Left Circumflex Coronary Artery Occlusion after Mitral Valve Annuloplasty

Abstract

The left circumflex coronary artery is susceptible to injury during mitral valve surgery because of its proximity to the mitral valve annulus. We report the case of a 73-year-old woman who had undergone mitral valve repair and experienced a perioperative myocardial infarction due to occlusion of the left circumflex coronary artery. After percutaneous coronary intervention, a fistulous communication had developed between the stented portion of the left circumflex coronary artery and the left atrium, which, to our knowledge, is the first report of such a complication. The patient underwent successful mitral valve replacement. Although injuries to the left circumflex coronary artery are rare during mitral valve surgery, we believe that increasing awareness of the risk will help to prevent potentially fatal complications. We also recommend that surgeons gather as much detail as possible about the patient's anatomy before operation, use careful and meticulous surgical techniques, and use transesophageal echocardiography to look for wall-motion abnormalities before closing the incision.

In 1967, Danielson and colleagues¹ were the first to describe injury to the left circumflex coronary artery (LCx) secondary to mitral valve surgery, and since then only a handful of cases have been reported.^1–6 Possible mechanisms of injury include either direct injury or distortion of the artery as it courses near the annulus.² We present a unique complication in a patient who experienced a perioperative myocardial infarction secondary to occlusion of the LCx after mitral valve repair. The patient developed a coronary artery-to-left atrial fistula after percutaneous coronary intervention to open the LCx occlusion.

Case Report

In September 2009, a 73-year-old woman who had been experiencing dizziness for several days sought treatment at another hospital. She had a long-standing history of mitral valve prolapse with mitral regurgitation, paroxysmal atrial fibrillation, hypertension, dyslipidemia, and hypothyroidism. She had quit smoking 10 years earlier. Her routine medications included warfarin, metoprolol, diltiazem, simvastatin, aspirin, and levothyroxine.

On physical examination, the patient had hypotension and junctional bradycardia, which were thought to be secondary to atrioventricular nodal blocking agents. The blocking agents were discontinued, and the patient was given intravenous fluids for hypotension. She subsequently developed congestive heart failure, requiring treatment with intravenous diuretics.

A transthoracic echocardiogram showed anterior mitral leaflet prolapse with severe mitral regurgitation and mild tricuspid regurgitation. The left ventricular (LV) ejection fraction was 0.60; LV end-diastolic dimension, 54 mm; and LV end-systolic dimension, 29 mm. Cardiac catheterization showed normal coronary arteries, a left-dominant coronary system, and severe mitral regurgitation. The LV ejection fraction was 0.65. Right-sided heart catheterization showed a pulmonary capillary wedge pressure of 14 mmHg and prominent v waves.

The patient underwent minimally invasive mitral valve repair through a right thoracotomy. The chordae were implanted to the A2 segment, annuloplasty was completed with a 26-mm annuloplasty ring (Carpentier-Edwards Physio; Edwards Lifesciences, LLC; Irvine, Calif), and Cox maze III biatrial cryoablation was performed. The surgery appeared to go well; however, while the patient was being weaned from cardiopulmonary bypass, ST-segment elevation was noted on the electrocardiogram (ECG). A perioperative transesophageal echocardiogram (TEE) revealed normal LV function, and Swan-Ganz monitoring revealed a cardiac index greater than 3 L/min/m². The decision was made to close the chest, and the patient was transferred to the cardiothoracic surgery intensive care unit. The ECG showed evidence of myocardial infarction with profound ST-segment elevations of 5 to 7 mm in leads II, III, and aVF, and ST-segment depressions of 5 to 12 mm with T-wave inversions in leads I, aVL, and V₂ through V₆, which led to a high suspicion of intraoperative arterial injury. Emergent coronary angiography revealed a single, discrete, total occlusion of the mid LCx. A single stent was placed, and the lesion was successfully revascularized. The patient tolerated the procedure well and remained stable. One week later, she underwent implantation of a permanent pacemaker for bradycardia-tachycardia syndrome.

During postoperative days 7 through 15, the patient had a persistent cough and mild dyspnea, and she was initially treated for bronchitis. On postoperative day 15, a transthoracic echocardiogram showed severe mitral regurgitation of unknown cause, moderate-to-severe tricuspid regurgitation, and an LV ejection fraction of 0.50 with akinesis from the basal inferior to the mid inferior wall, as well as in the inferolateral and inferoseptal walls. Because severe mitral regurgitation was present, the patient was transferred to our institution for further management.

