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Differentiating athlete's heart from inherited cardiac pathology: the challenge of repolarisation abnormalities presenting during anaesthesia.


This case report describes an asymptomatic healthy male professional athlete who underwent general anaesthesia for a routine orthopaedic operation. Peri-procedure, pronounced ST elevation suggestive of myocardial ischaemia manifested on the electrocardiogram lasting for four hours post-procedure, upon which the athlete developed deep and diffuse inferolateral T-wave inversion. These changes resolved spontaneously and the patient remained clinically stable throughout. This case demonstrates the clinical conundrum facing anaesthetists attempting to differentiate between repolarisation anomalies that are commonly observed in high-level athletes and those of inherited cardiac pathology, namely hypertrophic cardiomyopathy, which is the leading cause of sudden cardiac death in young athletes.

Key Words: repolarisation anomalies, athlete's heart syndrome, hypertrophic cardiomyopathy


A 26-year-old professional volleyball player of African-Caribbean ethnicity injured his left ankle in competition, sustaining ligamentous injury. He presented for ankle arthroscopy and operative repair. The patient gave informed consent for this case report to be published.

On attendance at the pre-admission clinic, he was assessed as American Society of Anesthesiologists Physical Status I. He reported no previous operative procedures, no medical issues, medications or allergies and was training several times a day (more than ten hours per week). He had no family history of cardiovascular disease or sudden cardiac death in a relative <35 years. He had been seen for routine pre-participation cardiovascular screening several months previously (electrocardiography and echocardiography are standard at our institution), with the athlete reporting that he had been cleared for professional competition. In summary, examination revealed an asymptomatic healthy, muscular athlete (92 kg, 2.07 m), with a normal airway and no cardiorespiratory abnormalities.

General anaesthesia was commenced (the patient had refused regional anaesthesia) with total intravenous anaesthesia (propofol and remifentanil infusions) and a laryngeal mask airway was inserted. Approximately 15 minutes after induction, pronounced ST elevation >2 mm was noticed on the anaesthetic monitor through Lead II and confirmed in CM5. This persisted throughout the procedure, which lasted 45 minutes and was uneventful. There were no other cardiovascular abnormalities present and all other aspects of the anaesthetic were unremarkable (Sp[O.sub.2] was 99% throughout, pulse remained between 60-65 beats per minute and blood pressure was constantly above a mean arterial pressure of 70 mmHg). Emergence from anaesthesia was unremarkable and he was transferred to the postanaesthetic care unit.

In the post-anaesthetic care unit, the ST segment elevation remained and a 12-lead electrocardiogram (ECG) revealed ST segment elevation in Leads II, V2-V6 with voltage criteria for left ventricular hypertrophy (Figure 1). He remained asymptomatic and pain-free throughout. The anaesthetist in charge at the time was unsure of the nature of the 'pronounced ST high take-off' and transferred the patient to the coronary care unit for observation, where serial troponin I's were reported as normal. Interestingly, serial ECGs demonstrated resolution of his ST segment elevation after four hours, upon which diffuse and deep inferolateral T-wave inversion became prevalent. A transthoracic echocardiogram demonstrated evidence of mild concentric left ventricular hypertrophy with an appropriately dilated left ventricular cavity and no evidence of regional wall abnormalities. He was subsequently discharged from hospital with no complications.

Subsequent review of the patient's pre-participation screening records revealed an ECG similar to his postoperative ECG, after ST segment elevation resolution (Figure 2). Accordingly, our cardiologist had characterised it as an uncommon and training-unrelated ECG (Table 1)', and as a result requested an echocardiogram, exercise stress ECG, 24-hour Holter ECG and cardiac magnetic resonance imaging with gadolinium in order to rule out cardiomyopathy pathology. These secondary investigations were within normal limits and pronounced as normal 'in the background of him being an athlete' by a specialist sports cardiologist. Despite the abnormal resting ECG, the unremarkable secondary cardiovascular examinations meant the patient had been cleared to play professional sport; thus, the patient believed that there had been no need to inform the anaesthetic team of this abnormal resting ECG prior to theatre.


