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 Table of Contents  
Year : 2019  |  Volume : 3  |  Issue : 1  |  Page : 21-26

Differentiation of T-wave inversion changes with borderline left ventricular hypertrophy in an asymptomatic young athlete – Case report and literature review

Department of Epidemiology, Cardiovascular Disease Prevention and Health Promotion, Institute of Cardiology, Warsaw, Poland

Date of Submission08-Aug-2019
Date of Acceptance26-Aug-2019
Date of Web Publication12-Nov-2019

Correspondence Address:
Dr. Lukasz A Malek
Department of Epidemiology, Cardiovascular Disease Prevention and Health Promotion, Institute of Cardiology, Niemodlinska Str 33, 04-635 Warsaw
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/hm.hm_26_19

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This is a case of initially 15 years of age, white, male from junior football team. He was completely asymptomatic, with no previous medical history or family history of sudden cardiac death and cardiac diseases. He has been playing football for 8 years. On periodic preparticipation screening, he presented T-wave inversions (TWIs) in leads V4–V6 and II, III, and aVF, which were not observed before on yearly screenings. Subsequently, he underwent echocardiography, which showed mildly increased myocardial thickness (13 mm) without other abnormalities. He was then referred to for further testing, which is discussed in the context of the current literature. Finally, management is presented.

Keywords: Athlete, electrocardiogram, left ventricle, hypertrophy

How to cite this article:
Malek LA. Differentiation of T-wave inversion changes with borderline left ventricular hypertrophy in an asymptomatic young athlete – Case report and literature review. Heart Mind 2019;3:21-6

How to cite this URL:
Malek LA. Differentiation of T-wave inversion changes with borderline left ventricular hypertrophy in an asymptomatic young athlete – Case report and literature review. Heart Mind [serial online] 2019 [cited 2023 May 31];3:21-6. Available from: http://www.heartmindjournal.org/text.asp?2019/3/1/21/270768

  Introduction Top

T wave inversion (TWI) in inferolateral electrocardiogram (ECG) leads (excluding lead III) is considered as unrelated to regular training and is not an element of physiological adaptation to exercise. This type of changes is also not a form of a “juvenile ECG,” where TWI extending to V3 (and not only present in V1 or V2) may be occasionally found in athletes <16 years of age or before puberty.[1],[2] For that reason, any case of TWI in the presented leads should undergo further investigation irrespective of athlete's age, gender, or race.[3] Particular attention should be given to screening for the presence of a quiescent form of cardiomyopathy.[3]

  Focus of the Analysis Top

  • The significance of inferolateral T-wave inversion (TWI) in athletes
  • The presence and forms of left ventricular hypertrophy (LVH) in athletes with particular focus on apical hypertrophic cardiomyopathy (HCM)
  • Discussion of further diagnostic workup to differentiate physiology from pathology in the presented athlete
  • Discussion on risk stratification, decision-making, and further management.

  Left Ventricular Hypertrophy in Athletes Top

Due to the new onset TWI in the inferolateral leads (V4–V6, II, III, and aVF), despite the lack of symptoms and normal ECGs on yearly screenings, the presented 15-year-old goalkeeper from a junior football team, who has been playing football for 8 years, was sent for echocardiography. It demonstrated mildly increased myocardial thickness (13 mm) with no other abnormalities.

Mild LVH has been reported in athletes as an element of structural adaptation to physical activity,[4],[5] but it generally does not exceed 12–13 mm as in the presented case. LVH is more typical for sports including strength exercise and less typical for pure endurance training.[6],[7] Football is an example of a mixed type of sports, where this form of LVH is more likely to be observed.[7] Cardiac magnetic resonance (CMR) data demonstrate that a significant increase of interventricular septal diameter (IVSd) and left ventricular (LV) mass has been observed already in boys between 8 and 12 years of age after 2 years of regular football training.[8] Recently published nomograms of basic echocardiographic linear dimensions in child and adolescent athletes (5–18 years of age) in comparison to normal pediatric population showed that mean values of all parameters are increased, but the most pronounced increase is observed for left atrial diameter and IVSd.[9]

At the time of initial screening, the presented athlete had a body surface area (BSA) of 2.0 m2 (185 cm of height and 77 kg of weight). Echocardiographic Z-score +2 for child and adolescent athletes with BSA of 2.0 m2 according to nomograms was calculated as 12.7 mm.[9] Because of the discrepancy between ECG pattern and a borderline LV thickness for junior athletes, he was sent for further testing.

