Interact CardioVasc Thorac Surg 2006;5:502-504. doi:10.1510/icvts.2005.127787
© 2006 European Association of Cardio-Thoracic Surgery
Case report - Transplantation |
Stenting of unprotected left main stem stenosis in cardiogenic shock after orthotopic heart transplantation
Andreas van de Looa,* and
Friedhelm Beyersdorfb
a Department of Cardiology, Marienkrankenhaus Hamburg and Universitätsklinik Freiburg, Hamburg, Germany
b Department of Cardiac Surgery, Universitätsklinik Freiburg, Hamburg, Germany
Received 2 January 2006;
received in revised form 5 March 2006;
accepted 10 March 2006
*Corresponding author. Department of Cardiology – Zentrum Innere Medizin, Marienkrankenhaus Hamburg and Universitätsklinik Freiburg, Alfredstr. 9, D-22087 Hamburg, Germany. Tel.: +49-40-25462101; fax: +49-40-25462100.
E-mail address: vandeloo.innere{at}marienkrankenhaus.org (A. van de Loo).
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Abstract
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We report the spectacular case of a young patient who developed cardiogenic shock caused by significant stenosis of the left main stem 8 years after orthotopic cardiac transplantation. Immediate percutaneous coronary intervention was a life saving procedure. The report illustrates the importance of early coronary angiography for the clinical management of heart transplant patients in cardiogenic shock as a relevant differential diagnosis to acute rejection. Allograft vasculopathy can develop unexpectedly even after years of uncomplicated follow-up.
Key Words: Heart transplantation; Transplant vasculopathy; Cardiogenic shock; Percutaneous intervention
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1. Introduction
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Transplant allograft vasculopathy is a major contributor to morbidity and mortality after cardiac transplantation. As clinical signs like angina pectoris are often subtle, coronary angiography and myocardial biopsies are regularly scheduled in order to identify patients at risk. This case report describes a patient who was under routine control, in stable clinical condition, 8 years after orthotopic heart transplantation and developed severe left main stenosis that could be successfully treated by emergency coronary stenting.
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2. Case report
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The 29-year-old male patient had orthotopic cardiac transplantation for terminal heart failure due to dilated cardiomyopathy in 1995. He was on the waiting list for 4 months. The perioperative course was uneventful and immunosuppression was started on cyclosporin A 250 mg/day, prednisolon 50 mg/day and azathioprine 100 mg/day. Systemic Cytomegalie viral infection occurred in 1995 and was successfully treated by ganciclovir. Twelve months later steroids were withdrawn according to the local protocol. In 1998, the patient had one episode of acute cardiac rejection that was graded IIb SHLT and treated with steroids. Outpatient control of risk factors, immunosuppression and infections were managed by the transplant center. Chronic medical therapy included simvastatin (20 mg/day), aspirin (100 mg/day) and diltiazem (180 mg/day) as prophylaxis against cardiac allograft vasculopathy (CAV). Coronary angiograms were performed once a year and no relevant allograft vasculopathy was identified conventionally. Diagnostic intracoronary ultrasound (IVUS) was not performed routinely. Cardiac function was normal, ejection fraction (EF) was 55% and regional wall motion abnormalities were not detected.
Five months after the last normal angiogram the patient developed tachycardia, weakness and shortness of breath on exertion. Within two days he was admitted to a local hospital in respiratory failure. Mechanical ventilation was initiated with the diagnosis of severe opportunistic pulmonary infection and the patient was referred to the transplant center. At admission the patient was in progressive cardiogenic shock (blood pressure 85/65 mmHg). Intravenous catecholamine infusion had to be increased continuously (epinephrine <0.5 µg/kg/min). Twelve-lead surface EKG showed sinus rhythm at 110 bpm and no characteristic ischemic alterations. Echocardiographic assessment showed a severely reduced LV-function (EF 20%). Lab results: C-reactive protein 15.8 mg/dl (normal range: 0.5–5.0); white blood count: 11.2 Tsd/ml (normal range: 5.0–10.0), Troponin T: 0.04 ng/ml (normal range: <0.01). In the emergency setting, it was decided to rule out transplant vasculopathy by coronary angiography and to obtain endomyocardial biopsies to identify acute rejection immediately as Troponin T was slightly elevated. At coronary angiography, an injection of contrast agent in the left coronary system showed a 95% concentrical stenosis of the main stem and a 60% stenosis of the left anterior descendent coronary artery (LAD) located distally to the first septal branch (see Fig. 1). Although blood pressure was extremely low, intracoronary nitrate (0.05 mg) was injected to rule out coronary spasm. After consulting the cardiac surgeon in the catheterization laboratory, to discuss all invasive options, the decision for acute coronary stenting was made because of the extremely rapid progession of cardiogenic shock within minutes and increasing catecholamine support. Systemic thrombolytic treatment was considered, but declined as morphology of the target stenosis was less suggestive for thrombus formation than for a lesion caused by graft vasculopathy (Fig. 1). Coronary spasm was ruled out by local low dose nitrate infusion via the guiding catheter. Intraaortic balloon pumping was initiated via the left femoral artery to improve coronary perfusion. A guiding catheter 6F JL 4 SH was placed near the LM ostium and a coronary stent (Cypher® 3.5/13 mm) was directly implanted into the left main stem. Abciximab (ReoPro®) was infused at recommended standard dose for 12 h.
