Abstract
Coronary artery perforation during percutaneous intervention is a rare but potentially life threatening complication. The treatment of coronary perforation can be challenging in view of potential life threatening consequences such as cardiac tamponade or myocardial infarction.
Presented is a clinical course of a 69 year-old female who developed cardiac tamponade as a result of presumed wire related perforation of the posterolateral branch of the right coronary artery. Her clinical course was further complicated by recurrent tamponade, atrial fibrillation, stress induced cardiomyopathy, heparin induced thrombocytopenia and cardiogenic pulmonary edema. Based on review of the medical literature a treatment algorithm for wire perforation is suggested.
Highlights
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Guidewire related coronary artery perforation is an infrequent but potentially life threatening complication.
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Treatment strategies depend on clinical and hemodynamic status of the patient, the presence of hemorrhagic pericardial effusion and tamponade, the location of perforation and the evolution of complications.
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Treatment can range from a simple conservative approach involving follow-up, reversal of anti-thrombotic agents, platelet transfusion, balloon occlusion and specific tools for CAP sealing along with pericardiocentesis and hemodynamic monitoring and support.
1
Introduction
With the advancements in medical technology, interventional cardiologists are attempting to treat more complex lesions. Consequently there is an increased incidence of rare, yet potentially life-threatening complication of coronary artery perforation (CAP). We are presenting a clinical course of a 69 year-old female who suffered a life threatening event of cardiac tamponade as a result of CAP during percutaneous intervention (PCI). Keeping her case as a focus, we have provided a brief account of various effective therapeutic strategies.
2
Case
A 69 year-old female with a history of hypertension, hyperlipidemia and severe depression was referred for cardiac catheterization in view of exertional substernal chest pain with minimal exertion despite good medical therapy. She underwent stress echocardiogram which revealed ischemia in the right coronary artery (RCA) distribution. Cardiac catheterization was performed via the right radial artery approach and revealed two-vessel coronary artery disease (CAD): 90% mid-RCA, 80% proximal RCA stenosis ( Fig. 1 ) and 70–80% mid-left anterior descending artery (LAD) stenosis. The therapeutic options were discussed with the patient who preferred PCI to the proximal & mid-RCA. The patient was loaded with Ticagrelor 180 mg and a left coronary bypass (LCB) 6F guide was chosen. Due to significant RCA tortuosity we used Whisper wire which was advanced into the right posterior descending artery (PDA). Pre-dilatation with a Sprinter 3.0 mm × 20 mm (Medtronic, Minneapolis, MN) balloon resulted in excessive nausea and retching resulting in loss of the guide catheter and wire access in the RCA. The Whisper wire was then re-advanced and a Resolute 3.0 mm × 32 mm (Medtronic, Minneapolis, MN) drug eluting stent (DES) was deployed in the proximal RCA. She continued to vomit and retch and the guiding catheter and whisper wire again were disengaged from the RCA. After repositioning the guide, the whisper wire was noted to traverse into a false lumen distal to the stent which created extensive dissection in distal RCA. A second Whisper wire was introduced into the true lumen initially into the proximal right posterolateral ventricular branch (PLV) and later repositioned into the PDA. A 6F Guideliner (Vascular Solutions, Maple Grove, MN) was advanced into the proximal RCA to secure the guiding catheter position. A second DES was deployed in the mid to distal RCA to cover the dissection. Due to slow flow and extensive stenting, and in view of the patient vomiting and inability to absorb the oral Ticagrelor, the patient received double bolus of Integrilin. After the Integrilin bolus a small perforation ( Fig. 2 ) was noted in the distal PLV, therefore no further Integrilin infusion was given.