On arrival at our cardiothoracic surgery unit, the patient was in stable condition. A repeat coronary angiogram revealed a patent LCx stent and a perforation with fistulous communication from the stent into the left atrium (Fig. 1). Echocardiography showed dehiscence of the mitral annuloplasty ring and severe paravalvular mitral regurgitation (Fig. 2A and 2B), in addition to severe left atrial enlargement and a color jet entering the posterior portion of the left atrium (Fig. 2C). Echocardiography also showed moderate segmental LV systolic dysfunction with severe hypokinesis of the basal and mid inferior septum and the inferior wall, severe right atrial enlargement, severe tricuspid regurgitation, severe pulmonary hypertension (systolic pulmonary artery pressure, 61 mmHg), trace pericardial effusion, and bilateral pleural effusion. The worsening tricuspid regurgitation—thought to have been caused by the recently implanted pacing wire—was expected to improve with surgical correction of the mitral annuloplasty ring dehiscence. The patient underwent reoperation for mitral valve replacement with a 27-mm bovine pericardial valve (Edwards Lifesciences) and direct closure of the coronary artery-to-left atrial fistula (Fig. 3).

Fig. 1 Coronary angiogram shows a patent stent in the left circumflex coronary artery (LCx) and a perforation with a fistulous communication from the stented portion of the LCx into the left atrium. LAD = left anterior descending coronary artery; OM = obtuse marginal branch

Fig. 2 Transthoracic echocardiograms show A) dehiscence of the mitral annuloplasty ring (apical 4-chamber view), B) severe paravalvular mitral regurgitation (apical 4-chamber view), and C) an unusual color jet entering the posterior portion of the left atrium (parasternal long-axis view). Ao = aorta; LA = left atrium; LV = left ventricle; MR = mitral regurgitant; MV = mitral valve; RVOT = right ventricular outflow tract

Fig. 3 Intraoperative photographs show A) dehiscence of the mitral valve (MV) annuloplasty ring (arrow), and B) the fistula opening (arrow) from the left circumflex coronary artery into the left atrium.

Six days postoperatively, repeat echocardiography showed a normally functioning bioprosthetic mitral valve with no mitral regurgitation. The patient recovered slowly over the next week and was eventually transferred to a rehabilitation facility. She was last seen by our doctors in February 2011, and she was doing well.

Discussion

Injury to the LCx during mitral valve surgery is a recognized complication.^2–6 Our case is unique, however, because it is the first in which postoperative percutaneous coronary intervention caused complications. In our patient, a fistulous communication from the LCx into the left atrium led to dehiscence of the mitral annuloplasty ring and recurrent mitral regurgitation, necessitating reoperation.

The LCx courses near the anterolateral commissure of the mitral valve, and the coronary sinus is adjacent to the annulus of the posterior mitral valve leaflet; both vessels lie within the left atrioventricular groove. Proximity of the vessels to the mitral annulus has been shown to be related to the dominance of the coronary circulation. In patients with left-dominant or codominant anatomy, the LCx runs near the mitral annulus and, thus, is susceptible to injury during mitral valve surgery.⁴ Our patient had left-dominant coronary anatomy, and the mechanism of injury was likely related to a suture impinging on the LCx. Stent angioplasty during the subsequent procedure disrupted the suture, creating a fistulous communication from the LCx to the left atrium. Partial disruption of the annuloplasty ring probably contributed to complete ring dehiscence.

When coronary artery occlusion occurs after mitral valve surgery, one of the main concerns is determining whether to return the patient to the operating room or to perform emergent cardiac catheterization. Currently, no evidence supports the superiority of one option over the other. In this case, the ST-segment elevation observed during the post-pump period of the original operation may have been enough reason to perform a coronary bypass to the distal LCx, which would have prevented the subsequent cascade of problems. Perhaps a mechanical problem with one of the coronary arteries would have been suspected earlier in the treatment course if such complications were more common.

Virmani and colleagues⁴ suggested that using intraoperative TEE to look for new wall-motion abnormalities might decrease mortality rates after mitral valve surgery. Increasing awareness of the potential for injuring the LCx during mitral valve surgery and following a few general principles can also help to prevent potentially fatal consequences. We recommend that surgeons gather as much detail as possible about the patient's anatomy before operation, use careful and meticulous surgical techniques, and use intraoperative TEE to look for wall-motion abnormalities before closing the incision.