  Further Diagnostic Workup for Differentiation of Left Ventricular Hypertrophy in Athletes Top

Medical history

Differentiation of physiological and pathophysiological LVH in athletes should start with collection of detailed medical history including questions about any symptom suggesting pathology such as chest pains, palpitations, dizziness, worsening physical performance, fatigue, fainting, or syncope related or not related to exercise. This should be supplemented by questions about family history with particular attention to signs of HCM, any cases of sudden cardiac death (SCD), especially in first-degree relatives or any case of unexplained death.

  None of This Was Present in the Presented Athlete Top


Apart from ECG changes observed in this case, there are some other abnormalities, which are more typical for HCM than physiological adaptation.[10] They are summarized in [Table 1] and described below:
Table 1: Normal findings and changes suggesting the presence of hypertrophic cardiomyopathy in athlete's electrocardiogram (please see text for details)

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  • Short PQ interval/preexcitation typical for storage diseases or mitochondrial disorders (short PR interval without preexcitation is also present in Anderson–Fabry disease)
  • Extreme forms of amplitude criteria for LVH (Sokołow–Lyon ≥50) may be present in storage diseases or in case of preexcitation
  • Low QRS voltage was rarely observed in HCM but may be present in amyloidosis
  • Pathological Q-waves particularly in inferolateral leads but usually with positive T-waves are suggestive of asymmetric LV hypertrophy, while broad Q-waves are suggestive of fibrosis
  • Concave ST-segment depression was typically found in cases of apical aneurysms formed due to the presence of mid-ventricular obstruction.

Of note, only in 6% of patients with HCM, there are no ECG changes, This percentage is even smaller in athletes with HCM.[10],[11]

Baseline ECG of the patient is presented in [Figure 1]. It shows sinus bradycardia of 58/min, normal heart axis, signs of early repolarization, the presence of amplitude criteria for LVH (Sokołow–Lyon of 45 mm), TWI in II, III, aVF, and V4–V6, normal PQ of 160 ms, and QTc of 420 ms.
Figure 1: Changes in diagnostic studies observed in the presented patient. Baseline electrocardiogram showing negative T-waves in II, III, aVF, and V4–V6

Click here to view


Echocardiography, which is a natural first-line imaging method, is an evaluation of suspected HCM also in athletes.

Traditionally, there were several features aside from LVH suggestive of HCM rather than athlete's heart:[10],[12]

  • Asymmetric pattern of LVH – in athletes, the between-segment difference in LVH does not usually exceed 2 mm.
  • Small cavity size and increased relative wall thickness (RWT) – end-diastolic LV diameter <5 mm and RWT >0.45
  • Disproportionate left atrial enlargement – in athletes alike in patients with HCM, there is a typically symmetrical enlargement of all heart chambers
  • LV outflow tract obstruction (LVOTO) with systolic anterior motion of the anterior mitral valve leaflet and the presence of more than mild mitral regurgitation
  • Other forms of LV obstruction such as mid-ventricular LV obstruction
  • Decreased LV ejection fraction
  • Decreased diastolic relaxation/filling (septal e' velocity <8 cm/s and/or E/A ratio <1).

