Tako-tsubo Cardiomyopathy on the First Day After Renal Transplantation d Case Report and Literature Review  skab, A. Dębska-Slizie a, M. Bohdanb, M. Gruchałab, and B. Rutkowskia J. Gołębiewskaa,*, I. Stopczyn n a Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland; and bFirst Department of Cardiology, Medical University of Gdansk, Gdansk, Poland

ABSTRACT Background. The etiology of tako-tsubo cardiomyopathy, defined as a transient left ventricular dysfunction in the absence of significant coronary artery stenosis, still remains unclear. This syndrome mainly occurs in postmenopausal women and is often associated with emotional stress or miscellaneous diagnostic and therapeutic procedures. Estimated prevalence of tako-tsubo cardiomyopathy is found in 1% to 2% of patients presenting with suspected acute coronary syndrome. So far there has been only one case report of tako-tsubo cardiomyopathy in a renal transplant recipient. Case report. We describe the case of a 68-year-old woman with a history of coronary artery disease and coronary artery bypass grafting in whom unspecific transient chest pain and hypotension were observed on the first day after renal transplantation. After transplantation, the patient was anuric with pulmonary congestion and toxic tacrolimus concentrations were observed. Electrocardiogram showed sinus rhythm with left bundle branch block (LBBB) that has not been described before. Plasma cardiac necrosis markers troponin I and creatine kinase MB were mildly elevated. Echocardiography showed severe left ventricular function impairment with characteristic shape of left ventricle. Subsequent cardiac catheterization revealed the absence of angiographic evidence of acute plaque rupture within both coronary arteries and bypass grafts. During the next few days there was marked clinical improvement with resolution of LBBB and full recovery of all biochemical parameters. On discharge, full functional recovery of the left ventricle in echocardiography was observed. Postulated mechanisms of tako-tsubo cardiomyopathy include catecholamine excess, coronary artery spasm, and microvascular dysfunction. On the other hand calcineurin inhibitors are known factors causing coronary epicardial endothelial dysfunction and negatively affecting vasomotor function. Conclusions. Tako-tsubo cardiomyopathy in patients after renal transplantation may be at least in part a manifestation of calcineurin inhibitor cardiotoxicity.

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AKO-TSUBO cardiomyopathy was first described by Sato et al in 1990 as systolic dysfunction of the apical and/or mid-segments of the left ventricle that mimics myocardial infarction, but in the absence of obstructive coronary artery disease [1]. This condition was initially considered a rare disease that affected only postmenopausal women exposed to great psychological stress such as the death of a spouse. Nowadays it is an increasingly reported clinical syndrome, affecting patients of different ages, both genders, and precipitated by a variety of physical and emotional stressors. Tako-tsubo cardiomyopathy has so far

been diagnosed in the setting of various medical conditions such as pneumothorax, status asthmaticus with beta2agonist overdose, incidental hypothermia and diabetic ketoacidosis, chemotherapy course for breast or renal cancer, snake bite, stroke caused by air embolism, severe burn

*Address correspondence to Justyna Gołębiewska, Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, ul. Debinki 7, 80-952 Gdansk, Poland. E-mail: [email protected]

0041-1345/14 http://dx.doi.org/10.1016/j.transproceed.2014.09.075

ª 2014 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710

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Transplantation Proceedings, 46, 2920e2922 (2014)