The patient was monitored for thirty minutes in the catheterization laboratory with no electrocardiographic or symptomatic changes. A transthoracic echocardiogram (TTE) showed no significant pericardial effusion. The patient was then transferred to the coronary care unit in stable condition, but after approximately thirty minutes the patients was noted to have profound hypotension and new ischemic ECG changes ( Fig. 3 ) and thus was brought emergently back to the catheterization laboratory. During transthoracic echo revealing cardiac tamponade ( Fig. 4 ) pericardiocentesis was performed emergently and 400 mL of blood was removed from the pericardial space and a 6F pericardial drain was left on negative pressure. Repeat coronary angiography was performed in view of significant ST-elevations in the inferior leads. The RCA and the recently placed stents were noted to be widely patent but the PLV perforation was noted to have more significant flow ( Fig. 5 ). The left coronary system was not feeding the perforation. Less than one hour after pericardiocentesis, the patient developed hypotension and was noted to have a moderate pericardial effusion with repeat tamponade physiology despite pericardial drainage ( Fig. 6 ). This was initially managed with fluids and inotropes, but ultimately she was brought back to the catheterization laboratory a few hours later with drain retraction approximately 5 cm and 350 mL of blood was again drained. At this time, the PLV perforation was sealed with a 2-mm coil via a Renegade (Boston Scientific, San Jose, CA) catheter with good angiographic result and resolution of perforation ( Fig. 7 ). Despite no further bleeding, she continued to have tamponade physiology on echocardiography with minimal anterior pericardial fluid ( Figs. 8 , 9 ). Initially attempts were made at repositioning the drain, as well as exchange of the drain, but this did not resolve her hemodynamic problem. Eventually the patient was referred for pericardial window and underwent window placement with resolution of her tamponade physiology. Her post-procedural course was complicated by atrial fibrillation, acute heart failure with reduced left ventricular function to 30% and new ischemic ECG changes (repeat coronary angiography showed no change in coronary anatomy) probably related to stress induced cardiomyopathy. She also developed heparin induced thrombocytopenia with platelet drop from 350,000 to 45,000, without thrombotic complications. She ultimately was managed expectantly and was discharged from the hospital in stable condition after 12 days.
2
Case
A 69 year-old female with a history of hypertension, hyperlipidemia and severe depression was referred for cardiac catheterization in view of exertional substernal chest pain with minimal exertion despite good medical therapy. She underwent stress echocardiogram which revealed ischemia in the right coronary artery (RCA) distribution. Cardiac catheterization was performed via the right radial artery approach and revealed two-vessel coronary artery disease (CAD): 90% mid-RCA, 80% proximal RCA stenosis ( Fig. 1 ) and 70–80% mid-left anterior descending artery (LAD) stenosis. The therapeutic options were discussed with the patient who preferred PCI to the proximal & mid-RCA. The patient was loaded with Ticagrelor 180 mg and a left coronary bypass (LCB) 6F guide was chosen. Due to significant RCA tortuosity we used Whisper wire which was advanced into the right posterior descending artery (PDA). Pre-dilatation with a Sprinter 3.0 mm × 20 mm (Medtronic, Minneapolis, MN) balloon resulted in excessive nausea and retching resulting in loss of the guide catheter and wire access in the RCA. The Whisper wire was then re-advanced and a Resolute 3.0 mm × 32 mm (Medtronic, Minneapolis, MN) drug eluting stent (DES) was deployed in the proximal RCA. She continued to vomit and retch and the guiding catheter and whisper wire again were disengaged from the RCA. After repositioning the guide, the whisper wire was noted to traverse into a false lumen distal to the stent which created extensive dissection in distal RCA. A second Whisper wire was introduced into the true lumen initially into the proximal right posterolateral ventricular branch (PLV) and later repositioned into the PDA. A 6F Guideliner (Vascular Solutions, Maple Grove, MN) was advanced into the proximal RCA to secure the guiding catheter position. A second DES was deployed in the mid to distal RCA to cover the dissection. Due to slow flow and extensive stenting, and in view of the patient vomiting and inability to absorb the oral Ticagrelor, the patient received double bolus of Integrilin. After the Integrilin bolus a small perforation ( Fig. 2 ) was noted in the distal PLV, therefore no further Integrilin infusion was given.
