Year : 2009  |  Volume : 12  |  Issue : 1  |  Page : 57--62

Intraoperative myocardial ischemia during renal transplantation caused by anomalous origin of the right coronary artery

Virendra K Arya1, Ashish Bangaari1, Subramanyam Rajeev1, Ashish Sharma2, Mukat Minz2, Manoj K Rohit3,  
1 Department of Anesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012, India
2 Department of Renal Transplant Surgery, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012, India
3 Department of Cardiology, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012, India

Correspondence Address:
Virendra K Arya
Department of Anesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012


Anomalous origin of the right coronary artery (AORCA) is a rare congenital anomaly with an incidence of 0.92% during routine cardiac catheterization. Its presence raises an important concern to the anaesthesiologist because it can lead on to myocardial ischaemia manifesting as either angina pectoris or myocardial infarction, or sudden death in young patients with minimal exertion, even in the absence of atherosclerosis. Patients with AORCA may be intolerant to stress and the high cardiac output condition owing to volume loading. Such a therapeutic manoeuvre may be desirable during renal transplantation to enable better perfusion of the renal graft immediately after grafting the kidney, in order to improve its function. Hence, haemodynamic goals in renal transplant recipient with AORCA can be contradictory during surgery, thereby rendering anaesthetic management challenging. We report a case of acute myocardial ischemia precipitated by fluid loading conditions in a patient with AORCA during renal transplant that was successfully treated with emergent intra-aortic balloon pump therapy intraoperatively. Judicious intraoperative fluid replacement is recommended, and volume overload must be avoided in AORCA patients undergoing surgery.

How to cite this article:
Arya VK, Bangaari A, Rajeev S, Sharma A, Minz M, Rohit MK. Intraoperative myocardial ischemia during renal transplantation caused by anomalous origin of the right coronary artery.Ann Card Anaesth 2009;12:57-62

How to cite this URL:
Arya VK, Bangaari A, Rajeev S, Sharma A, Minz M, Rohit MK. Intraoperative myocardial ischemia during renal transplantation caused by anomalous origin of the right coronary artery. Ann Card Anaesth [serial online] 2009 [cited 2022 Jan 27 ];12:57-62
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Full Text

Anomalous origin of the right coronary artery (AORCA) from the left sinus of Valsalva is a rare congenital anomaly that was first described in 1948 by White and Edwards. [1] The incidence of this anomaly is 0.92% during routine cardiac catheterization. [2] Although not considered clinically important in the past, [3] the presence of AORCA is of special concern to the anaesthesiologist as it can lead to angina pectoris, myocardial infarction (MI), or sudden death in young patients with minimal exertion, even in the absence of atherosclerosis. [4],[5],[6] In contrast to the normal right coronary artery (RCA) originating from the right aortic sinus [Figure 1a], AORCA has been found to arise from various regions as demonstrated by angiography: left sinus of Valsalva, non-facing aortic sinus, left main coronary, left anterior descending (LAD) coronary artery, left circumflex artery and pulmonary trunk or pulmonary artery. There are three subtypes of AORCA from the left sinus of Valsalva based on the path of the anomalous artery. They are as follows: interarterial, retro-aortic, and anterior to the pulmonary trunk. The interarterial subtype of AORCA from the left sinus of Valsalva [Figure 1b] and AORCA from the pulmonary artery are considered "malignant anomaly" and associated with a high risk of exercise-induced ischaemia, MI, and sudden cardiac death. [7],[8]

We report a case of acute myocardial ischaemia precipitated by haemodynamic alterations occurring during renal transplant (RT) surgery in a patient with interarterial subtype of AORCA that required emergent intra-aortic balloon pump (IABP) therapy. Further implications of peri-operative issues related to this condition requiring special care are discussed.