TAKO-TSUBO CARDIOMYOPATHY

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injury, heavy alcohol overdose, heroin/methadone withdrawal, and procedures both with and without general anesthesia such as emergency colostomy, bladder hydrodistention, urgent ureteral stenting, total gastrectomy, cataract extraction, laparoscopic cholecystectomy, repair of uterine prolapse, cesarean section, and many more. CASE REPORT A 68-year-old woman with end-stage renal disease secondary to glomerulonephritis underwent a renal transplantation (RTx) from a 45-year-old deceased male donor who died of subarachnoid hemorrhage. She had a history of hypertension and coronary artery disease (CAD) and underwent coronary artery bypass grafting (CABG) surgery 3 years before RTx. Her medical history also included cholelithiasis, coxarthrosis, and appendectomy. Her family history was insignificant (in particular with regard to cardiovascular and cerebrovascular diseases). She had been maintained on hemodialysis for the preceding 4 years. At the time of RTx she was in a good general condition. Cardiologic evaluation before RTx revealed positive exercise electrocardiogram (ECG) test at workload of 7 METs. On echocardiography, normal heart chambers with good global and segmental contractility were observed with no significant valves abnormalities. The consulting cardiologist concluded that this was consistent with stable coronary heart disease and required no further action. Doppler ultrasound showed good blood flows within lower extremities arteries. Doppler ultrasound of carotid arteries was not performed. The kidney donor was of B category according to deceased donor score [2]. His estimated glomerular filtration rate (eGFR; CockroftGault) and plasma creatinine level were 107  29.9 mL/min/1/73 m2 and 0.85  0.23 mg/dL, respectively. Total ischemic time was 12 hours and 30 minutes; HLA mismatching was 0:0:1 (A, B, DR), respectively. Anesthesia and surgery were uneventful, with good initial kidney perfusion. However, the operating surgeon observed atherosclerotic plaques in the recipient’s external iliac artery. Initial maintenance immunosuppression consisted of glucocorticosteroids, mycophenolate mofetil (1.0 g twice daily) and tacrolimus (0.1 mg/kg bw twice daily), without induction. On day 1 after RTx, the patient presented with unspecific, transient chest pain. Arterial hypotension (85/50 mm Hg) and moderate sinus tachycardia (100 bpm) were observed. Patient was anuric with pulmonary congestion. ECG showed a left bundle branch block (LBBB) that has not been described before. Mild troponin I (TnI) and creatine kinase MB (CKMB) elevation (TnI 1.62 ng/mL and CKMB 15.9 U/L) was observed. Other biochemical parameters and their evolution during the patient’s hospitalization are presented in Table 1.

Table 1. Evolution of the Biochemical Parameters During Hospitalization Time After RT (d)

Level of biochemical parameters

1

2

3

5

14

21

Tacrolimus (mg/mL) TnI (ng/mL) CKMB (U/L) Creatinine (mg/dL) BUN (mg/dL) Kþ (mmol/L)

d 1.62 15.9 3.65 30.6 3.4

40.5 1.91 9.9 3.73 42.0 3.9

d 5.35 18.7 5.43 63.3 3.8

22.5 5.28 7.1 4.08 52.6 4.6

14.4 1.52 2.8 3.14 51.3 4.8

9.5 d d 0.87 24.6 4.7

Abbreviations: RT, renal transplantation; TnI, troponion I; CKMB, creatine kinase MB; BUN, blood urea nitrate; Kþ, potassium.

Transthoracic echocardiography showed severe left ventricular function impairment (ejection fraction ¼ 35% to 40%) with shape of left ventricle consistent with tako-tsubo cardiomyopathy. However, due to the patient’s significant history of CAD and ECG and laboratory symptoms consistent with acute coronary syndrome, she was referred for urgent coronary angiography. No angiographic evidence of acute plaque rupture and thrombosis within both coronary arteries and bypass grafts was revealed. Ventriculography showed an apical ballooning pattern with contrast retention in the apex. Because of the risk of hemorrhage on the first day after vascular surgery and echocardiography strongly suggestive of takotsubo cardiomyopathy diagnosis, the patient was only maintained on low-molecular-weight heparin and aspirin and received no clopidogrel before coronary angiography. Tacrolimus level was measured on the second day after transplantation and was 40.5 ng/mL; since that time it was rapidly tapered to maintain a blood level between 10 and 12 ng/mL. Within the days of reducing the tacrolimus trough level there was observed a marked clinical improvement with resolution of LBBB and full recovery of all biochemical parameters. In echocardiography on discharge the left ventricle apical wall abnormalities resolved and systolic function normalized with EF 65% whereas the tacrolimus level decreased to 9.5 ng/mL. Because of delayed graft function, the patient required six hemodialysis sessions. The initial transplant ultrasound scanning showed no abnormalities, with good Doppler blood flows. However, on the third day after RTx there was an increase in resistive index and reduction of intrarenal flow velocities consistent with tacrolimus toxicity. Allograft function slowly improved and the patient was discharged on the postoperative day 22 with a serum creatinine concentration of 0.87 mg/dL, a creatinine clearance of 55 mL/min, and an eGFR modification of diet for renal disease (MDRD) score of >60 mL/min/1.73 m2. The discharge transplant ultrasound scanning showed no abnormalities, with good Doppler blood flows.

