ADVERTISEMENT
Case Report
Iatrogenic Coronary Artery Stenosis at the Ostium of Left Anterior Descending Artery After Aortic Valve Replacement: A Case Report with Imaging and Histological Findings
December 2010
ABSTRACT: Iatrogenic coronary artery stenosis (ICAS) after aortic valve replacement (AVR) is a rare but potentially fatal complication. Immediate traumatic lesions or late stenoses caused by insertion of an antegrade cardioplegia catheter during AVR mostly occur at the site of the left main trunk or right coronary ostium. Here, we report a rare case of ICAS after AVR at the ostium of left anterior descending artery. Intravascular ultrasound provided helpful information to choose and perform directional coronary atherectomy (DCA) as the strategy of percutaneous coronary intervention. Histological examination of the specimen taken by DCA demonstrated intimal hyperplasia and no findings of atheromatous plaque with lipid core or thrombus. The patient has been asymptomatic after the procedure and the follow-up multidetector computed tomography at 1 year showed no restenosis.
J INVASIVE CARDIOL 2010;22:E206–E208
Key words: aortic valve replacement, antegrade cardioplegia, iatrogenic coronary artery stenosis, intravascular ultrasound, directional coronary atherectomy
————————————————————
Iatrogenic coronary artery stenosis (ICAS) after aortic valve replacement (AVR) is a rare but potentially fatal complication. The causes of this critical condition are possibly related to insertion of a perfusion catheter for antegrade cardioplegia. Insertion of a perfusion catheter during AVR may produce immediate traumatic coronary lesions and late stenoses. Stenoses of the left main trunk or the ostium of the right coronary artery after AVR have been repeatedly reported since the first report by Roberts and Morrow in 1967.1 The incidence of iatrogenic coronary ostial stenosis has been estimated between 1–5%.2–7 However, few reports demonstrated ICAS after AVR at the ostium of the left anterior descending artery (LAD).8 We report a rare case of ICAS at the ostium of LAD that developed in 4 months after AVR, which was successfully treated by directional coronary atherectomy (DCA).
Case Report. A 64-year-old man with a history of hypertension was referred to our hospital because of fatigue and dyspnea on exertion. Physical examination revealed a grade 3/6 to-and-fro murmur at the second intercostal right sternum border. The electrocardiogram (ECG) showed a normal sinus rhythm without left ventricular (LV) hypertrophy by Sokolow-Lyon voltage criteria, but the echocardiogram indicated severe aortic regurgitation and mild aortic stenosis with a peak pressure gradient of 55 mmHg, a mean gradient of 34 mmHg and a calculated aortic valve area of 1.30 cm2.
His left ventricle was dilated with LV end-diastolic/end-systolic dimensions of 59/40 mm 
and LV ejection fraction was slightly decreased to 55%. Preoperative coronary angiography showed no significant coronary lesions (Figure 1). Aortic valve replacement was performed with a Carpentier-Edwards 25-mm prosthesis (Edwards Lifesciences, Irvine, California). During the surgical intervention, myocardial protection was achieved by antegrade direct cannulation of both coronary ostia using flexible, balloon-tipped cannulae (cardiopulmonary bypass time, 100 minutes; aortic clamp time, 76 minutes). The post-operative period evolved without complications and the patient was discharged 14 days after surgery on oral warfarin. Four months after the surgery, the patient was referred to our hospital because of worsening effort angina of recent onset. The ECG showed newly-appeared terminal T-wave inversion in precordial leads V2–V6. 
Physical examination indicated normal prosthetic valve sounds and no signs of heart failure, and the echocardiogram confirmed the normally functioning aortic prosthesis and normal LV function. Multidetector computed tomography (MDCT) imaging revealed significant stenosis at the ostium of the LAD (Figure 2).
Coronary angiography (CAG) (Figure 3) also demonstrated a severe stenosis at the
ostium of the LAD and no other significant lesions. Coronary bypass surgery was recommended as a therapeutic option, but was rejected by the patient. Thus, the patient underwent percutaneous coronary intervention (PCI). Intravascular ultrasonography (IVUS) demonstrated localized severe stenosis with a homogeneous echo pattern in the proximal LAD (Figure 4). A total of 9 cuts were performed using a directional atherectomy (DCA) device (Guidant Corporation, Indianapolis, Indiana) 
without subsequent stenting. The maximum balloon pressure during cutting was 30 psi. Histological examination of the DCA specimen showed intimal hyperplasia and no findings of atheromatous plaque with lipid core or thrombus (Figure 5). The patient has been asymptomatic after the procedure and the follow-up MDCT at 1 year showed no restenosis. 