 Case Report

A 45-year-old male, weighing 57 kg, with end-stage renal disease (ESRD) receiving bi-weekly renal replacement therapy, was scheduled for RT. He had a surgically created arterio-venous fistula on left upper forearm and his preoperative haemoglobin was 9 gm%. He had well-controlled hypertension and diabetes mellitus. He also gave history of episodic atypical chest pain. Coronary angiography and CT angiography after an episode of chest pain performed a month prior were significant for diffuse mid-segment left anterior descending artery (LAD) narrowing of 25%-30%, dominant RCA circulation with anomalous origin from left sinus of Valsalva [Figure 2a] and interarterial course of AORCA on multi-slice-CT 3D reconstructed image [Figure 2b]. Attending cardiologist considered the LAD lesion insignificant and suggested no intervention for AORCA. Pre-operative electrocardiogram (ECG) revealed sinus rhythm with right bundle-branch block and strain pattern. Echocardiography showed concentric LV hypertrophy (septum: 18 mm, post wall: 16 mm) with mild diastolic dysfunction (diagnosed by E:A ratio), ejection fraction of 72% and no regional wall motion abnormalities (RWMA). Medications included daily aspirin 150 mg, atenolol 100 mg, amlodipine 10 mg and insulin. All cardiac medications were continued on the day of surgery, except aspirin.

Combined epidural and general anaesthesia was chosen as the anaesthetic technique. Monitoring included 5-lead ECG, pulse-oximetry (SpO 2 ), end-tidal capnometry (EtCO 2 ), invasive blood pressure (IBP), pulmonary artery pressure (PAP), pulmonary artery occlusion pressure (PAOP), temperature and urine output. The baseline arterial pressure, central venous pressure (CVP), PAP, PAOP and cardiac index (CI) were 104/68 mmHg, 3 mmHg, 22/8 mmHg, 5 mmHg and 2 L/min/m 2 , respectively. Serum electrolyte values measured on the morning of surgery were normal. An epidural catheter was inserted in L 1-2 interspace and sensory block of T 8 -L 1 dermatomes was achieved by 10 ml of 0.5% bupivacaine with 50 g fentanyl after confirming its position. Subsequently, general anaesthesia was induced intravenously with fentanyl 50 g, thiopentone 250 mg and suxamethonium 125 mg. Anaesthesia was maintained with 66% nitrous oxide in oxygen, isoflurane and atracurium. The patient was infused with 4 L of normal saline and 200 ml of 20% albumin over 2 h to build up PAOP to 15 mmHg. The CI at this time increased to 4.7 L/min/m 2 . The target PAOP was achieved at approximately 30 min before the declamping of graft vessels and despite further restriction of fluids, PAOP was increasing, so did the CVP and PAP. The authors noted a gradual fall in the systemic pressures and SpO 2 , despite decreasing the depth of anaesthesia and increasing FiO 2 [Figure 3]. Injection frusemide 80 mg and 100 ml of 20% mannitol were infused prior to the declamping of renal vessels as per renal transplantation protocol, and one unit of blood was transfused slowly (Haemoglobin at this point was 8.5 gm%,) after establishing graft reperfusion and urine output. Post graft perfusion, CVP remained high (> 20 mm Hg) and tall 'cv' waves with no 'x' decent appeared in the CVP waveform, which was suggestive of tricuspid regurgitation (TR). However, PAP and PAOP gradually decreased reversing the PAOP to CVP gradient [Figure 3]. Systemic pressures further decreased and remained low with no change in the heart rate from baseline despite fluid challenges, phenylephrine 100 mg boluses and light plane of anaesthesia. Dopamine followed by dobutamine and adrenaline were gradually added when IBP dropped to 80/40 mmHg. The patient continued to remain hypotensive despite the vasopressor support (20 g/kg/min of dopamine and dobutamine each; 0.04 g/kg/min of adrenaline) and urine output stopped from the transplanted kidney. Significant ST-segment elevation appeared in leads II, III, and aVF. Combination of nitroglycerine (1-3 g/kg/min) with ionotropes also failed to improve the haemodynamic parameters. Fluid administration was restricted in view of absence of urine output.

