Vol.47 - Número 4, Octubre/Diciembre 2018 Imprimir sólo la columna central

Ironman Heart. What is the limit of health? Role of cardiac imaging
Dicamen-Hospital Italiano. (5500) Mendoza, Argentina
Recibido 25-MAY-18 – ACEPTADO despues de revisión el 21-JUNIO-2018
There are no conflicts of interest to disclose.



Athlete's heart includes a series of morphological and functional adaptations directly related to the type of exercise, as well as to the degree of demand. We will analyze the characteristics in an elite male triathlete of high performance.
We analyze the current role of cardiac imaging in cardiac structural and functional characterization in high performance athletes. With the incorporation and development of different echocardiography techniques, such as tissue Doppler, speckle tracking, strain rate, multislice coronary CT and cardiac MRI.
These methods allow us to better understand adaptations in high performance athletes, with the ultimate goal of detecting pathologies, mainly cardiomyopathies that could cause SCD (sudden cardiac death) during sports practice
Key words: Heart of Ironman. Ironman. Cardiac imaging. Healthy limit.


The term athlete’s heart described more than a century ago is characterized by an increase in chamber volumes and electrocardiographic changes. It is characterized by structural, functional and peripheral cardiac adjustments, the goal of which is to improve flow and tissue extraction of oxygen [1,2].

In the last 30 years, an exponential increase occurred in sports long-distance competitions, with 200,000 participants per year in international marathon circuits and 70,000 participants in long-distance triathlon competitions of the “ironman” type [3].

In February 1978, a group of 15 athletes participated in one of the biggest competitions of human resistance known till then, a long-distance triathlon called Ironman, made in Waikiki, Hawaii. It consisted of 3.7 km of swimming in the sea, 180 km of cycling, and 42,195 km of running (marathon) [4].

A resistance test with an extended exercise component and with isotonic predominance, it leads to physiological hypertrophy and eccentric predominance.


Male, 38-year-old patient, with no pathological history, elite triathlete in competitions with no interruptions starting when he was 12 to this date (for 26 years). He was a finalist 9 times in the Ironman competition that entails 3.7 km of swimming, 180 km of cycling, and 42,195 km of running. He finished these competitions in an average of 9 hours. With a weekly training of 6 days and a load of 3 hours per day in average. No alarming symptoms during the practice of sports.

Physical examination within normal limits; 1.70 m of height, weight 72 kg, BMI 23, normotensive, symmetrical pulses, no murmurs. Electrocardiogram: sinus bradycardia with no conduction disorders or signs of hypertrophy. Lab tests within normal limits, including lipids. Ergometer test was negative enough for ischemia; DP 35,000, Mets 15, VO2max 61 ml/min/kg. Doppler echo with preserved volumes with normal systolic and diastolic function, including tissue Doppler echo and longitudinal-radial strain.

Coronary multislice CT (128 slices) was conducted as screening for coronary anomalies due to “chest discomfort, atypical sharp pain”, with no evidence of atherosclerotic coronary lesions (Agatston score 0), muscle bridges or congenital coronary anomalies.



Echocardiographic assessment.
Doppler echo constitutes the first additional study to differentiate physiological vs pathological hypertrophy.

The variables analyzed constitute parietal thickness, diameters, ventricular mass, volumes and systolic and diastolic function among others (Figure 1).

Figure 1. Echocardiogram with preserved volumes and physiological hypertrophy; LV mass 169 gr/m2.

In a series of 1309 athletes, 55% had increase in diastolic diameters, but only 15% showed diameters of more than 60 mm, always in the presence of preserved systolic function [5]. Larger diameters are described in elite cyclists [5].

In 947 elite athletes, parietal thickness rarely exceeds 12 mm; only 1.7% presented thickness ≥13 mm, with smaller septal thicknesses in women in regard to men [6]. Parietal thickness is symmetrical in sportsmen according to the volume overload. On the other hand, in hypertrophic cardiomyopathy thicknesses generally exceed 14 mm, and affect the basal septum preferentially; with 20% of cases presenting associated anomalies like mitral systolic anterior motion (SAM) and mesosystolic-aortic closure.

Physiological hypertrophy shows regression of it with periods of suspension of training for at least 3 months; while chamber volumes remain increased for up to 12 months according to literature [7]. These findings that do not revert in the case of primary hypertrophic cardiomyopathy or use of anabolic steroids.

Left atrium.
Atrial dimensions should be measured by modified Simpson technique, indexing BSA (body surface area) with limits beyond normality around 34 mL/m2, observing in sportsmen higher average values in 3.2% of cases [8,9]. Atrial strain has also been used to differentiate pathological hypertrophy, with increased values in athletes [11].