Athletes are perceived as the "epitome of health", due to their lifestyle and physical achievements. However, a small but notable proportion of athletes die suddenly from sudden cardiac death (SCD). About 80% of non-traumatic sudden deaths in young athletes (<35 years) are caused by inherited or congenital structural and functional cardiovascular abnormalities. These appear to provide a substrate for arrhythmias predisposing to SCD. These pathologies include hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy, idiopathic concentric left ventricular hypertrophy, congenital anomalous coronary arteries, Wolff-Parkinson-White syndrome, Long QT syndrome and Marfan's syndrome (2-6).

Identifying asymptomatic athletes with underlying cardiovascular disease is important because SCD may be prevented by lifestyle modification, including (when necessary) restriction from competitive sports, but also prophylactic treatment by drugs, implantable cardioverter defibrillator and/or other therapeutic options. Athletes carrying an increased cardiac risk may have a favourable long-term outcome if there is timely identification and appropriate clinical management.

However, electrocardiographic alterations are common in athletes and usually reflect a physiologically benign remodelling of the heart (structural and electrical) as a response to regular intensive exercise (7-11), so called 'Athlete's Heart' syndrome.

While considered to be physiologically benign, it is important to differentiate the athlete's heart from a number of inherited cardiac pathologies, which may predispose the apparently young and healthy athlete to serious arrhythmia and the potential for SCD (12). With athletes frequently undergoing surgical procedures, this case illustrates the importance of the anaesthetic team understanding the common findings associated with the athlete's heart and how this can be differentiated from the leading cause of SCD in athletes, HCM (Figure 3) (12-14).

T-wave inversion is a particularly difficult conundrum in athletes as it may represent the only sign of an inherited heart muscle disease, even in the absence of any other features and before structural changes in the heart can be detected (15). T-wave inversion in Leads V5-V6 is nearly always associated with cardiomyopathy and should be viewed with suspicion (16), although there are other cases as well as ours that indicate that this finding is not completely foolproof (13). It is also important for the anaesthetist to note that T-wave inversion in the inferior and lateral leads is identified in 1.5-1.8% of adult and Caucasian athletes. However, T-wave inversions in the lateral leads appears to be confined to males and has been identified in only 0.3%. In contrast, T-wave inversion is identified in 10% of black athletes (6% inferior leads and 4% lateral leads), but as with Caucasian athletes, T-wave inversion in the lateral leads is usually absent in black female athletes (17).

The significance of these changes is unclear and further research, including genetic testing, is ongoing. Pelliccia et al (18) followed up 81 athletes with abnormal ECGs and found that 6% of these subsequently developed cardiomyopathies. It is postulated that these abnormal ECGs may be the earliest phenotypic expression of pathological cardiac genotypes. By contrast, Basavarajaiah and Whyte describe a series of athletes with similar ECG abnormalities that resolved with a relatively short period of de-training, thus highlighting the difficulty in diagnosing pathology (19-20). However, missing a pathological diagnosis is potentially catastrophic to all concerned.

There are two important ECG changes that are specific to HCM, which may assist in the differentiation between athlete's heart syndrome and HCM. First, the ECG is abnormal in approximately 90% of patients with HCM (i.e. HCM patients usually demonstrate a combination of T-wave inversion not including V1, III and aVR, ST-segment depression, left bundle branch block, left axis deviation, pathological Q-waves, left atrial enlargement and voltage criterion for left ventricular hypertrophy). Second, 'isolated' voltage criterion for left ventricular hypertrophy (a commonly observed feature within athletes) occurs in only 2% of HCM patients (16).

It is unclear why perioperative 'pronounced ST high take-off' occurred in our patient post-induction, or why it spontaneously resolved; perhaps early repolarisation was in fact previously present which predisposed to ST-segment elevation. As mentioned, early repolarisation is thought to occur in up to 90% of elite athletes (21) and the membrane stabilising effects of general anaesthetics may in fact have compounded this (however, other [Na.sup.+] channel blockers are not thought to accentuate this in practice (22)). Indeed, careful examination of the resting ECG (Figure 2) reveals T-wave inversion (grey arrows) without ST-segment depression but with early repolarisation in Leads V2-V4 (black arrows). Alternatively, a decrease in vagal tone during anaesthesia may have been responsible for these changes, although after checking the athletes previous exercise stress test, the ST segment changes noted during anaesthesia were not present while exercising. Coronary artery disease or spasm has been ruled out. The precise mechanism remains unclear. We have followed this athlete for four years and he remains asymptomatic, fit and well, without significant changes on echocardiography, exercise stress testing and cardiac magnetic resonance imaging.