Arterial blood gas analysis at this time showed pH of 7.33, partial pressure of oxygen 64 mmHg, partial pressure of carbon dioxide 36 mmHg, bicarbonate 19 mmol/L, base excess - 4, SpO 2 91% with fractional inspired oxygen concentration of 1.0 and haemoglobin 10.5 gram%. The measured CI values were between 3.1 and 4.1 L/min/m 2 during the hypotensive period [Figure 3] that were contrary to clinical signs (diminishing urine output, soft feel of grafted kidney by surgeon, cool extremities and low amplitude SpO 2 waveform), which were suggestive of low CI. Hence, irrespective of the measured values, low CI secondary to myocardial ischaemia, possibly predominant right ventricular involvement was suspected on the ECG and reversed PAOP to CVP gradient findings (CV P > PAOP), and no further CI measurements by bolus thermodilution technique were performed intraoperatively as they were time consuming, leading to further fluid load, as well as misleading. Keeping in view the intraoperative status, ongoing ischaemia and haemodynamic instability despite medical therapy, the attending cardiologist decided to support the failing ventricle by inserting an intra-aortic ballon pump (IABP), which was inserted through femoral artery on the side opposite to the grafted kidney under fluoroscopic guidance. Transthoracic echocardiography at this time revealed dilated hypokinetic right ventricle with moderate tricuspid regurgitation, paradoxical motion of the interventricular septum, inferior wall hypokinesia and left ventricular (LV) ejection fraction of 30%-35%. After completion of the surgery, the patient was transferred to the renal transplant intensive care unit. The haemodynamic parameters and SpO 2 gradually improved with IABP support. A 12-lead ECG in intensive care unit revealed significant ST elevation in leads II, III (ST elevation in III > II), aVF, and V 1 to V 4 R. Troponin-T test performed by using a semi-quantitative kit after 6 h in the ICU was found reactive (Troponin-T level > 0.1 ng/ml), which was suggestive of MI.

Eight hours after the IABP therapy, ST segment changes reverted and ionotropes were tapered with marked improvement in urine output. IABP augmentation was gradually reduced and discontinued after 12 h. The patient was extubated on the first post-operative day and discharged on the seventh post-operative day with normally functioning transplanted kidney. A repeat echo showed normal-sized right ventricle with no RWMA, and left ventricle EF of 50%-55%.


The haemodynamic management during renal transplantation is usually based on the maintenance of adequate intravascular volume, preferably higher side of normal filling pressure (CVP 10-15 mmHg and pulmonary diastolic pressure > 15 mm Hg) and systemic blood pressures (systolic > 130 mmHg, mean > 85 mmHg) at the time when reperfusion to transplanted kidney is established. [9],[10] Immediate graft function has been associated with a blood volume greater than 70 ml/kg and a plasma volume greater than 45 ml/kg. [10] Patients with CAD and/or decreased cardiac reserve may not tolerate volume loading because it may result in increased cardiac work and dilutional anaemia in an already anaemic ESRD patient. This may worsen the ratio of myocardial oxygen demand and supply, thus precipitating myocardial ischaemia. Hence, the intention to assure adequate volume status must be balanced against the danger of fluid overload in such patients. Despite these recommendations, the authors administered intravenous fluids as per their protocol because they were of the opinion that their patient had good myocardial reserve capable of tolerating the fluid challenge. We were not aware of any recommendations in literature recommending fluid restriction in patients with AORCA similar to patients with poor cardiac reserve while managing this case.

In the present case, myocardial ischaemia seems to have been primarily initiated due to AORCA precipitating RCA block at its interarterial part or at slit-like ostium in the left aortic sinus or at both sites due to high normal volume loading conditions resulting in distension of aorta and pulmonary artery. Other factors such as dilutional anaemia, volume load, pre-existing LAD lesion and LV hypertrophy, if at all, might have contributed secondarily. The pre-existing insignificant LAD lesion and given volume load cannot explain the entire intraoperative clinical course of the patient. ECG changes of ST elevation in inferior and right chest wall leads along with reversed CVP to PAOP gradient were representative of ischaemia in RCA territory, [11] which had no atherosclerotic lesion on angiography. Ischaemia in the LAD territory could be secondary due to persistent hypotension and LV hypertrophy. Intraoperative transoesophageal echocardiography (TEE) could have confirmed this diagnosis much earlier; [12] however, this was unfortunately not available in our renal transplant set up. However, transthoracic echocardiographic findings in the ICU showing dilated hypokinetic right ventricle and paradoxical motion of the interventricular septum with inferior wall hypokinesia were consistent with the findings observed during ischaemia of right ventricle and inferior wall of left ventricle leading to low CI and hypotension. [13] The other differential diagnosis for this type of echocardiographic findings could be pulmonary thromboembolism or air embolism that seems to be a remote possibility.

