Mitral Annuloplasty Causing Left Circumflex Injury and Infarction: Novel Use of Intravascular Ultrasound to Diagnose Suture Inju

Mitral annuloplasty with Cosgrove-Edwards ring is a widely accepted and less morbid surgical alternative to mitral valve replacement in a selected group of patients.^1,2 Injury of the left circumflex artery during suture placement is unusual but has been reported in the surgical literature initially in the 1960s.³ This injury appears to be more common in patients with coronary left dominance, where the coronary artery typically courses in closer proximity to the posterior mitral valve leaflet.⁴ The incidence of left circumflex territory ischemia is likely under-recognized and under-reported in the literature. It may have devastating repercussions including postoperative myocardial infarction and death. We present a report of two patients with left circumflex artery injury after mitral annuloplasty. Case 1. A 61-year-old male with no known coronary artery disease risk factors presented to the outside hospital with mild symptoms of progressive exertional dyspnea and fatigue. His physical examination revealed a 3/6 holosystolic murmur best heard at the axilla. Echocardiography showed severe mitral regurgitation with mildly thickened mitral leaflets (consistent with myxomatous mitral disease) but no mitral stenosis and normal ejection fraction of 60%. No wall motion abnormalities were noted. Preoperative coronary angiography showed a left dominant system without angiographically apparent coronary artery disease (Figure 1A). The ejection fraction as assessed by left ventriculography was 56%. Cardiac index was 5.4 L/minute. There was severe mitral regurgitation with large V-waves on the pulmonary wedge tracing and left ventricular end-diastolic pressure that was elevated at 20 mmHg. There was mild pulmonary hypertension. The patient underwent mitral valve annuloplasty and repair, which involved resection of P3 leaflet and placement of 28 mm physio annuloplasty ring. His postoperative course was complicated by ventricular tachycardia requiring amiodarone infusion and oral amiodarone administration. The patient’s creatinine kinase peaked at 3,317 IU/L with MB fraction of 455 ng/ml, index if 15.3 and peak troponin-T of 75.9. His postoperative echocardiogram revealed markedly reduced ejection fraction of 24% with inferolateral wall akinesis and left ventricular dilation. The mitral valve prosthesis was well seated and there was no paravalvular leak or mitral stenosis (valve are of 1.5 cm2 and gradient of 4 mmHg). There was trivial mitral regurgitation. Exercise stress test showed good exercise capacity (10 minutes on modified Bruce protocol) but revealed PR interval prolongation with exercise. The patient continued to have ventricular ectopy and was referred to this hospital for consideration of internal cardioverter-defibrillator placement. His ECG showed sinus rhythm at the rate of 61 with first degree AV conduction delay, right bundle branch block and left axis deviation, Q-waves in the inferior limb leads suggestive of prior inferior myocardial infarction as well as inferolateral T-wave flattening. Cardiac catheterization revealed a left dominant system, where left circumflex coronary artery was a large vessel supplying both the posterior descending and posterior left ventricular branches. The left circumflex artery had a 70% lesion proximal to the origin of a large obtuse marginal artery (OM). Other coronary vessels were free of disease (Figures 1B and D). Left ventriculography showed left ventricular hypokinesis with a classic “double-density” appearance of the inferolateral wall consistent with left circumflex territory infarction (Figure 1C). A possibility of suture injury of the vessel was raised rather than de novo atherosclerotic lesion. Intracoronary ultrasound (Boston Scientific Corp., Natick, Massachusetts) pullback demonstrated that the vessel had only mild intraluminal plaqueing and that the 70% lesion was predominantly due to external compression or anatomic distortion (Figures 2 A–D; arrows). Cardiac surgery consultation was obtained regarding the safest management of this lesion and the decision was made to proceed with stenting of the left circumflex lesion. A single 3.5 mm x 13 mm sirolimus-eluting stent was delivered successfully and postdilated to 4.0 mm, resulting in a negligible residual stenosis (Figures 3A and B). The patient subsequently underwent an electrophysiologic study of the AV nodal and His Purkinje system conduction, which showed AV nodal block, but no evidence of His bundle injury. Case 2. A 48-year-old female presented to the emergency room with complaints of severe progressive shortness of breath, paroxysmal nocturnal dyspnea and orthopnea over 1 month preceded by 1 year of exertional dyspnea. She denied any chest pain. On examination she was tachycardic but normotensive. Her jugular venous pressure was elevated and chest had decreased breath sounds at the bases, and bilateral crackles. Cardiac exam revealed regular tachycardia with normal S1 and S2. There was a 3/6 holosystolic murmur best heard over the axilla and a soft diastolic murmur. Her echocardiogram revealed global left ventricular hypokinesis with dilation (left end diastolic diameter of 6.1 cm) and an estimated ejection fraction of 20%. There was severe eccentric mitral regurgitation and mild aortic regurgitation. She was