A preoperative ECG was not requested for this patient in the pre-anaesthetic assessment, in keeping with current American College of Cardiology/ American Heart Association guidelines (23). If it had been requested, pre-existing T-wave inversion in the inferolateral leads would have been observed and resulted in further investigation prior to general anaesthesia. Alternatively, further informed discussion regarding a regional technique may have altered the anaesthetic approach for this case. The patient has since been informed that should there be a need for further anaesthetics, this information could be useful to future anaesthetists and he has been given a copy of his ECGs. Most professional athletes are subject to rigorous screening procedures before being given clearance to play (24), but these ECG irregularities may catch the unsuspecting anaesthetist out if they are unaware of their existence preoperatively.

In conclusion, this case highlights an athlete with resting abnormal ECG changes which were exacerbated by the intraoperative experience. While ultimately the outcome was good, there was a significant time and resource burden imposed as a result. This highlights the need for vigilance when dealing with apparently healthy athletes; taking a full functional history and examination may suffice in the vast majority of these patients, but occasionally further investigation is warranted before proceeding to anaesthesia.

Caption: Figure 1: 12-Lead electrocardiogram immediately post-procedure demonstrating pronounced ST segment elevation (grey arrows) in Leads II, V2-V6 with voltage criteria for left ventricular hypertrophy.

Caption: Figure 2: 12-Lead electrocardiogram four hours post-procedure demonstrating T-wave inversion in the inferolateral leads (grey arrows), with ST segment elevation in V2-V4 (black arrows) and voltage criteria for left ventricular hypertrophy.

Caption: Figure 3: Clinical criteria used to help differentiate athlete's heart from hypertrophic cardiomyopathy in individuals with borderline abnormalities. HCM=hypertrophic cardiomyopathy, LVH=left ventricular hypertrophy, LVEDD=left ventricular end-diastolic diameter, LVWT=left ventricular wall thickness, LA=left atrium, LVOTO=left ventricular outflow tract obstruction, TDI=tissue Doppler imaging, E'=peak early mitral annular velocity, E/E'=ratio of early diastolic transmitral E-wave velocities to tissue doppler mitral annulus early diastolic E'-wave velocities, ECG=electrocardiography, V[O.sub.2]=volume of oxygen per unit time.


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P. DZENDROWSKYJ *, B. HAMILTONt, M. G. WILSON ([double dagger])

Department of Anaesthesia, Qatar Orthopaedic and Sports Medicine Hospital, Doha, Qatar

* BSc(Hons), MBBS, FRCA, FANZCA, FCICM, Specialist Anaesthetist.

([dagger]) MB, ChB, FCASE Consultant in Sports Medicine, Department of Sports Medicine.

([double dagger]) BSc, PhD, Cardiovascular Physiologist, Department of Sports Medicine.

Address for correspondence: Dr P. Dzendrowskyj, Department of Anaesthesia, ASPETAR, Qatar Orthopaedic and Sports Medicine Hospital, PO Box 29222, Doha, Qatar. Email: Peter.Dzendrowskyj(a

Accepted for publication on January 24, 2013

Table 1

Classification of abnormalities of the ECG in athletes

Group 1: Common and training-   Group 2: Uncommon and training-
related ECG changes             unrelated ECG changes

* Sinus bradycardia             * T-wave inversion (except in leads
* Marked sinus arrhythmia         aVR, Lead 3, V1-V2)
* First-degree AV block         * ST-segment depression
* High degree of AV block       * Pathological Q-waves
* Incomplete RBBB               * Left atrial enlargement
* Early repolarization          * Left axis deviation/left anterior
* Isolated QRS voltage            hemiblock
  criteria for left             * Right axis deviation/left posterior
  ventricular hypertrophy,        hemiblock
  with normal axis              * Right ventricular hypertrophy
                                * Ventricular pre-excitation/WPW
                                * Complete LBBB or RBBB
                                * Long or short QT interval
                                * Brugada-like early repolarization
                                * More than one supra-ventricular
                                  premature contraction, and all
                                  forms of premature ventricular beats

ECG=electrocardiogram, AV=atrioventricular, RBBB=right bundle
branch block, LBBB=left bundle branch block, WPW=Wolff-
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Author:Dzendrowskyj, P.; Hamilton, B.; Wilson, M.G.
Publication:Anaesthesia and Intensive Care
Article Type:Case study
Date:Mar 1, 2013
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