HCM Versus Athlete’s Heart: A String of Pearls
- Mild hypertrophy <16 mm may occur in competitive athletes who undergo rigorous training. It does not occur with casual athletics or mild training.
- In athletes with wall thickness of 13-16 mm, the so-called “gray zone,” ancillary findings of small relative LV cavity size, abnormal diastolic function, or systolic anterior motion supports a diagnosis of hypertrophic cardiomyopathy.
- In ambiguous cases, cardiac MRI evaluation may be helpful, including (if necessary) 3 months of deconditioning and repeat
If hypertrophic cardiomyopathy (HCM) is marked by thickening of the left ventricle without clinical cause, how often does such hypertrophy occur in athletes who have physiological thickening caused by training? Several studies have helped answer this question. In an analysis of 947 elite athletes, 1.7% had LV thickening of about 12 mm, suggesting a rough upper limit of physiologic cardiac hypertrophy.1 In that study, mean age was 22.5 years; as for highly trained younger athletes, ages 14 to 18, there is some thickening, but less than that seen in adult athletes.2
Another study looked at athletes before joining the United Kingdom’s Olympic team and found thickening between 13-16 mm in 1.5% of athletes,3 similar to a study of 156 professional football players, 6% of whom had thickening >13 mm.4
In terms of distinguishing HCM from the athletic heart, there is a “gray zone,” defined in 1995 by Maron et al as being between 12-16 mm as measured by echocardiography.5 There are other ancillary findings: HCM patients have asymmetric patterns in the LV cavity <45 mm; conversely, individuals with athlete’s heart will have LV cavity dilatation to accommodate training-related volume changes of 55 mm or greater.
An abnormal flow Doppler waveform in athletes with LV hypertrophy strongly suggests HCM; however, a normal Doppler filling pattern does not exclude diagnosis of HCM because of pseudo-normal flow patterns. In these cases, tissue Doppler is useful to show a good separation between pathologic hypertrophy, physiologic hypertrophy of athletes, and normal non-hypertrophic hearts.
One important note: different echo units acquire tissue Doppler differently.6 Studies performed on one machine may have a different diastolic tissue velocity when performed on another echo system. Mark V. Sherrid, MD, advises “know your machine and know the ‘normals’ of your machine.”
Looking at systolic anterior motion (SAM) of the mitral valve and determining whether mitral leaflets are elongated can help with the diagnosis. Sometimes this occurs in HCM even when the walls are not particularly thickened. If this occurs, especially in the presence of mitral-septal contact either at rest or with exercise, hypertrophic cardiomyopathy is likely. Stress exercise echo is an optimal way to provoke such patients and can provide more information than at rest.
In athletic patients whose wall thickness is in the “gray zone,” deconditioning is a final approach that can help with diagnosis.7 Three-month deconditioning should be enough time to see if the heart shows reduced hypertrophy or stays the same. If imaging reveals a decrease of ≥2 mm with deconditioning relative to peak training, that’s more consistent with the remodelling that occurs with athlete’s heart. Patients with HCM typically experience no change over time in wall thickness from deconditioning.
Cases, especially those of professional or elite athletes, are often freighted with emotional overtones and patients want a full workup. MRI and gadolinium enhancement can be performed as well and may help identify scarring. MRI doesn’t generally show much more than the echo, but it is better if the cardiologist reviews the images personally to make sure wall thicknesses are accurately measured. The kind of careful measurement to assess the effects of deconditioning, for example, can be achieved with cardiac magnetic resonance (CMR) as it allows for very accurate maximal wall thickness measurements.
When these same patients undergo contrast enhanced MRI with intravenous gadolinium, the tracer will be taken up in areas of extra expanded cellular space indicative of fibrosis and scarring. About 60% of patients with HCM will have some evidence of this late gadolinium enhancement (LGE) when scanned with this technique. However, up to this point, there’s no strong evidence that the athlete’s heart will demonstrate LGE. It’s a structurally normal substrate even in those athletes immediately after marathons or triathlons who have very small activity-related troponin leaks and who have been imaged by contrast-enhanced CMR.
One area in which CMR doesn’t perform as well: the assessment of diastolic function. Tissue Doppler or spectral Doppler techniques help raise the suspicion of abnormal diastolic function that would be much more consistent with HCM than athlete’s heart.
Clearly, there are strengths for both techniques that can assist in the diagnosis of these patients.References
- Pelliccia A. N Engl J Med. 1991; 324:295-301.
- Sharma S, et al. J Am Coll Cardiol. 2002;40:1431-6. http://content.onlinejacc.org/cgi/content/abstract/40/8/1431
- Basavarajaiah S, et al. J Am Coll Cardiol. 2008;51:1033-9. http://content.onlinejacc.org/cgi/content/abstract/51/23/2256
- Abernethy W, et al. J Am Coll Cardiol. 2003; 41:280-4. http://content.onlinejacc.org/cgi/content/abstract/41/2/280
- Maron BJ, et al. Circulation. 1995;91:1596-601.
- McCulloch M. J Am Soc Echocardiogr. 2006;19:744-8.
- Pelliccia A, et al. Circulation. 2002;105:944-9.
To listen to an interview with Mark V. Sherrid, MD, visit youtube.cswnews.org. The interview was conducted by Alfred Bove, MD, PhD.
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