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A jogger with tightness of the chest

Clinical case


Renée B.A. van den Brink - Academic Medical Center, Amsterdam, Netherlands

Educational Resource:

ESC Core Curriculum Chapter 3 (Non-invasive imaging), Chapter 10 (Myocardial Disease), Chapter 19 (Exercise Physiology)


Frequently in athletes the clinical cardiologist is confronted with the question of whether an abnormality on the ECG or echocardiogram fits an athlete’s heart or indicates cardiac pathology.

A 50 year old Caucasian male patient was referred by a sports physician for evaluation. His medical history was unremarkable. He liked jogging and ran half-marathons. During the last months his exercise tolerance was decreased due to “tightness of the chest”, which he described as difficulty to take a deep breath. He did not have chestpain, orthopnea, nocturnal dyspnea, palpitations or exertional dizziness.  At physical examination his blood pressure was 125/65 mmHg, length 1.88m, weight 72kg, BSA 1.97 m². Cardiac auscultation revealed normal heart sounds and a short 2/6 ejection murmur at the left sternal border. He had no risk factors for coronary artery disease. He used no medication, drugs or anabolic steroids. There was no family history of heart disease. His resting ECG is reproduced in figure 1.

Question 1
How would you interpret the ECG in this patient?


The patient underwent echocardiography. The left ventricle (LV) showed concentric hypertrophy  (LV wall thickness: 14mm), LV mass was 118 g/m² ( normal: 49-115 g/ m²). There was no LV dilatation (LV end-diastolic diameter 41 mm, LV end-systolic diameter 23 mm, LV shortening fraction 36%). End-diastolic LV volume was: 44 ml/ m² (normal: 35-75 ml/m²)  , end-systolic volume was 11 ml/m² (normal 12-30 ml/m²); LV ejection fraction 75%.  LA volume was 19 ml/m² (normal < 29 ml/m²).  RV anterior wall thickness 7 mm. Relevant echocardiographic findings are shown in figure 2 and movie 1 (Transthoracic echocardiogram: 1a, 1c, 1d, 1e, 1f).

Question 2
How would you interpret echocardiographic findings?


The patient performed a treadmill exercise test. He stopped after 12 minutes stage V (15 METS) due to fatigue and dyspnea. He had no chest pain. His heart rate was 142 bpm  (84% of predicted) and his blood pressure raised from 125/80 mmHg to 135/80 mmHg. The exercise test revealed no rhythm- or conduction abnormalities. The ECG was non-diagnostic for ischemia, due to repolarisation abnormalities at rest Figure 3. A coronary angiography was performed that was normal. Pulmonary function was also normal. It was said to him that he had no cardiac pathology.
However, the patient was not able to resume jogging and gradually (within 1 year) developed progressive dyspnoea (NYHA class 2/4), fatigue and oedema.  At physical examination his blood pressure was 100/60 mmHg, heart rate 65 bpm. His jugular venous pressure was elevated.  At cardiac auscultation he had normal heart sounds and a short grade 2/6 ejection murmur. There were mild pulmonary crackles, hepatomegaly and pitting oedema of both legs. The ECG showed sinus rhythm, a horizontal electrical axis, low QRS voltage in the the limb leads, no voltage criteria for LV hypertrophy in the precordial leads; figure 4. Echocardiography was repeated. In comparison with 1 year prior LV wall thickness was increased from 14 to 19mm, LV mass from 118 to 196 g/m2. There was no LV dilatation and LV end-diastolic diameter had decreased from 41 to 37 mm, LV end-systolic diameter and shortening fraction were unchanged (24 mm, 37% respectively). LA volume was virtually unchanged: 21 ml/m2. End-diastolic LV volume decreased from 44 ml/m² to 16 ml/m²; normal: 35-75 ml/m². Relevant echocardiographic findings are shown in figure 5, Movie 2 (Transthoracic echocardiogram 1 year later: movie 2a2c, 2d, 2e, 2f) and 3 (Comparison of initial transthoracic echo and trans thoracic echo 1 year later: 1a/2a; 1c/2c; 1d/2d).

Question 3
What is your diagnosis?

Additional laboratory investigation demonstrated an impaired renal function (creatinin 187 umol/l); free kappa 21 mg/l, free lambda 825 mg/l, ratio VK/VL 3,6. Serum albumin 28 g/l. NT-Pro BNP 38.524 ng/l. Rectum biopsy showed no signs of amyloidosis. However, renal biopsy showed signs of AL amyloidosis. This was due to monoclonal gammopathy of undetermined significance (MGUS of IgG lambda type). See figure 6. The patient was treated with furosemid 80 mg o.d.d., thalidomid 100 mg o.d.d. and dexamethason 40 mg o.d.d. (adriamycin was not given due to its cardiotoxicity). In spite of this treatment his clinical situation further deteriorated and he died.


LV hypertrophy can be secondary to athletic sports, hypertension and aortic stenosis. LV hypertrophy can also be due to an inherited heart muscle disorder caused by mutations in sarcomeric proteins, resulting in myocyte disarray, with or without fibrosis, myocardial hypertrophy and small-vessel disease.
In hypertrophic cardiomyopathy it is important to always consider non-sarcomeric variants of HCM, termed ‘phenocopies’, such as  Fabry’s disease (prevalence 4% of HCM). Also one should keep in mind that thickening of the LV wall can be caused by amyloidosis (amyloid depositions) and sarcoidosis (granulomatous disease).
It is difficult to distinguish morphologically mild HCM (wall thickness 13–15mm) from hypertrophy in athletes. Diagnosis of HCM is facilitated by the presence of repolarisation abnormalities (ST depression and/or negative T-waves in the lateral and/or inferior leads) or pathological Q waves on the ECG.
Echocardiography may be helpful as the LV mass is  <134 g/m² in males or  <110 g/m² in females, LV cavity (> 55 mm) is commonly enlarged in athletes but small (< 45 mm) in HCM; diastolic function is normal or enhanced in athletes but usually impaired in HCM; and left atrial size is normal in athletes but often increased in HCM. VO2 max is > 50 ml/kg/min in athletes but not in HCM; see figure 7. [10]  [11]
If in serious doubt over the nature of hypertrophy – a period of detraining would reverse the hypertrophy associated with training, but not in a pathological state. [12]  [13]  
The period of detraining required is short because physiological hypertrophy regresses to normal, on average within 13 weeks, irrespective of the duration of the preceding training.[14]


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