The mechanism of coronary ischaemia in patients with interarterial subtype of AORCA has been speculated to be due to abnormal course and slit-shaped ostium. [2],[4],[5],[6],[7],[14] Because the RCA arises from contra-lateral sinus of Valsalva, it must cross the base of the heart, which creates an acute angulation at its origin exposing it to compression between the aorta and the main pulmonary artery [Figure 1b],[Figure 2b]. Myocardial ischaemia is, therefore, associated with trivial exhaustion or events associated with increased CI as may occur due to sympathetic stimulation frequently encountered in surgical patients. [2],[4],[5],[7] Sudden onset of myocardial ischaemia even during resting conditions has also been reported in patients with malignant type of AORCA due to vasospasm. [5],[15] Compression of AORCA between aorta and main pulmonary trunk during systole has been shown during multi-detector computed tomography and ionotropes are unlikely to benefit hypotension in this situation. [7],[16] Some reports have suggested that compression or kinking phenomenon could also result in some degree of intimal disruption and subsequent vasospasm at proximal portion of anomalous coronary artery. [5],[15],[17] In our patient, the timing of haemodynamic instability coincided with increasing CI and graft reperfusion when filling pressures were raised towards the high normal range. The measured CI values remained higher than the baseline value during the hypotensive episode, which were misleading. Various studies have reported error in cardiac output measurement by thermodilution technique during acute TR. [18],[19] Once hypotension occurred, it was imperative to achieve early haemodynamic stability to prevent acute tubular necrosis in the transplanted kidney. Moreover, a high dose of ionotropes is also considered detrimental to the transplanted kidney. [9] Hence, using IABP support intraoperatively was the only option left without any previous literature supporting its use in RT. The author's decision was in accordance with the American College of Cardiology/American Heart Association guidelines for the management of acute MI that considered IABP as a class-I indication for cardiogenic shock that is not quickly reversed by pharmacological therapy. [20] IABP improved myocardial perfusion by improving coronary flow, and it may have improved the survival of the transplanted kidney by improving CI.

The management of patients with AORCA from the left sinus of Valsalva remains controversial, and there are no available guidelines for peri-operative management. However, from this report, one can retrospectively conclude that the author's decision to build up PAOP towards high normal side by giving liberal fluids may be incorrect and responsible for subsequent problems. Fluid management plan in AORCA patients undergoing surgery should be judicious and in renal transplant it should be modified in favour of maintaining just adequate filling pressures to maintain baseline haemodynamics and give additional fluids as per need once diuresis from the grafted kidney starts after reperfusion. Therefore the authors suggest that fluid overload must be prevented during surgery in such patients. In addition, their patient may have benefited by intraoperative transoesophageal echocardiogram monitoring, which would have revealed the occurrence of RWMA and tricuspid regurgitation early, and the authors could have withheld intravenous fluids. Some reports have advocated the use of nitrates, beta blockers and calcium channel blockers for reducing vasospasm in AORCA. [21] Our patient was already receiving calcium channel blocker and beta blocker. The trial of intraoperative nitroglycerine use was unsuccessful may be due to mechanical nature of RCA obstruction precipitated by fluid overload and perhaps it was used for a short period of time that was insufficient to take off a large preload. It was used for a short time period because it caused further fall in BP (from 96 to 80 mmHg).

The author's case report highlights peri-operative implications during the anaesthetic management of patients with AORCA. This condition is now considered to be of class-III severity in clinical relevance-based classification of coronary artery anomalies in the adults and recognized as an important causative factor in sudden death and MI. [22] Till any definitive preoperative intervention is recommended for these patients, anaesthetists must be aware of the patho-physiological conditions that can precipitate coronary ischaemia in these patients peri-operatively.

In conclusion, conditions causing sympathetic stimulation, distension of major vessels, increasing PA pressure and cardiac output should be prevented or controlled in AORCA patients during surgery. Intraoperative fluid replacement should be carefully titrated to requirement and fluid overload must be avoided prospectively, given the problems associated with fluid overload when a transplanted kidney is either slow to function or failing. Thus, the normal appropriate goals for fluid management during renal transplant are even more critical in a patient with AORCA. Utility of early IABP use in relieving refractory myocardial ischaemia precipitated by this condition must be kept in mind considering the mechanical nature of RCA obstruction.