Discussion. Myocardial ischemia by ICAS is an infrequent but serious complication following AVR. Several factors may contribute to the pathophysiologic mechanisms for this complication: 1) microintimal injuries and local pressure necrosis by infused cardioplegia; 2) direct traumatic injury by the catheter tip for antegrade cardioplegia; and 3) immunological reaction to the heterograft.
Tukiji et al reported a rare case of bilateral coronary ostial stenosis after AVR with stentless bioprosthesis.9 The pathological feature was the intimal fibrous thickening in the aortic root and proximal artery along with mucinous degeneration and hyaline degeneration but no evidence of ruptured plaques or thrombotic species. They concluded that the mechanism of ICAS might be related to an immunological reaction to the heterograft. This hypothesis appears acceptable to explain the mechanism of ICAS occurred at the ostium of left main trunk or right coronary artery attached to the heterograft. Indeed, most previous reports described ICAS in these lesions.
However, microintimal injuries by infused cardioplegia or direct traumatic injury by the catheter tip may be more appropriate to explain the mechanism of ICAS in the present case, which occurred at the LAD ostium remotely located to the heterograft. Although the problem of ICAS after AVR was described in the 60s and 70s, it remains a problem even today, in spite of the developments in the manufacture of catheters for selective cardioplegia solution infusion and in techniques for myocardial preservation. Retrograde cardioplegia administration via the coronary sinus reduces the need for manipulation of the coronary ostia and could perhaps provide a solution.10,11
However, retrograde cardioplegia alone might not be effective in the entire myocardial protection including right ventricle due to anatomic variations of the coronary sinus. Therefore, the best method of cardioplegia still remains uncertain.
In the present case, we treated ICAS at the LAD ostium by DCA, since the localization and IVUS findings suggested that the lesion was suitable for DCA. This gave us the opportunity to analyze the histopathology of ICAS. The pathological feature of the DCA specimen was the intimal fibrous thickening, but there was no evidence of atheromatous plaque with lipid core or thrombus.
The histological findings suggested that the mechanism of unstable angina in the present case might be different from typical unstable angina caused by local thrombus formation at ruptured or eroded unstable plaque. MDCT could provide useful information on the lesion characteristics. An intermediate CT density (50–119 HU) was reported to correspond to the presence of fibromuscular tissue.12 The minimum CT density of ICAS in the present case was 73.5 HU, which is compatible with fibrous tissue. The IVUS imaging also revealed localized and severe stenosis with a homogeneous echo pattern in the proximal LAD. The findings of imaging modalities were consistent with a proliferative fibrotic reaction, which developed gradually and locally during the post-operative 4 months.
Compared with procedures for non-bifurcation lesions, PCI of ostial bifurcation lesions is associated with a lower procedural success rate, an increased rate of subsequent major cardiac events and restenosis. Considerably high rates of restenosis and target lesion revascularization in bifurcation lesions still limit the clinical benefit of PCI in the era of drug-eluting stents; a target lesion revascularization rate remains as high as 19%.13 The best techniques for the treatment of the ostial bifurcation lesions have yet to be determined, and debulking techniques such as DCA may be a potential alternative strategy even in the drug-eluting stent era. Furthermore, with regard to efficacy and feasibility of debulking, DCA could be more useful in the present case, since ICAS was caused by formation of fibrous tissue, a process distinct from conventional unstable angina.
Conclusion. We report a rare case of ICAS at the ostium of LAD after AVR, which was successfully treated by DCA. Although the present case is indeed rare, physicians as well as surgeons should be aware of the potential complication after AVR.
Acknowledgements. We thank Yukihiro Imai, MD, at the Department of Diagnostic Pathology, Kobe City Medical Center General Hospital, for analysis of the pathological findings of this report.
————————————————————
From the Department of Cardiovascular Medicine, Kobe City Medical Center General Hospital, Kobe, Japan.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted February 4, 2010, provisional acceptance given March 1, 2010, final version accepted March 23, 2010.