Recent findings suggest that at least some of these abnormalities may not be present in athletes with HCM.[6],[7],[11] A reason for that is that previous echocardiographic studies, used in the guidelines,[10] compared athletes with sedentary HCM patients and did not include subsets of athletes with HCM. Newer studies demonstrated that in comparison to sedentary HCM patients, athletes with HCM have smaller maximal LV thickness, larger end-diastolic cavity dimensions, lower RWT, and preserved diastolic function.[6],[7],[11] The new proposed end-diastolic LV diameter discriminating HCM and athlete's heart has been set at 54 mm. It can be explained by the fact that individuals with more pronounced forms of HCM are usually eliminated from sports at early stage, as they are likely to be symptomatic, have early changes on screening, or just feel generally unfit for sports. It is supported by observation that apical HCM, which is considered as a benign form of HCM, seems more frequent in athletes.[11]

Baseline echocardiography of the patient is presented in [Figure 2]a and [Figure 2]b. It shows mildly increased wall thickness (13 mm), with no other abnormalities (normal cavity sizes, ejection fraction, diastolic function, and flow through the valves).
Figure 2: Baseline echocardiography in four-chamber view apical view and short-axis parasternal view showing borderline myocardial thickness of the left ventricular wall (a and b). Cardiac magnetic resonance in short-axis apical view showing apical obliteration during systole (c) and small subendocardial perfusion deficit during hyperemia in the lateral apical segment (d)

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  Cardiac Magnetic Resonance Top

CMR is a second-line imaging method when suspecting HCM, providing additional information. In inconclusive echocardiographic cases, it can show less visible features of HCM and give insight into the presence of fibrosis or less often storage diseases.[6],[7],[10]

CMR findings, which may be suggestive of HCM, other than visible in echocardiography, include:

  • Presence of bizarre pattern of myocardial structure (varying thickness of the myocardial wall with small regional differences)
  • Presence of apical forms of HCM, which if borderline may not be detected in echocardiography due to problems with acoustic window in that region. This is often accompanied by characteristic systolic contraction in that region on four- or two-chamber view with almost complete obliteration of the apex. It forms a “mouse tail” pattern of contraction, where LV cavity at the apex is the tail and the body of the mouse is the other part of the LV
  • Presence of crypts in the myocardium, which has been shown to precede ECG changes and full manifestation of HCM in some but not all studies [13],[14]
  • Presence of myocardial edema or perfusion deficits suggestive of ongoing ischemia in T2-weighted images or during pharmacologically provoked hyperemia, respectively [15]
  • Presence of nonischemic, mid-wall late gadolinium enhancement (LGE) usually in the most hypertrophied segments.

The presented athlete underwent three CMR scans in the course of 3 years.

The first one done early in 2016 when he was 15 years of age during initial workup demonstrated a crypt in the basal inferoseptal segment, myocardial thickness of 12–13 mm in the apical segments, and no signs of fibrosis (stress testing was not done at that time).

The second one repeated a year after suggested the presence of a “mouse tail” pattern of apical LV contraction with LV thickness in that region of 13 mm and a subendocardial perfusion deficit in apical septal segment during hyperemia. Again, there were no signs of fibrosis. This CMR is presented in [Figure 2]c and [Figure 2]d.

The third one done in 2018 showed similar myocardial morphology and consistently no signs of fibrosis, but this time no perfusion deficits were observed. Given the fact that the detection of perfusion deficits in the apical regions is difficult due to motion artifacts, it might be possible that ischemia detected in one of the scans was a dark rim artifact.

Twenty-four-hour Holter monitoring

Ambulatory ECG monitoring can reveal runs of nonsustained ventricular tachycardia (nsVT) present in 24% of adult patients with HCM and/or paroxysmal supraventricular arrhythmias present in 38% of patients with HCM.[10]

The presented athlete did not demonstrate arrhythmias of 24-h Holter monitoring. The recording was repeated 3 times in the last 3 years.