1White NK, Edwards JE. Anomalies of the coronary arteries: Report of four cases. Arch Pathol (Chic) 1948;45:766-71.
2Angelini P, Velasco JA, Flamn S. Coronary anomalies: Incidence, pathophysiology and clinical relevance. Circulation 2002;105:2449-54.
3Alexander RW, Griffith GC. Anomalies of the coronary arteries and their clinical significance. Circulation 1956;14:800-5.
4Assiri AS. Acute coronary syndrome caused by anomalous origin of the right coronary artery from the left sinus of Valsalva. West Afr J Med 2005;24:278-9.
5Kaku B, Kanaya H, Ikeda M, Uno Y, Fujita S, Kato F, et al . Acute inferior myocardial infarction and coronary spasm in a patient with an anomalous origin of the right coronary artery from the left sinus of Valsalva. Jpn Circ J 2000;64:641-3.
6Boissier F, Coolen N, Nataf P, Tchetche D. Sudden death related to an anomalous origin of the right coronary artery. Ann Thorac Surg 2008;85:1077-9.
7Ichikawa M, Sato Y, Komatsu S, Hirayama A, Kodama K, Saito S. Multislice computed tomographic findings of the anomalous origins of the right coronary artery: Evaluation of possible causes of myocardial ischemia. Int J Cardiovasc Imaging 2007;23:353-60.
8Komatsu S, Sato Y, Ichikawa M, Kunimasa T, Ito S, Takagi T, et al . Anomalous coronary arteries in adults detected by multislice computed tomography: Presentation of cases from multicenter registry and review of the literature. Heart Vessels 2008;23:26-34.
9Lemmens HJ. Kidney transplantation: Recent developments and recommendations for anaesthetic management. Anesthesiol Clin North Am 2004;22:651-62.
10Baker J, Yost S, Niemann CU. Organ transplantation. In: Miller RD, editor. Miller's Anaesthesia. 6th ed. Philadelphia, Pennsylvania: Elsevier Churchill Livingstone; 2005. p. 2231-83.
11Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med 2003;348:933-40.
12Uchida T, Ishihara M, Dote K, Tateishi H, Sato S. Quantitative evaluation of right ventricular function by transesophageal echocardiography: Report of a case with classical right ventricular infarction. J Cardiol Suppl 1991;26:25-33.
13Elkayam U, Halprin SL, Frishman W, Strom J, Cohen MN. Echocardiographic findings in cardiogenic shock due to right ventricular myocardial infarction. Catheter Cardiovasc Diagn 1979;5:289-94.
14Beique F, Tran QH, Ma F, Rudski L, Daves S, Angelini P. Anomalous right coronary originating from the left sinus of valsalva. J Cardiothorac Vasc Anesth 2004;18:788-98.
15Ichikawa M, Komatsu S, Asanuma H, Iwata A, Ishiko T, Hirayama A, et al . Acute myocardial infarction caused by "malignant" anomalous right coronary artery detected by multidetector row computed tomography. Circ J 2005;69:1564-7.
16Ghersin E, Litmanovich D, Ofer A, Lessick J, Dragu R, Rispler S, et al . Anomalous origin of right coronary artery: Diagnosis and dynamic evaluation with multidetector computed tomography. J Comput Assist Tomogr 2004;28:293-4.
17Maddoux GL, Goss JE, Ramo BW, Raff GL, Heuser RR, Shadoff N, et al . Angina and vasospasm at rest in a patient with an anomalous left coronary system. Catheter Cardiovasc Diagn 1989;16:95-8.
18Heerdt PM, Blessios GA, Beach ML, Hogue CW. Flow dependency of error in thermodilution measurement of cardiac output during acute tricuspid regurgitation. J Cardiothorac Vasc Anesth 2001;15:183-7.
19Heerdt PM, Pond CG, Blessios GA, Rosenbloom M. Inaccuracy of cardiac output by thermodilution during acute tricuspid regurgitation. Ann Thorac Surg 1992;53:706-8.
20Ryan TJ, Antman EM, Brooks NH, Califf RM, Hillis LD, Hiratzka LF, et al. 1999 update: ACC/AHA Guidelines for the Management of Patients with acute myocardial infraction: Executive summary and recommendations: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infraction. Circulation 1999;100:1016-30.
21Kaku B, Shimizu M, Yoshio H, Ino H, Mizuno S, Kanaya H, et al . Clinical features and prognosis of Japanese patients with anomalous origin of the coronary artery. Jpn Circ J 1996;60:731-41.
22Rigatelli G, Rigatelli G. Congenital coronary artery anomalies in the adult: A new practical viewpoint. Clin Cardiol 2005;28:61-5.