referred to this hospital for cardiac catheterization, which revealed elevated left ventricular filling pressures (LVEDP = 30 mmHg) and moderately elevated pulmonary pressures (45 mmHg). Left ventriculography confirmed severe mitral regurgitation with severe global hypokinesis and an ejection fraction of 20% (Figure 4C). The coronary arteries in this right dominant system had no angiographically apparent disease in the left main, LAD, LCX and RCA (Figure 4A). She underwent mitral valve posterior cleft leaflet repair and placement of a 28 mm St. Jude Medical (St. Paul, Minnesota) mitral annuloplasty ring. In the postoperative period there was difficulty weaning inotropic support, and her cardiac index was noted to decrease. She was also noted to have runs of supraventricular tachycardia but no other EKG changes were apparent. Echocardiogram showed a well-seated mitral valve ring without paravalvular leak, with residual 1–2+ mitral regurgitation, and a normal transvalvular gradient. The left ventricle was hypokinetic, as was the right ventricular free wall and the ejection fraction was 15%. The patient gradually stabilized. Her follow-up echocardiogram at 6 months showed worsening mitral regurgitation (3+) and persistently depressed ejection fraction. She was referred for cardiac catheterization, which in addition to severe mitral regurgitation and globally depressed ventricular function, revealed a new total occlusion of the proximal left circumflex coronary artery with robust collaterals from the LAD (Figure 4B). The remaining coronary vessels remained free of angiographically apparent disease. Given the chronicity of the occlusion and presence of collaterals, the decision was made to manage her worsening mitral regurgitation by redo mitral annuloplasty. Intraoperative transesophageal echocardiogram also raised concern for worsening aortic regurgitation (2+). Therefore in addition to redo mitral annuloplasty with a 27 mm St. Jude ring, a 21 mm supra-aortic valve ring was also placed. The patient had no postprocedural complications and was discharged to home in stable condition. Her two-months follow up echocardiogram showed an ejection fraction of 30% and mild mitral regurgitation. Discussion Mitral annuloplasty has been used successfully not only in degenerative and rheumatic mitral valve disease but also in ischemic mitral regurgitation.5,6 With the reports of higher mortality in patients with asymptomatic mitral regurgitation and higher mitral regurgitant orifice areas, early mitral valve repair is recommended more often.⁷ Suture injury of the left circumflex artery has been reported in the past but is quite unusual, except for patients with left dominant and codominant coronary system.^3,4,8 Patients with left dominant coronary system have left circumflex arteries, which course much closer to the posterior mitral annulus. Typical distance of 8.4 mm in patients with right coronary dominance is reduced to 4 mm (range from 3 mm to 6.5 mm) in patients with dominant left circumflex. Thus, sutures securing the annular ring are more likely to distort or frankly injure the left circumflex artery in these patients. Virmani⁴ reported three cases of patients that died in the immediate postoperative period from inferolateral infarction. Although the prevalence of left dominance is only 8%, identification of such patients during preoperative coronary angiography should alert the referring cardiologist and cardiac surgeon to the possibility of closer proximity of the left circumflex artery to the annulus. Case 1 is unique in that we managed this complication of mitral annuloplasty with percutaneous coronary angioplasty and stenting of the 70% left circumflex stenosis, with good immediate angiographic result and without injury to the myocardium. Only one such case has been reported to date in literature.⁹ In addition, the novelty in this case is that we were able to distinguish the mechanical compression of the left circumflex injury due to suture injury from obstructive atherosclerotic disease by intravascular ultrasound (Figures 2 A–D). Although development of de novo atherosclerotic disease is unusual in such a short period of time, intravascular ultrasound imaging allowed us to definitively rule out this possibility. To our knowledge this is the first such application of intravascular ultrasound in diagnosing left circumflex artery suture injury. Case 2 was unusual in that suture injury occurred in a patient with right dominant system. Hemodynamic instability in the postoperative period, supraventricular tachycardia and worsening cardiac index may have alerted her physicians to the possibility of left circumflex coronary artery injury after valvular prosthesis problems have been ruled out by echocardiography. Global severely depressed ejection fraction likely made focal wall motion abnormalities difficult to appreciate. ECG is often unrevealing as left circumflex injury is often electrocardiographically silent. Given the total occlusion of the left circumflex artery, and its chronicity of 7 months with good collaterals, percutaneous management with recanalization and stenting were unlikely to succeed. Therefore, redo mitral annuloplasty to treat ischemic mitral regurgitation was the chosen course of action.