Ann Thorac Surg 2005;79:693-696
© 2005 The Society of Thoracic Surgeons
Case report
Intraoperative Fracture of the Right Coronary Artery: Recognition and Management
Michael A. Borger, MD, PhD*,a,
Tirone E. David, MDa,
Nicolas Doll, MDb,
Friedrich W. Mohr, MD, PhDb
a Division of Cardiovascular Surgery, Toronto General Hospital, University of Toronto, Toronto, Canada
b Clinic for Heart Surgery, Heart Center, University of Leipzig, Leipzig, Germany
Accepted for publication September 8, 2003.
* Address reprint requests to Dr Borger, Division of Cardiovascular Surgery, Toronto General Hospital, Room EN 13-217, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4
michael.borger{at}uhn.on.ca
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Abstract
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We describe the recognition and management of two patients who developed intraoperative fracture of the right coronary artery (RCA). Both patients had a calcified RCA without a hemodynamically significant stenosis. Compression of the right atrioventricular groove during the surgical procedure resulted in fracture of the RCA, leading to ventricular arrhythmias and hemodynamic instability. Coronary bypass grafting without cardioplegic arrest was used for definitive diagnosis and treatment. Both patients made a rapid and uneventful recovery.
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Introduction
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Rupture of the right coronary artery (RCA), as a complication of blunt chest trauma, has been described in several previous case studies [1–3]. We present two patients who developed intraoperative fracture of the RCA, with particular focus on the recognition and management of this uncommon problem.
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Case Reports
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Patient 1
The first patient was a 62-year-old male who presented with a several month history of increasing angina, as well as a positive exercise stress test. He had hypertension, hyperlipidemia, and type II diabetes mellitus for several years. He also had a 50 pack per year smoking history and mild chronic obstructive pulmonary disease, with a forced expiratory volume in 1 second (FEV1) of 1.8 L. Cardiac catheterization revealed a 50% left main stenosis, 90% proximal left anterior descending (LAD) stenosis, and a heavily calcified RCA without any significant stenosis. The patient's left ventricular ejection fraction was mildly impaired at 54%.
The patient was booked for urgent bypass of the LAD and obtuse marginal arteries. Intraoperative digital palpation revealed severe calcification of the ascending aorta, extending from the sinotubular junction up to the aortic arch ("porcelain aorta"). A decision was therefore made to perform off-pump coronary bypass without clamping of the ascending aorta. Deep pericardial retraction sutures were placed and a beating heart retractor and stabilizer were employed. A radial artery T graft was constructed end-to-side on the skeletonized left internal mammary artery (LIMA), and the distal LIMA was subsequently anastomosed to the mid-LAD. The obtuse marginal artery was too small to bypass and we therefore constructed a radial artery-to-circumflex anastomosis in the left atrioventricular groove. The exposure during this anastomosis was very difficult because of the location of the target, the hyperinflated lungs, and the intact right pericardium. The right atrioventricular groove was therefore compressed on the sternal retractor during the exposure.
Upon releasing the arms of the stabilizer and the pericardial retraction sutures, the patient immediately developed refractory ventricular fibrillation. Defibrillation was unsuccessful and therefore cardiac massage was instituted. An arterial cannula was emergently inserted into the ascending aorta just above the right coronary artery, as this was the only portion free of calcification. The patient was placed on full cardiopulmonary bypass (CPB) and an intraaortic balloon pump was inserted through the left femoral artery. Defibrillation of the heart was temporarily successful, but the patient continued to experience recurrent ventricular arrhythmias. There were diffuse, nonlocalizable acute ST segment changes. Doppler transit-time measurements revealed good flow in the LIMA and radial artery. A transesophageal echocardiography probe was not inserted preoperatively and therefore was not immediately available.
We considered a diagnosis of fracture of the RCA secondary to a combination of vessel wall calcification and excessive compression during exposure of the circumflex artery. We subsequently opened the posterior interventricular (PIV) artery during CPB support, but without cardioplegic arrest. We found a complete absence of antegrade coronary flow, thereby confirming our diagnosis. We bypassed the PIV with a segment of saphenous vein, with the proximal end constructed as an end-to-side T graft off of the LIMA. After 20 minutes of reperfusion, the patient was easily weaned from CPB without any ventricular arrhythmias. The patient was hemodynamically stable thereafter and awoke without any neurologic deficits. The balloon pump was removed on postoperative day 2 and the patient was transferred to the nursing floor on day 4. He was discharged home a few days later.
Patient 2
The second patient was a 56-year-old male who presented two years before his cardiac investigations with flushing, wheezing, and diarrhea. A diagnosis of carcinoid syndrome was made and the patient's symptoms were successfully controlled with octreotide. In the 6 months prior, the patient developed an increase in fatigue, ascites, and peripheral edema. Echocardiography revealed findings consistent with severe carcinoid involvement of the heart [4]. The patient had severe combined pulmonary insufficiency and stenosis (valve area 0.8 cm2), as well as severe tricuspid regurgitation. Contrast computed tomography (CT) of the abdomen revealed multiple liver nodules consistent with metastatic carcinoid disease.
The patient was managed medically with furosemide and spironolactone, but required several admissions for worsening right-sided heart failure. During the most recent hospital admission, the patient was aggressively diuresed, resulting in a 20-kg weight loss. The patient was essentially bedridden because of severe fatigue and edema. Echocardiography confirmed severe pulmonary insufficiency(stenosis) and severe tricuspid regurgitation. In addition, the patient had global right ventricular hypokinesis with preserved left ventricular function. Cardiac catheterization revealed minor irregularities in the circumflex territory, generalized calcification of the RCA with a 40% proximal stenosis (see Fig 1), and a normal left anterior descending artery.