Right chambers.
Volume overload is accompanied by right atrial and ventricular enlargement, associated to mild functional tricuspid valve insufficiency and vena cava dilatation with preserved partial respiratory collapse [11]. In a series of 127 male elite athletes, right ventricular dilatation was observed with associated parietal thickening ≥5 mm, from the long subcostal or parasternal axis [12]. Parietal thickness can also be measured in two dimensions in end-diastolic volume, at tricuspid valve chordal level. Right ventricular diameters should be measured at basal level and in the base-apex axis from the apical four-chamber view (Figure 2).

Figure 2. Three-leaflet aortic valve. Right chambers within normal limits.


Increased diameters should be differentiated in ARVC (arrhythmogenic right ventricular cardiomyopathy), analyzing: presence of symptoms or not, electrocardiographic alterations and anomalies in echocardiography. In ARVC, there is RV systolic function, shown by decreased TAPSE (tricuspid annular plane systolic excursion), tissue S wave ≤8 cm/sec and presence of ventricular aneurysms [13], requiring cardiac NMR to complete the evaluation.

Coronary ostia.
Coronary ostia could be seen by echocardiography in 90% of sportsmen from a modified short axis; however, there are no records about the sensitivity to detect congenital coronary artery anomalies [14].

Tissue Doppler echo and strain rate
Myocardial deformation evaluation techniques, such as tissue Doppler echo, speckle tracking and strain rate allow a proper functional assessment both of systole and diastole, with greater independence in regard to variables like preload, heart rate and less intra- and inter-observer variation [15,16].

Modifications such as the increase in diastolic velocity during the rapid filling phase, are related to the degree of training and the subsequent aerobic capacity.

Systolic function could be analyzed by tissue Doppler echo as fiber and not chamber index, using tissue S wave; a value ≥9 cm/sec has 87% sensitivity and 97% specificity to differentiate pathological hypertrophic cardiomyopathy (HTN or primary) vs physiological hypertrophy [17] (Figure 3).

Figure 3. Tissue Doppler at lateral level of the tricuspid annulus with preserved function; S wave 14 cm/sec.

Diastolic function analyzed by pulsed and tissue Doppler echo remains normal, even observing a supernormal pattern, characterized by prominent E wave and E/a ratio of more than 2. The E/e’ ratio is also used, with e’ values in sportsmen of 8 cm/sec.

The strain rate technique shows less global longitudinal strain (GLS) values in pathological vs physiological hypertrophy. Normal values in sportsmen are -20% [18] (Figure 4).

Figure 4. Longitudinal strain images, with preserved values. GLS (global longitudinal strain 20%).


The previously described findings are related to the activity performed, and individual factors such as gender, race and body surface area among others.

Indicators of pathological hypertrophy

  • Parietal thickness of more than 16 mm, asymmetrical distribution.
  • LV diastolic diameter of less than 45 mm.
  • Left atrial enlargement ≥34 mL/m2.
  • Diastolic dysfunction by mitral valve pulsed-wave and tissue Doppler echo.
  • Lack of hypertrophy regression by suspending physical activity (8 to 12 weeks).
  • Electrocardiographic patterns.
  • Family history of hypertrophic cardiomyopathy.

Stress Doppler echo

Accessible test, that is affordable, more accepted than pharmacological stress test in sportsmen. It provides data on systolic and diastolic function in strain. It evaluates contractile reserve in athletes with borderline ejection fraction in rest (EF 45-50%) and capacity for exercise.

Very useful in the screening of atherosclerotic CAD with sensitivity and specificity (76%-88% respectively) [19].

Useful in the evaluation of patients with settled hypertrophic cardiomyopathy when evaluating the presence of mitral systolic anterior motion (SAM) and associated dynamic gradients.


In relation to nuclear cardiology tests by SPECT and PET CT, there is limited and scant evidence on the evaluation of asymptomatic sportsmen. In some investigation studies, coronary flow, oxygen consumption and use of free fatty acids were evaluated by PET CT, detecting decrease in consumption in regard to perfused myocardial mass, which could be interpreted as physiological adaptation in the myocardial consumption of energy [20].

There are no levels of current recommendations for these tests in sportsmen.

Coronary tomography angiography.
With 128-slice CT, that enables a better temporospatial resolution and using less amount of iodine-based contrast, the following can be assessed: coronary arteries, aortic vascular diameters, aortic valve structure, pulmonary artery and evaluating venous drainage (Figure 5). Moreover, we may complete the evaluation of chamber volumes and systolic function indices by volumetric methods.

Figure 5. Coronary CT angiography of 128 slices, with origin of coronary ostia and preserved trajectories. No evidence of obstructive lesions. (Courtesy of Dr. Andrea Astesiano).


CT angiography provides the chance of evaluating coronary arteries in a noninvasive manner, thus enabling the detection of congenital anomalies in aortic birth or in its trajectory to the myocardium and myocardial bridges. By quantifying the calcium score it is possible to identify atherosclerotic disease in a subclinical way.