Biochemical markers

To rule out concomitant diseases and ongoing myocardial injury, initial first-line assessment should include the following markers: whole blood count, glucose concentration, markers of myocardial necrosis (troponin and creatine kinase-MB) or myocardial dysfunction (such as brain natriuretic peptide [BNP] or its terminal part – N-terminal prohormone of BNP [NT-proBNP]) as well as creatine kinase, transaminases, renal function, pH, electrolytes, and lactic acid.[10]

The presented athlete had periodically assessed values of troponin and NT-proBNP, which were always within the reference range (troponin I <0.014 ng/ml and NT-proBNP <125 pg/ml).

Exercise testing and/or cardiopulmonary exercise testing

Despite the fact that HCM is a relative contraindication to exercise testing, it should be a part of initial workup for HCM, especially in athletes. It is also useful in prognosis assessment.[10] Exercise provocation can demonstrate:

  • The onset or increase of ventricular extrasystolic beats or more complex ventricular arrhythmias during exercise
  • Lack of increase of arterial blood pressure (BP) during exercise by >20 mmHg from the initial values or drop in BP of >20 mmHg from the highest recorded values, which also carries a prognostic significance [10]
  • Decreased performance in relation to age and sex. A study by Sharma et al.[16] showed that athletes with physiological LVH are more likely to achieve >50 ml/min/kg of maximal oxygen consumption (max VO2) or over 120% of predicted max VO2 for age, sex, and size in comparison to patients with HCM
  • Pseudonormalization of ECG changes on exercise, which was demonstrated in patients with apical forms of HCM [17] but remains of undetermined significance.

The presented athlete underwent exercise testing on a treadmill and then cardiopulmonary exercise testing on a treadmill. He did not present arrhythmias, showed good BP response, and achieved V02 max of 50 ml/min/kg (the test was performed after 3 months of detraining). There was also a pseudonormalization of TWIs on exercise.


In case of athlete's heart, any findings suggestive of HCM should attenuate or even disappear after 6–8 weeks of detraining, but they persist in true HCM cases.[7]

The presented athlete was asked to refrain from training for 3 months. There were no changes in echocardiography, but ECG changes were periodically pseudonormalizing (TWI returned to normal).

Genetic testing

In majority of the cases, HCM is transmitted in an autosomal dominant way, with a 50% risk of inheritance.[10] However, there may be also de novo mutations, lack of full disease penetration visible in parents, or autosomal recessive transmission. It has been also shown that similar mutations often cause different patterns of disease or even different cardiomyopathies.[10] Sequencing of genes producing sarcomere proteins leads to identification of mutation in 60% of cases. Probability to identify mutation is higher in familial forms of HCM and lower in elderly patients or in case of atypical presentation. Genetic testing is indicated in patients with diagnosis of HCM and may be considered in subjects with borderline changes, Importantly, genetic testing should be an element of detailed analysis by a specialized team with adequate genetic counseling.[10]

The presented athlete underwent whole-exome sequencing, which did not disclose any mutations characteristic for HCM.

  Summary of Findings and Diagnosis in the Presented Case Top

The most likely diagnosis in the presented case is apical HCM. In favor of that diagnosis, there was an inferolateral TWI characteristic for this form of HCM, which pseudonormalized during detraining. CMR pattern was also suggestive of this diagnosis. It included borderline myocardial thickness of apical segments, “mouse tail” contraction pattern in that region, crypt in the left ventricle, and single test of myocardial perfusion deficit during hyperemia in the apical septal segment.

Flett et al.[18] presented a group of similar patients with only relative apical wall thickening (apical: basal wall thickness >1) and a higher prevalence of features consistent with HCM than in the control group.

All of the other tests performed in the presented athlete did not disclose any feature of HCM.