DISCUSSION

So far there have been several reports of tako-tsubo cardiomyopathy soon after orthotopic liver transplantation [3e8], a single report of tako-tsubo cardiomyopathy directly preceding lung transplantation [9], and a single description of spontaneously occurring biventricular tako-tsubo cardiomyopathy in a heart transplantation patient [10]. It has also been postulated that heart dysfunction observed in a braindead donor and recipient after heart transplantation may be an extreme variant of tako-tsubo cardiomyopathy resulting from a “catecholamine storm” associated with a rapidly increasing intracranial pressure [11]. To our knowledge, this is the second description of tako-tsubo cardiomyopathy in an RTx patient [12]. The pathogenesis of this disorder is not well determined. The onset is frequently but not always triggered by an acute medical illness or by intense emotional or physical stress. Postulated mechanisms of tako-tsubo cardiomyopathy include catecholamine excess, coronary artery spasm, and microvascular dysfunction. Renal calcineurin inhibitor (CNI) toxicity is a frequent adverse effect of immunosuppression with CNIs in solid organ transplantation, leading to acute and chronic renal failure. Acute CNI toxicity is due to tubular epithelial cell

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vacuolation, atrophy, and microcalcification and vasoconstriction of the vasa afferens and efferens and vacuolization of smooth muscle cells leading to vessel lumen narrowing [13]. CNIs are also known factors causing coronary epicardial endothelial dysfunction and negatively affecting vasomotor function [14,15]. Tacrolimus has been shown to accelerate the progression of coronary microangiopathy to a greater extent than cyclosporine, both in animal models [16,17] and human studies [18]. This discrepancy may result from the fact that tacrolimus induces endothelial dysfunction independently of calcineurin inhibition [19]. Because the etiology of tako-tsubo is still unknown, the management of this cardiomyopathy remains undetermined. It is important to seek and eliminate underlying causes. The prognosis is good and the goal of the treatment is to relieve symptoms and avoid complications. Kurisu et al [20] observed left ventricular apical thrombosis in 5.3% of takotsubo patients. Therefore, it is believed that anticoagulant therapy should be implemented and continued until the left ventricle contraction improves. In some patients, persistent left ventricular wall motion abnormalities are observed [21]. According to some authors, such patients should be given beta-blockers, angiotensin-converting enzyme inhibitors, or angiotensin II type 1 receptor blockers [22]. This case shows the potential role of tacrolimus toxicity in causing both severe coronary epicardial and intrarenal vasoconstriction with tubular damage. In the described patient, after reduction of the tacrolimus serum level, both cardiac and renal function improved markedly. Therefore, we postulate that it is necessary to consider tacrolimus toxicity in patients presenting with tako-tsubo cardiomyopathy and delayed graft function early after renal transplantation. REFERENCES [1] Sato H, Taiteishi H, Uchida T. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon M, editors. Clinical aspect of myocardial injury: From ischemia to heart failure. Tokyo, Japan: Kagakuhyouronsha, Tokyo; 1990. pp. 56. [2] Nyberg SL, Baskin-Bey ES, Kremers W, et al. Improving the protection of donor kidney quality: deceased donor score and resistive indices. Transplantation 2005;80:925. [3] Tachotti Pires LJ, Cardoso Curiati MN, Vissoci Reiche F, et al. Stress-induced cardiomyopathy (takotsubo cardiomyopathy) after liver transplantation-report of two cases. Transplant Proc 2012;44:2497. [4] Eagle SS, Thompson A, Fong PP, et al. Takotsubo cardiomyopathy and coronary vasospasm during orthotopic liver