In sportsmen, with low cardiovascular risk and favorable lipid levels, the true risk is usually underestimated. There are controversial observations, where marathon athletes compared to controls with the same age and equal cardiovascular risk, presented a higher calcium score, proposing as the possible cause, inflammatory cytokine release [21]. In a study evaluating male sportsmen >45 years (318 patients), CT angiography could detect 19% of asymptomatic CAD when stress test was negative [22].

Although coronary CT angiography is not a first-line test in the evaluation of sportsmen at competitive level, it is indeed useful in patients in moderate/high risk or in whom the initial tests are not conclusive to rule out CAD.

A very important test when the goal is identifying the main cardiomyopathies, providing tissue and even myocardial perfusion characterization. It allows assessing volumes, ventricular mass and global and regional contractile function [23]. The late gadolinium enhancement (LGE) technique allows to differentiate ischemic and nonischemic myocardial impairment patterns. Nonischemic patterns of myocardial impairment include the enhancement of the subendocardial ring (myocardial amyloidosis), patchy enhancement (hypertrophic cardiomyopathy - HCM) or mesocardial and epicardial enhancement (myocarditis or Fabry disease) [24,25].

In the diagnosis of HCM, it has 80% of sensitivity and 90% specificity; greater than that of echocardiogram, obtaining a diagnostic superiority of 6% in comparison to echocardiogram, with a better measurement of parietal thicknesses in 20% and constituting the gold standard to identify the apical variant of HCM [26,29].

It is important to highlight that HCM may present a small prevalence of late gadolinium enhancement with non-hypertrophic segments, emphasizing that late enhancement is observed only in 65% of confirmed cases of HCM. More than half of patients with HCM present anomalies in mitral leaflets (elongated and redundant leaflets) and around 25%, alterations in chords (elongation) and papillary muscles (hypertrophy, bifid papillary muscles, apical shift and direct insertion of anterior leaflet). This could even be the primary phenotypical expression of HCM [27,28,29].

In high-performance sportsmen, increase in left ventricular trabeculations is observed, as a response to volume overload, with NMR constituting a useful tool to differentiate it from noncompaction cardiomyopathy [30].

Detection of ischemia by NMR
Perfusion imaging with stress NMR may help in the diagnosis of atherosclerotic CAD in athletes and the general population, but it is limited by being less available than stress echo, coronary CT angiography and gamma-camera [30]. Current guidelines recommend it in patients with suspicion of atherosclerotic CAD and pre-test intermediate probability. NMR may play a significant role in detecting coronary arteries anomalies in athletes by coronary magnetic resonance angiography (CMRA). It is a noninvasive technique that could be used in people younger than 35 years with low probability of CAD [31].

High-intensity exercise. What is the limit of its benefits?
The benefit of training on contractile reserve is well known; preload is increased in high-performance sportsmen, associated to characteristic bradycardia and increase in volumes.

However, there are observational studies referring to the so-called “cardiac fatigue” with transient reduction in systolic and diastolic function, measured by echocardiography and increase in plasma markers: troponins and B natriuretic peptide [32,33]. Although the clinical impact of such findings is unknown, they are objectified.

Transient dysfunction mainly affects the right ventricle, with alterations in the contractile function that may persist up to one month after the competition [34].

Pulmonary pressure values in rest may also be increased, with values of 40 mmHg, coinciding with the increase in ventricular systolic volume, but with no theoretical increase in pulmonary vascular resistances.

In triathlon athletes participating in the Ironman competition, transient decreases have been described in ejection fraction values, diastolic dysfunction and transitory alterations in regional contractility. Using strain rate techniques, a decrease was observed in longitudinal, radial and circumferential strain values [35]. However, a prospective study of 114 Olympic athletes, participating in 2 to 5 consecutive Olympic games, did not display deterioration in cardiac function variables, or greater risk of arrhythmias [36].


Cardiac imaging enables a better cardiac anatomical and functional characterization in more complex scenarios, in relation to the increasing participation in high-performance and long-duration sports disciplines like triathlons.

Echocardiogram is the first-line technique to assess sportsmen with previous pathologies, mainly hypertension, as well as being a screening technique before uncertain findings in physical examination and/or electrocardiogram. It may also confirm coronary artery anomalies and differentiate gray areas between athlete’s heart and the main cardiomyopathies: hypertrophic, dilated, arrhythmogenic right ventricular cardiomyopathy, and noncompaction cardiomyopathy, among others.


  • A special acknowledgement to Drs. Martín Córdoba, Augusto Ortego, Gabriela García, Sebastián Wolff, David Wolff, for their invaluable contribution to prepare this document.


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Publication: December 2018


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