Address for correspondence: Yoshimori An, MD, Department of Cardiovascular Medicine, Kobe City Medical Center General Hospital, 4-6, Minatojima-nakamachi, Chuo-ku, Kobe, Japan, 650-0046. E-mail: yan527@hotmail.com
and LV ejection fraction was slightly decreased to 55%. Preoperative coronary angiography showed no significant coronary lesions (Figure 1). Aortic valve replacement was performed with a Carpentier-Edwards 25-mm prosthesis (Edwards Lifesciences, Irvine, California). During the surgical intervention, myocardial protection was achieved by antegrade direct cannulation of both coronary ostia using flexible, balloon-tipped cannulae (cardiopulmonary bypass time, 100 minutes; aortic clamp time, 76 minutes). The post-operative period evolved without complications and the patient was discharged 14 days after surgery on oral warfarin. Four months after the surgery, the patient was referred to our hospital because of worsening effort angina of recent onset. The ECG showed newly-appeared terminal T-wave inversion in precordial leads V2–V6. 
Physical examination indicated normal prosthetic valve sounds and no signs of heart failure, and the echocardiogram confirmed the normally functioning aortic prosthesis and normal LV function. Multidetector computed tomography (MDCT) imaging revealed significant stenosis at the ostium of the LAD (Figure 2).
Coronary angiography (CAG) (Figure 3) also demonstrated a severe stenosis at the
ostium of the LAD and no other significant lesions. Coronary bypass surgery was recommended as a therapeutic option, but was rejected by the patient. Thus, the patient underwent percutaneous coronary intervention (PCI). Intravascular ultrasonography (IVUS) demonstrated localized severe stenosis with a homogeneous echo pattern in the proximal LAD (Figure 4). A total of 9 cuts were performed using a directional atherectomy (DCA) device (Guidant Corporation, Indianapolis, Indiana) 
without subsequent stenting. The maximum balloon pressure during cutting was 30 psi. Histological examination of the DCA specimen showed intimal hyperplasia and no findings of atheromatous plaque with lipid core or thrombus (Figure 5). The patient has been asymptomatic after the procedure and the follow-up MDCT at 1 year showed no restenosis. 
Discussion. Myocardial ischemia by ICAS is an infrequent but serious complication following AVR. Several factors may contribute to the pathophysiologic mechanisms for this complication: 1) microintimal injuries and local pressure necrosis by infused cardioplegia; 2) direct traumatic injury by the catheter tip for antegrade cardioplegia; and 3) immunological reaction to the heterograft.
Tukiji et al reported a rare case of bilateral coronary ostial stenosis after AVR with stentless bioprosthesis.9 The pathological feature was the intimal fibrous thickening in the aortic root and proximal artery along with mucinous degeneration and hyaline degeneration but no evidence of ruptured plaques or thrombotic species. They concluded that the mechanism of ICAS might be related to an immunological reaction to the heterograft. This hypothesis appears acceptable to explain the mechanism of ICAS occurred at the ostium of left main trunk or right coronary artery attached to the heterograft. Indeed, most previous reports described ICAS in these lesions.
However, microintimal injuries by infused cardioplegia or direct traumatic injury by the catheter tip may be more appropriate to explain the mechanism of ICAS in the present case, which occurred at the LAD ostium remotely located to the heterograft. Although the problem of ICAS after AVR was described in the 60s and 70s, it remains a problem even today, in spite of the developments in the manufacture of catheters for selective cardioplegia solution infusion and in techniques for myocardial preservation. Retrograde cardioplegia administration via the coronary sinus reduces the need for manipulation of the coronary ostia and could perhaps provide a solution.10,11
However, retrograde cardioplegia alone might not be effective in the entire myocardial protection including right ventricle due to anatomic variations of the coronary sinus. Therefore, the best method of cardioplegia still remains uncertain.
In the present case, we treated ICAS at the LAD ostium by DCA, since the localization and IVUS findings suggested that the lesion was suitable for DCA. This gave us the opportunity to analyze the histopathology of ICAS. The pathological feature of the DCA specimen was the intimal fibrous thickening, but there was no evidence of atheromatous plaque with lipid core or thrombus.