The patient was scheduled for urgent pulmonic and tricuspid valve surgery. A median sternotomy was performed and the heart was arrested with antegrade cold blood cardioplegia. Direct inspection confirmed the diagnosis of carcinoid valvular disease, with severe thickening and retraction of the pulmonic and tricuspid valve leaflets. The pulmonic valve was replaced with a #27 pericardial tissue valve and a Dacron graft was used to enlarge the right ventricular outflow tract. Hand-held atrial retractors were used to expose the tricuspid valve, and occasionally substantial retraction pressure was required. The tricuspid valve was also replaced with a #27 pericardial valve. Although the operation proceeded without incident during CPB, we immediately encountered difficulty during weaning. The patient developed diffuse ST segment changes and increased pulmonary artery pressures, quickly followed by ventricular fibrillation requiring reinstitution of CPB. A second attempt at weaning was similarly unsuccessful. Transesophageal echocardiography (TEE) revealed good function of both prosthetic valves, as well as right ventricular and inferior left ventricular hypokinesis.
A diagnosis of intraoperative fracture of the RCA was made, presumably secondary to coronary arterial wall calcification and excessive pressure on the right atrioventricular groove during atrial retraction. During CPB support, and without cardioplegic arrest, we opened the PIV and confirmed a lack of antegrade blood flow. A segment of saphenous vein was used to bypass the PIV and the patient was subsequently weaned from CPB without difficulty. The patient developed increased renal and liver function tests on the first day postoperatively, but these normalized 2 to 3 days thereafter. He also developed a thrombosis of the left common femoral vein one week postoperatively, requiring treatment with warfarin. The patient's recovery was otherwise unremarkable and he was discharged home on postoperative day 14. Six-month follow-up revealed that the patient is doing very well, with no signs or symptoms of right heart failure.
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Comment
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Rupture of the RCA is a well-described but uncommon complication of blunt chest trauma. Common causes of acute intraoperative right coronary artery insufficiency include embolism, air, or vasospasm. However, we do not believe these factors occurred in our two patients. We do not think our patients suffered from particulate embolism because the ascending aorta was not opened and because neither patient had a thrombus in the left atrium or ventricle. It is also unlikely that air embolism was the causative factor, given that there was virtually no flow in the PIV artery when it was opened. It should be stressed that the retraction sutures were released after the PIV artery was opened to confirm that antegrade flow was severely compromised. Finally, it is unlikely that vasospasm was the cause since these two patients had no prior history or risk factors for vasospasm. We therefore believe fracture of the RCA (ie, fracture of the calcified RCA lesion) was the cause of our two patients sudden hemodynamic deterioration.
Review of these two patients reveals the importance of rapid diagnosis of intraoperative RCA fracture. Both patients presented with intractable ventricular arrhythmias. Ischemia in the RCA territory is a well-recognized cause of ventricular tachycardia and fibrillation [5]. Although our patients developed ventricular arrhythmias only, it is also possible to present with sinus and atrioventricular dysfunction after acute RCA occlusion. Acute ST changes were also observed in our two patients, but they were diffuse and nonlocalizable. Intraoperative TEE was somewhat helpful in that it revealed new inferior wall hypokinesis in one patient, but it may not be readily available when a rapid diagnosis is needed.
Our experience would suggest that the most important factor for making a diagnosis of intraoperative RCA fracture is a high degree of suspicion based on the preoperative angiogram. Both patients had calcification and minor, nonhemodynamically significant lesions in the RCA. The combination of RCA vessel wall calcification and excessive pressure on the right atrioventricular groove resulted in sudden RCA occlusion. In both cases, we confirmed our diagnosis by performing an arteriotomy and demonstrating a lack of antegrade coronary flow.
Management of intraoperative RCA fracture simply involves construction of a saphenous vein bypass graft to the artery distal to the site of injury. We performed this procedure in both patients with CPB support, but without cardioplegic arrest. We preferred this approach because it enabled the definitive diagnosis to be made (ie, lack of RCA blood flow) while still allowing continuous perfusion of the left coronary system. In both patients, simple bypass of the PIV resulted in a dramatic improvement in hemodynamic status and elimination of ventricular arrhythmias. Both patients made a relatively uneventful recovery thereafter.
In conclusion, intraoperative fracture of the RCA is a rare but imminently treatable cause of hemodynamic instability. It should be suspected in patients with a calcified RCA who had mechanical compression of the right atrioventricular groove during their surgical procedure. The diagnosis can be confirmed by opening the RCA without cardioplegic arrest, and is easily treated with the construction of a saphenous vein bypass graft. Rapid diagnosis and treatment results in immediate improvements in hemodynamic status and the elimination of ventricular arrhythmias, resulting in satisfactory outcomes.
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References
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- Trotter TH, Knott-Craig CJ, Ward KE. Blunt injury rupture of tricuspid valve and right coronary artery. Ann Thorac Surg. 1998;66:1814–1816[Abstract/Free Full Text]
- Pringle SD, Davidson KG. Myocardial infarction caused by coronary artery damage from blunt chest injury. Br Heart J. 1987;57:375–376[Abstract/Free Full Text]
- Patel R, Samaha FF. Right coronary artery occlusion caused by blunt trauma. J Invasive Cardiol. 2000;12:376–378[Medline]
- Pandya UH, Pellikka PA, Enriquez-Sarano M, Edwards WD, Schaff HV, Connolly HM. Metastatic carcinoid tumor to the heart: echocardiographic-pathologic study of 11 patients. J Am Coll Cardiol. 2002;40:1328–1332[Abstract/Free Full Text]
- Hoch DH, Rosenfeld LE. Tachycardias of right ventricular origin. Cardiol Clin. 1992;10:151–164[Medline]
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Abstract
Introduction