   ET AL GOŁĘBIEWSKA, STOPCZYNSKA, DĘBSKA-SLIZIE N transplantation: separate entities or common mechanism? J Cardiothorac Vasc Anesth 2010;24:629. [5] Saner FH, Plicht B, Treckmann J, et al. Tako-Tsubo syndrome as a rare cause of cardiac failure in liver transplantation. Liver Int 2010;30:159. [6] Phillips MS, Pruett TL, Berg CL, et al. Takotsubo cardiomyopathy in a liver transplant recipient: a diagnosis of exclusion? J Cardiothorac Vasc Anesth 2009;23:268. [7] Tiwari AK, D’Attellis N. Intraoperative left ventricular apical ballooning: transient Takotsubo cardiomyopathy during orthotopic liver transplantation. J Cardiothorac Vasc Anesth 2008;22:442. [8] Lee HR, Hurst RT, Vargas HE. Transient left ventricular apical ballooning syndrome (Takotsubo cardiomyopathy) following orthotopic liver transplantation. Liver Transpl 2007;13:1343. [9] Michel-Cherqui M, Felten ML, Liu N, et al. Management of takotsubo cardiomyopathy in a lung transplant recipient. Transplantation 2010;90:692. [10] Behnes M, Baumann S, Borggrefe M, et al. Biventricular takotsubo cardiomyopathy in a heart transplant recipient. Circulation 2013;128:e62. [11] Berman M, Ali A, Ashley E, et al. Is stress cardiomyopathy the underlying cause of ventricular dysfunction associated with brain death? J Heart Lung Transplant 2010;29:957. [12] Chrapko BE, Tomaszewski A, Jaroszy nski AJ, et al. Takotsubo syndrome in a patient after renal transplantation. Med Sci Monit 2012;18:CS26. [13] Finn WF. FK506 nephrotoxicity. Ren Fail 1999;21:319e29. [14] Moien-Afshari F, McManus BM, Laher I. Immunosuppression and transplant vascular disease: benefit and adverse effects. Pharmacol Ther 2003;100:141. [15] Keogh A. Calcineurin inhibitors in heart transplantation. J Heart Lung Transplant 2004;23(suppl):S202. [16] Arai S, Teramoto S, Senoo Y. The impact of FK506 on graft coronary disease of rat cardiac allograft d a comparision with cyclosporine. J Heart Lung Transplant 1992;11:757. [17] Meiser BM, Billingham ME, Morris RE. Effects of cyclosporin, FK506, and rapamycin on graft-vessel disease. Lancet 1991;338:1297. [18] Abu-Quaoud MS, Soletniy LN, Chen D, et al. Lack of relationship between microvascular and macrovascular disease in heart transplant recipients. Transplantation 2012;94:965. [19] Eguchi R, Kubo S, Ohta T, et al. FK506 induces endothelial dysfunction through attenuation of Akt and ERK1/2 independently of calcineurin inhibition and the caspase pathway. Cell Signal 2013;25:1731. [20] Kurisu S, Inoue I, Kawagoe T, et al. Incidence and treatment of left ventricular apical thrombosis in Tako-tsubo cardiomyopathy. Int J Cardiol 2011;146:E58. [21] Kurisu S, Inoue I, Kawagoe T, et al. Persistent left ventricular dysfunction in takotsubo cardiomyopathy after pacemaker implantation. Circ J 2006;70:641. [22] Kurisu S, Kihara Y. Tako-tsubo cardiomyopathy: clinical presentation and underlying mechanism. J Cardiology 2012;60:429.

Tako-tsubo cardiomyopathy on the first day after renal transplantation - case report and literature review.

The etiology of tako-tsubo cardiomyopathy, defined as a transient left ventricular dysfunction in the absence of significant coronary artery stenosis,...
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