The histological findings suggested that the mechanism of unstable angina in the present case might be different from typical unstable angina caused by local thrombus formation at ruptured or eroded unstable plaque. MDCT could provide useful information on the lesion characteristics. An intermediate CT density (50–119 HU) was reported to correspond to the presence of fibromuscular tissue.12 The minimum CT density of ICAS in the present case was 73.5 HU, which is compatible with fibrous tissue. The IVUS imaging also revealed localized and severe stenosis with a homogeneous echo pattern in the proximal LAD. The findings of imaging modalities were consistent with a proliferative fibrotic reaction, which developed gradually and locally during the post-operative 4 months.
Compared with procedures for non-bifurcation lesions, PCI of ostial bifurcation lesions is associated with a lower procedural success rate, an increased rate of subsequent major cardiac events and restenosis. Considerably high rates of restenosis and target lesion revascularization in bifurcation lesions still limit the clinical benefit of PCI in the era of drug-eluting stents; a target lesion revascularization rate remains as high as 19%.13 The best techniques for the treatment of the ostial bifurcation lesions have yet to be determined, and debulking techniques such as DCA may be a potential alternative strategy even in the drug-eluting stent era. Furthermore, with regard to efficacy and feasibility of debulking, DCA could be more useful in the present case, since ICAS was caused by formation of fibrous tissue, a process distinct from conventional unstable angina.
Conclusion. We report a rare case of ICAS at the ostium of LAD after AVR, which was successfully treated by DCA. Although the present case is indeed rare, physicians as well as surgeons should be aware of the potential complication after AVR.
Acknowledgements. We thank Yukihiro Imai, MD, at the Department of Diagnostic Pathology, Kobe City Medical Center General Hospital, for analysis of the pathological findings of this report.
References
1. Roberts WC, Morrow AG. Late postoperative pathological findings after cardiac valve replacement. Circulation 1967;35:I48–I62. 2. Lesage CH Jr., Vogel JH, Blount SG Jr. Iatrogenic coronary occlusive disease in patients with prosthetic heart valves. Am J Cardiol 1970;26:123–129. 3. Pande AK, Gosselin G. Iatrogenic left main coronary artery stenosis. J Invasive Cardiol 1995;7:183–187. 4. Pennington DG, Dincer B, Bashiti H, et al. Coronary artery stenosis following aortic valve replacement and intermittent intracoronary cardioplegia. Ann Thorac Surg 1982;33:576–584. 5. Sethi GK, Scott SM, Takaro T. Iatrogenic coronary artery stenosis following aortic valve replacement. J Thorac Cardiovasc Surg 1979;77:760–767. 6. Yates JD, Kirsh MM, Sodeman TM, et al. Coronary ostial stenosis, a complication of aortic valve replacement. Circulation 1974;49:530–534. 7. Kincaid EH, Cordell AR, Hammon JW, et al. Coronary insufficiency after stentless aortic root replacement: Risk factors and solutions. Discussion 8. Ann Thorac Surg 2007;83:964–968. 8. Graf R, Verani MS. Rapid development of coronary arterial stenosis following valve replacement: An unusual cause of myocardial ischemia. Tex Heart Inst J 1986;13:305–307. 9. Tsukiji M, Akasaka T, Wada N, et al. Bilateral coronary ostial stenosis after aortic valve replacement with freestyle stentless bioprosthesis: A case report. J Cardiol 2004;44:207–213. 10. Menasche P, Kural S, Fauchet M, et al. Retrograde coronary sinus perfusion: A safe alternative for ensuring cardioplegic delivery in aortic valve surgery. Ann Thorac Surg 1982;34:647–658. 11. Menasche P, Subayi JB, Piwnica A. Retrograde coronary sinus cardioplegia for aortic valve operations: A clinical report on 500 patients. Discussions 63–64. Ann Thorac Surg 1990;49:556–563. 12. Schroeder S, Kopp AF, Baumbach A, et al. Noninvasive detection and evaluation of atherosclerotic coronary plaques with multislice computed tomography. J Am Coll Cardiol 2001;37:1430–1435. 13. Palmerini T, Sangiorgi D, Marzocchi A, et al. Ostial and midshaft lesions vs. bifurcation lesions in 1,111 patients with unprotected left main coronary artery stenosis treated with drug-eluting stents: Results of the survey from the Italian Society of Invasive Cardiology. Eur Heart J 2009;30:2087–2094.
