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Year : 2020  |  Volume : 30  |  Issue : 1  |  Page : 33-34

The significance of “contractile reserve” in the echocardiographic assessment of athletic heart syndrome

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA

Date of Submission18-Sep-2019
Date of Decision11-Jun-2019
Date of Acceptance23-Feb-2020
Date of Web Publication13-Apr-2020

Correspondence Address:
Krishnaswamy Chandrasekaran
Department of Cardiovascular Medicine, Mayo Clinic, 200 1st Street SW, Rochester 55905, MN
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcecho.jcecho_48_19

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The clinical distinction between athlete's heart and structural heart disease in the echocardiography laboratory is often challenging. We present a case where athletic heart syndrome was promptly differentiated from pathology with a simple maneuver during echocardiography.

Keywords: Athlete's heart, echocardiography, ejection fraction

How to cite this article:
Christopoulos G, Barrett-O'Keefe Z, Chandrasekaran K. The significance of “contractile reserve” in the echocardiographic assessment of athletic heart syndrome. J Cardiovasc Echography 2020;30:33-4

How to cite this URL:
Christopoulos G, Barrett-O'Keefe Z, Chandrasekaran K. The significance of “contractile reserve” in the echocardiographic assessment of athletic heart syndrome. J Cardiovasc Echography [serial online] 2020 [cited 2021 Jun 17];30:33-4. Available from: https://www.jcecho.org/text.asp?2020/30/1/33/282331

  Introduction Top

We present a case of a young athletic male with left ventricular enlargement and low ejection fraction. We demonstrated contractile reserve as a means of differentiating athletic heart syndrome from dilated cardiomyopathy.

  Case Report Top

A 56-year-old male was referred for transthoracic echocardiogram to evaluate a systolic cardiac murmur. The patient was a noncompetitive runner who had no prior known cardiac history and no cardiovascular complaints. His vital signs were remarkable for bradycardia (41 beats/min), blood pressure was 124/70 mmHg, and his body mass index was 20.8 kg/m2. Echocardiography revealed normal wall thickness (parasternal long-axis septal thickness 10 mm and posterior wall thickness 10 mm), mild left ventricular (LV) enlargement (parasternal long-axis diastolic LV dimension of 51 mm, systolic LV dimension of 40 mm, and apical biplane volume index of 120 mL/m2), mild right ventricular (RV) enlargement (apical four-chamber base-apex diastolic RV diameter of 99 mm), and mild left atrial enlargement. Biplane LV ejection fraction was calculated as 47% (linear ejection fraction by M mode at 44%), and wall motion analysis was consistent with mild generalized hypokinesis without regional wall motion abnormalities [Figure 1] and Video 1].

LV stroke volume index was calculated as 94 mL (inde × 56 ml/m2 square), and cardiac output was calculated as 4.15 L/min (cardiac inde × 2.19 L/min/m2). The average longitudinal LV strain was normal at − 20%. Diastolic function was normal (medial mitral annulus tissue Doppler velocity 0.09 m/s with a normal transmitral flow). The patient's heart rate increased to 80 beats/min after repetitive squatting, and repeat imaging showed a significant improvement of biplane ejection fraction to 64% (two-dimensional ejection fraction by M mode 57%) and decrease of end-systolic biplane volume from 121 to 59 mL [Figure 1] and Video 2]. These findings were consistent with the athlete's heart and no further evaluation was performed.
Figure 1: (a) Parasternal long-axis two-dimensional view and (b) apical four-chamber view at rest (40 beats/min) demonstrating mild left ventricular enlargement. M-mode assessment at rest (c) and after squatting (80 beats/min) (d) demonstrating significant decrease in end-systolic dimension and increase in calculated ejection fraction with squatting

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  Discussion Top

Identification of the athletic heart and differentiation from structural heart disease is often challenging, particularly when resting echocardiography demonstrates LV dilation with or without decreased resting LV systolic function. The degree of LV dilation in athletes is variable, and a study of 1309 elite Italian athletes showed that LV end-diastolic dimension was larger than 54 mm in 45% and larger than 60 mm in 15% of cases.[1] In addition, low-normal or mildly depressed ejection fraction is a common finding among highly athletic individuals. Ejection fraction <52% was reported in 11.6% of professional (Group A1) cyclists who participated in the 1995 “Tour de France” race.[2]

