3 Coronary perforation is associated with a high risk of severe hemodynamic compromise and death. A report by Gunning et al retrospectively analyzed 52 cases of arterial perforation with pericardial effusion, nearly half of which (46%) resulted in cardiac tamponade requiring drainage, and a third (33%) needing surgical repair. The authors reported a total mortality of 25% for this complication.4 Another report reviewing 31 consecutive cases of cardiac tamponade following PCI reported 42% mortality, 39% emergency surgery and 29% myocardial infarction during in-hospital follow up of these patients.5
PTFE-covered stent implantation at the site of rupture6 has become a widespread technique to treat proximal coronary artery perforations. In cases of distal guidewire perforation, however, it is often impossible to deliver such a device. In these cases, occlusion by means of gelfoam embolization has been reported as a possible therapy.7 Fischell and al reported 2 cases of hydrophilic guidewire distal perforation successfully treated by local injection of thrombin followed by prolonged balloon inflation.8 Other solutions include microcoil embolization for treatment of similar complications,9 injection of polyvinyl alcohol10 or of autologous thrombus11 into the distal coronary bed. Ellis Type I and Type II perforations are, however, usually managed more conservatively with simple measures such as stenting, reversal of heparinization and platelet transfusion in cases where abciximab has been used. Following any of these procedures, serial echocardiographic monitoring of any pericardial effusion should be routine. Delayed tamponade is a rare event in this setting, sometimes associated with isolated left atrial compression.12 We have found reports of delays varying from a few hours13 to 36 hours after PCI.14 Maruo et al reported a case of an extremely delayed pericardial effusion with symptoms of chest pain and anterolateral ST-segment elevation occurring 4 days after coronary intervention.15 Unusual presentation mimicking extensive acute myocardial infarction (left main occlusion or severe diffuse spasm ECG type in case 1) is exceptional.
A recent study showed that more than half of all coronary perforations are guidewire-related and follow the use of a hydrophilic wire in 50% of cases.3 Well-recognized mechanisms of perforation with wires include vessel piercing while crossing the lesion, distal migration and wire fracture.3 We suppose that hydrophilic guidewire looping is the cause of the 2 perforations we report, because retrospective angiographic analysis revealed an unusual tip conformation of the wires at the level of contrast extravasation. A loop in the distal portion of a wire is often thought of as being safe because it reduces the risk of wire migration and lodgment in small collateral branches. We believe that when using hydrophilic wires, this “loop configuration” represents an extremely dangerous situation that must be carefully avoided. In this configuration, the wire can act as a blade, cutting easily through the vessel intima and protruding into the pericardial cavity. This potential hazard is greatest in small vessels where elastic guidewire recoil tension is increased and vessel wall resistance is lower. As illustrated by our cases, covert coronary perforation may result in actual hemodynamic impairment even days later, seriously threatening the patient’s life.
References
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