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Fig. 1. Emergency coronary angiogram showing the 95% stenosis of the left main stem (arrow). LAD: Left anterior descendant coronary artery; Catheter: Standard 5 F Judkins 4 cm, diagnostic.
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After intervention the patient could be weaned from inotropic support within 24 h and was discharged home one week later. His ejection fraction was 40%. At his scheduled control angiography 6 weeks later the LAD stenosis was successfully stented (Fig. 2).
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Fig. 2. Control coronary angiogram after coronary stent placement. LAD: Left anterior descendant coronary artery; LCX: left circumflex coronary artery; tip of guide wire in small septal branch; epicardial pacing electrodes implanted at transplantation.
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Three years later the patient is well and clinically stable. He had repeated coronary angiograms with normal findings
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3. Discussion
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Cardiac allograft vasculopathy, as one manifestation of chronic rejection, is the major cause of morbidity and mortality among up to 50% of patients after heart transplantation [1,2]. Compared to conventional atherosclerosis, narrowing is more diffuse and less focal [3]. The left main stem is rarely involved significantly and acute plaque rupture seems to be rare as compared to conventional atherosclerosis. Predisposing factors for the development of cardiac allograft vasculopathy are initial endothelial injury by ischemia and reperfusion [4], immunosuppression, episodes of rejection, older donor age, cytomegalie viral infection, hypercholesterolemia [5], and others [3]. Our patient experienced one episode of allograft rejection proven by endomyocardial biopsy, one cytomegalie viral infection and hypercholesterolemia as predisposing condition for accelerated graft vasculopathy. As patients do not exhibit typical anginal symptoms regularly scheduled coronary angiograms are recommended during elective follow-up. Doshi documented a series of percutaneous interventions for allograft vasculopathy and found a mean interval of 7.8 years between transplantation and the need for revascularization [6] as in the presented case. The role of percutaneous coronary balloon angioplasty, and stenting, and bypass surgery for revascularization of patients with significant graft vasculopathy has been described before [6–8]. However, stenting of the unprotected left main stem in cardiac transplant patients has only been published in very few case reports [9,10]. This is the first report documenting direct emergency stenting of unprotected left main stenosis in cardiogenic shock for transplant vasculopathy. For the patient, it proved to be a successful strategy in a 2-year follow-up.
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4. Conclusions
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Cardiac allograft vasculopathy can develop unexpectedly in stable transplant recipients. In patients presenting with acute heart failure after cardiac transplantation, it is crucial to identify allograft vasculopathy as differential diagnosis to acute rejection early in the clinical course. As complex atypical coronary pathology might be identified, a well reflected interdisciplinary surgical or interventional strategy must be developed immediately.
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References
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- Kirklin JK, McGriffin DC, Benza RL, Tallaj J. Cardiac allograft Vasculopathy (chronic rejection) 2002;New York: Churchill Livingstone.
- Lietz K, Miller LW. Current understanding and management of allograft vasculopathy. Semin Thorac Cardiovasc Surg 2004; 16:386–394.[CrossRef][Medline]
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- El-Hamamsy I, Stevens LM, Vanhoutte PM, Perrault LP. Injury of the coronary endothelium at implantation increases endothelial dysfunction and intimal hyperplasia after heart transplantation. J Heart Lung Transplant 2005; 24:251–258.[CrossRef][Medline]
- Kobashigawa JA. Statins and cardiac allograft vasculopathy after heart transplantation. Semin Vasc Med 2004; 4:401–406.[CrossRef][Medline]
- Doshi AA, Rogers J, Kern MJ, Hauptman PJ. Effectiveness of percutaneous coronary intervention in cardiac allograft vasculopathy. Am J Cardiol 2004; 93:90–92.[CrossRef][Medline]
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- Chan AW, Carere RG, Khatri S, Della Siega A, Ignaszewski AP, Webb JG. Unprotected left main coronary artery stenting for cardiac allograft vasculopathy. J Heart Lung Transplant 2001; 20:776–780.[CrossRef][Medline]
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Abstract
1. Introduction