The pathophysiologic mechanism of depressed ejection fraction in athletes is often linked to LV dilation, and it is presumed that athletes require a lower percentage of their LV end-diastolic volume to meet resting strove volume demands. In addition, intensive training results in cardiovascular adjustment to a high output state and as a result, athletic individuals may appear preload reduced when evaluated at rest.[3] As the athletic heart is extremely compliant, it tends to operate at the steeper slope of the Frank Starling curve, which results in decreased cardiac contractility at rest.[4],[5] A significant subset of athletes do not demonstrate impressive LV dilation.[1] LV dyssynchrony could explain the lower ejection fraction in such patients. A recent study demonstrated significant delay between multiple systolic parameters (such as QRS onset and lateral LV systolic peak wave or interventricular septum systolic peak wave) in athletes with low versus normal ejection fractions.[6] Whether this dyssynchrony is pathologic is unclear because QRS duration and peak aerobic performance were not significantly changed in athletes with low ejection fractions.

Athlete's heart has been differentiated from pathology (hypertrophic or dilated cardiomyopathy) based on normal relaxation, absence of myocardial scarring, and reversibility of enlargement or hypertrophy with detraining.[7] Sports cardiologists use any of the above algorithms to differentiate athletic heart syndrome from pathology, and a multimodality imaging approach has been commonly proposed.[8] The evaluation usually starts with a thorough history and physical examination. Electrocardiography is a useful and simple clinical tool and may reveal many findings indicating pathology (such as increased QRS duration, left bundle branch block, ST/T wave changes, or abnormal QRS configuration).[9] Cardiac magnetic resonance imaging (CMR), with or without exercise, can be a superior modality to echocardiography in uncertain cases. CMR can accurately quantify chamber size and ejection fraction and may demonstrate pathologic late gadolinium enhancement.[10] Contractile reserve is a distinguishing feature of athletic heart syndrome that could be easily demonstrated with both exercise echocardiography and exercise CMR.[10] Although a multimodality imaging approach is essential in establishing the accurate diagnosis, it could be associated with less efficiency and increased cost. On the contrary, simple maneuvers (such as squatting during standard echocardiography) may be used to establish the correct diagnosis and defer further unnecessary cardiac workup.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Pelliccia A, Culasso F, Di Paolo FM, Maron BJ. Physiologic left ventricular cavity dilatation in elite athletes. Ann Intern Med 1999;130:23-31.  Back to cited text no. 1
Abergel E, Chatellier G, Hagege AA, Oblak A, Linhart A, Ducardonnet A, et al. Serial left ventricular adaptations in world-class professional cyclists: Implications for disease screening and follow-up. J Am Coll Cardiol 2004;44:144-9.  Back to cited text no. 2
Colan SD. Mechanics of left ventricular systolic and diastolic function in physiologic hypertrophy of the athlete's heart. Cardiol Clin 1997;15:355-72.  Back to cited text no. 3
Levine BD. Regulation of central blood volume and cardiac filling in endurance athletes: The Frank-Starling mechanism as a determinant of orthostatic tolerance. Med Sci Sports Exerc 1993;25:727-32.  Back to cited text no. 4
Levine BD, Lane LD, Buckey JC, Friedman DB, Blomqvist CG. Left ventricular pressure-volume and Frank-Starling relations in endurance athletes. Implications for orthostatic tolerance and exercise performance. Circulation 1991;84:1016-23.  Back to cited text no. 5
Boraita A, Sánchez-Testal MV, Diaz-Gonzalez L, Heras ME, Alcocer-Ayuga M, de la Rosa A, et al. Apparent ventricular dysfunction in elite young athletes: Another form of cardiac adaptation of the athlete's heart. J Am Soc Echocardiogr 2019;32:987-96.  Back to cited text no. 6
Wasfy MM, Weiner RB. Differentiating the Athlete's heart from hypertrophic cardiomyopathy. Curr Opin Cardiol 2015;30:500-5.  Back to cited text no. 7
Galderisi M, Cardim N, D'Andrea A, Bruder O, Cosyns B, Davin L, et al. The multi-modality cardiac imaging approach to the Athlete's heart: An expert consensus of the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2015;16:353.  Back to cited text no. 8
Sharma S, Drezner JA, Baggish A, Papadakis M, Wilson MG, Prutkin JM, et al. International recommendations for electrocardiographic interpretation in athletes. Eur Heart J 2018;39:1466-80.  Back to cited text no. 9
Claessen G, Schnell F, Bogaert J, Claeys M, Pattyn N, de Buck F, et al. Exercise cardiac magnetic resonance to differentiate athlete's heart from structural heart disease. Eur Heart J Cardiovasc Imaging 2018;19:1062-70.  Back to cited text no. 10


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