^5,6 This illustrates the importance of prompt identification of left circumflex injury and occlusion as a complication of annuloplasty in patients with persistently low cardiac index in the postoperative period. As we develop new technologies to treat mitral regurgitation such as percutaneous mitral rings that are placed in the coronary sinus and reduce the mitral annulus diameter by 20–25%, one should be very mindful of this complication and perform simultaneous coronary angiography in addition to intraprocedure echocardiographic assessment. While the pre-clinical studies in a limited number of animals assure us of excellent safety without any injury to the coronary vessels,^10,11 this claim will need to be verified. As part of the preoperative surgical planning, the distance between the annulus and the left circumflex artery could be measured using new imaging technologies such as cardiac magnetic resonance or multislice computer tomography. This could help guide the surgeon during the procedure to avoid such suture injuries.^12,13 In addition, in our own institution we have recently inaugurated a combined operating room with angiographic capabilities. It allows us to perform combined surgical and percutaneous interventions. In this case an angiogram obtained at the end of the mitral annuloplasty procedure may identify any potential injury to the left circumflex vessel. This would allow us to identify stenosis due to suture injury in addition to acute occlusions in an expeditious manner and allow for surgical or percutaneous correction. Only the latter would be immediately identifiable by intraoperative transesophageal echocardiography as a new wall motion abnormality. Conclusion Suture injury of the left circumflex coronary injury and infarction after mitral valve annuloplasty may be an under-recognized complication. Cardiologists and cardiac surgeons should be vigilant about this possible complication particularly in patients with left dominant and codominant coronary systems. Use of novel technologies such as cardiac magnetic resonance or multislice computer tomography to delineate the anatomic relationship of the mitral annulus and the left circumflex artery may be useful in identifying patients at high risk of such complications in whom alternative surgical approaches or early postoperative imaging might be considered. Our cases also illustrate a potential role for early coronary angiography in patients who have persistent hemodynamic instability or ventricular irritability, which may be related to left circumflex artery injury after annuloplasty. As illustrated by Case 1, this potentially devastating complication of mitral annuloplasty can be diagnosed by use of intravascular ultrasound to distinguish suture injury from atherosclerotic lesion. It is likely in this case that earlier identification and treatment with stenting may have provided more benefit. Finally, this complication has to be kept in mind as we introduce the new percutaneous mitral valve annuloplasty technologies into the clinical arena. Acknowledgement. We would like to thank Drs. Joseph P. Carrozza and Ralph Delatorre for their invaluable expertise in the management of these cases.

References 1. Cosgrove DM 3rd, Arcidi JM, Rodriguez L,et al. Initial experience with the Cosgrove-Edwards Annuloplasty System. Ann Thorac Surg 1995;60:499–503; Discussion 503–504. 2. Carpentier A, Deloche A, Dauptain J, et al. A new reconstructive operation for correction of mitral and tricuspid insufficiency. J Thorac Cardiovasc Surg 1971;61:1–13. 3. Danielson GK, Cooper E, Ifuku M. Severance of mitral prosthesis fixation sutures by annulus calcification. J Thorac Cardiovasc Surg 1967;53:858–863. 4. Virmani R, Chun PK, Parker J, McAllister HA Jr. Suture obliteration of the circumflex coronary artery in three patients undergoing mitral valve operation. Role of left dominant or codominant coronary artery. J Thorac Cardiovasc Surg 1982;84:773–778. 5. Tibayan FA, Rodriguez F, Langer F, et al. Undersized mitral annuloplasty alters left ventricular shape during acute ischemic mitral regurgitation. Circulation 2004;110(Suppl 1):II98–II102. 6. Lai DT, Timek TA, Tibayan FA, et al. The effects of mitral annuloplasty rings on mitral valve complex 3-D geometry during acute left ventricular ischemia. Eur J Cardiothorac Surg 2002;22:808–816. 7. Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, et al. Quantitative determinants of the outcome of asymptomatic mitral regurgitation. N Engl J Med 2005;352:875–883. 8. Cornu E, Lacroix PH, Christides C, Laskar M. Coronary artery damage during mitral valve replacement. J Cardiovasc Surg 1995;36:261–264. 9. Hassan W, El Shaer F, Hegazy H. Successful bailout percutaneous coronary intervention for immediate surgical complication. J Invasive Cardiol 2004;16:516–517. 10. Liddicoat JR, Mac Neill BD, Gillinov AM, et al. Percutaneous mitral valve repair: A feasibility study in an ovine model of acute ischemic mitral regurgitation. Catheter Cardiovasc Interv 2003;60:410–416. 11. Daimon M, Shiota T, Gillinov AM, et al. Percutaneous mitral valve repair for chronic ischemic mitral regurgitation: A real-time three-dimensional echocardiographic study in an ovine model. Circulation 2005;111:183–189. 12. Plein S, Greenwood JP, Ridgway JP, et al. Assessment of non-ST-segment elevation acute coronary syndromes with cardiac magnetic resonance imaging. J Am Coll Cardiol 2004;44:2173–2181. 13. Hoffmann MH, Shi H, Schmitz BL, et al. Noninvasive coronary angiography with multislice computed tomography. JAMA 2005;293:471–2478.