  Risk Stratification, Decision-Making, and Management Options in Patients With Hypertrophic Cardiomyopathy Top

The use of HCM risk-SCD calculator is contraindicated in athletes, as it was not validated in this population.[10] Therefore, in this subset of patients, it is really hard to assess the true risk of SCD. Early registry reports demonstrated that HCM was the main cause of SCD in young athletes.[19] In a prospective analysis of all young people in the Veneto region of Italy, it has been also demonstrated that the estimated relative risk ratio of SCD in athletes was 2.8 higher in comparison to nonathletes. Among athletes, the risk of SCD was strongly related to underlying cardiovascular diseases.[20]

For these reasons, guidelines on HCM take a very conservative stand indicating cessation of any competitive sports and intensive physical activity in patients with HCM, especially in those with risk factors of SCD and/or LVOTO.[10],[21],[22] Athletes with HCM may engage only in low-intensity sports (such as bowling, cricket, golf, or yoga). According to those guidelines, competitive sports may be considered only in asymptomatic, genotype-positive, but phenotype negative forms of HCM. Type of sports and mutation as well as results of frequently repeated tests should also be taken into consideration.[23]

The same guidelines state that most of the cases of SCD occur without exercise, while exercise-induced ventricular tachycardia is rare in patients with HCM.[10] This has been already observed in the Veneto region study, where HCM was a reason of SCD in 7.7% of cases (23 out of 300 SCD). SCD occurred only in one athlete while all other cases of HCM-related SCD were observed in nonathletes.[20] In fact, since publication of the guidelines, there has been mounting evidence that exercise may not necessarily trigger or modulate the risk in HCM, as it was believed before.[24],[25],[26],[27],[28],[29] German nationwide registry on sports-related SCD rarely found cardiomyopathies to be the cause, including HCM in only 2 cases of 144 SCDs.[26] However, in relation to the presented case, over 40% of all SCDs was related to football. The relatively low percentage of HCM-related deaths in athletes (8% of all SCDs) was also reported in the US National Collegiate Athletic Association with the structurally normal hearts as the main cause of SCD.[25] This was not different in the UK Regional Registry on SCD in sports (with only 6% of all SCDs due to HCM).[27]

The latter study showed that there was no difference in the incidence of SCD in HCM on exertion or at rest. The only independent predictors of SCD during exercise in multivariate analysis were arrhythmogenic right ventricular cardiomyopathy and the presence of LV fibrosis. A recent small study by Pellicia et al.[28] demonstrated that over 9 years of follow-up, event-free survival was not significantly different between low- and intermediate-risk HCM patients who trained and competed in comparison to those who dismissed any physical activity.[28] Those who experienced events were more likely to have a positive family history for HCM, burst of nsVT, higher prevalence of LGE on CMR, and lower e' velocity on Doppler imaging. The other group suggested that troponin elevation might be a useful factor in decisions of exercise prescription.[29],[30] Furthermore, an implantable cardioverter-defibrillator Sports Safety Registry demonstrated that the proportion of shock during sports competitions and practice was not more common that during other physical activities, including patients with HCM.[31]

Finally, a study on patients with apical HCM reported benign prognosis (annual mortality of 0.1% in comparison to 1.4% reported earlier for the whole HCM population), especially in pure forms of the disease.[32] Good prognosis in subjects with apical HCM was also reported in another study.[33]

In light of the above considerations, the current view is to formulate a decision on continuation of competitive sports in relation to symptoms and integrated information from multimodality testing with implementation of shared decision-making between parents, junior athletes, trainers, and sports associations.[29] Patients should be instructed to avoid dehydration and electrolytic imbalance as well as to restrain from supplementation with performance-enhancing drugs. Other supplements should be used wisely. There should be a close monitoring of these athletes with reporting of any symptom. All personnel engaged in training of an athlete with HCM should be certified in basic life support (BLS) and automated external deffibrilator (AED) should be available on hand.

In case of the presented athlete, after consultation with parents and a team manager, the joint decision was made to allow him to continue sports career. He currently plays professionally in a regional football club and has remained uneventful during 3 years of follow-up under close monitoring with ECG, Holter monitoring, echocardiography, exercise testing annually, and periodic CMR scan for the presence of fibrosis.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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  [Figure 1], [Figure 2]

  [Table 1]


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