Identifying the aetiology of left ventricular hypertrophy in an athlete: importance of lifestyle modification

Abstract

The aetiology of left ventricular hypertrophy (LVH) in an athlete is often difficult to identify. We describe a 29-year-old fitness instructor who was referred for investigation of syncope. He gave a history of intensive weight lifting and anabolic steroid use at supra-therapeutic doses for the preceding 6 years. Electrocardiography showed inferolateral repolarisation abnormalities and a transthoracic echocardiogram demonstrated asymmetrical LVH with reduced left ventricular cavity dimensions. There was no left ventricular outflow tract obstruction or systolic motion of the anterior mitral valve leaflet. These findings were confirmed on cardiac magnetic resonance imaging (CMR). The differential diagnosis included athlete’s heart, steroid-induced cardiomyopathy and non-obstructive hypertrophic cardiomyopathy. The patient was advised to discontinue both steroid use and intensive training. After 3 years of steroid abstinence but continued training, the syncopal episodes and the ECG abnormalities completely resolved, associated with regression of LVH on echocardiography and CMR.

Background

Advising and encouraging patients to desist from harmful lifestyles is a vital part of clinical practice. This case illustrates how, in a case of pathological left ventricular hypertrophy (LVH), removing possible aetiological lifestyle factors is able to establish the diagnosis and at the same time treat the patient. A one-off assessment of clinical findings and imaging may be insufficient to reach a definitive diagnosis and could be misleading.

Case presentation

A 29-year-old professional fitness instructor with a history of asthma was referred with recurrent cough syncope. He trained in weight lifting 8 h a day for 6 days a week. Over the last 6 years he had regularly taken high doses of anabolic steroids, such as Trenbolone and Sustenonein, for 3-month courses prior to competitions. There was no history of hypertension and no family history of heart disease or unexplained sudden death.

Investigations

Physical examination revealed prominent musculature (body mass index (BMI) 31) but was otherwise unremarkable. ECG showed left axis deviation with inferolateral repolarisation abnormalities and borderline LVH by voltage criteria (figure 1).

Figure 1.

ECG at presentation.

Transthoracic echocardiography demonstrated moderate asymmetrical LVH (IVSd 1.9 cm, LVPWd 1.5 cm) with reduced left ventricular cavity dimensions (LVESD 2.2 cm, LVEDD 3.8 cm) (figure 2). There was no left ventricular outflow tract obstruction (LVOTO) and no systolic motion of the anterior mitral valve leaflet (SAM) to suggest obstructive hypertrophic cardiomyopathy.

Figure 2.

Echocardiography at presentation. Left: apical four chamber view; right: parasternal short axis view.

Holter monitoring revealed sinus rhythm throughout, although no recording was acquired during syncopal episodes.

Differential diagnosis

Based on the finding of LVH and clinical presentation, the differential diagnosis included hypertrophic cardiomyopathy (HCM), athlete’s heart and steroid-induced cardiomyopathy. Features suggestive of HCM included: (1) syncopal episodes triggered by coughing, ie, a Valsalva manoeuvre, raising the suspicion of outflow tract obstruction; (2) asymmetrical LVH; (3) repolarisation changes as seen on the initial ECG; and (4) small LV cavity on echocardiogram.

Other features of HCM such as SAM of the mitral valve or LVOTO were absent, although these are not distinguishing features of HCM and LVOTO only occurs in 30% of HCM cases, thus making the non-obstructive form of HCM a distinct possibility in our patient. In addition, cardiac magnetic resonance imaging (CMR) did not show late enhancement with gadolinium, a sensitive marker of myocardial scarring, which, depending on the study quoted, is present in 81%¹ or 69%² of patients with HCM; however, to a lesser degree late enhancement with gadolinium is also detected in other forms of LVH.³ In addition, there was no family history of HCM, although spontaneous mutations do occur. Although absence of these features does not exclude HCM, it makes the diagnosis less likely.

The history of longstanding weight training in conjunction with the ECG changes would support a diagnosis of athlete’s heart. Athlete’s heart is defined as the constellation of concentric LVH, increased ventricular mass and an increase in diastolic diameter associated with long-term training. Often non-specific ECG findings are detectable. However, the small LV cavity in our patient argues against this diagnosis.

Steroid-induced cardiomyopathy is a less well-defined clinical entity. In athletes, steroid use may present as concentric LVH with dilated cavity dimensions, thereby augmenting the physiological changes detected in athlete’s heart.⁴ However, it can also manifest as asymmetrical LVH with a small cavity.^5,6 Often it is accompanied by diastolic dysfunction.⁷ A comparative overview of the conditions can be found in table 1.

Table 1.

Summary of typical findings for hypertrophic cardiomyopathy, athlete’s heart and steroid-induced LVH

	Athlete's heart	Hypertrophic cardiomyopathy	Steroid-induced hypertrophic cardiomyopathy
LVH	Symmetrical	Asymmetrical	Symmetrical or asymmetrical
LVEDD	>55 mm	<45 mm	Variable
LVOTO	No	30%	Rarely present
LV filling	Normal	Abnormal	Often abnormal
Reversibility of LVH	Yes	No	Often partial reversibility only

LVEDD, left ventricular end diastolic diameter; LVH, left ventricular hypertrophy; LVOTO, left ventricular outflow tract obstruction. It must be emphasised that while the features listed above are the “classical” features of these conditions, not all features may be present in any one condition and there may be considerable overlap between these conditions both clinically and echocardiographically.

Treatment

A presumptive diagnosis of steroid-induced cardiomyopathy was made. The patient was advised to desist from using anabolic steroids, and to cease physical training, in the hope of inducing regression of LVH.

Outcome and follow-up

After 6 months of steroid abstinence the syncopal episodes ceased. CMR performed after 18 months of steroid abstinence but ongoing training continued to show inter-ventricular septal hypertrophy (figure 3) and septal dyssynchrony. There was no enhancement in the late phase after gadolinium contrast.

Figure 3.

Cardiac MRI 18 months after discontinuation of steroids, but continuation of training. Left: four chamber view, right: short axis view.

Three years after steroid cessation and with reduced training, the ECG had completely normalised with resolution of the previous repolarisation changes (figure 4). In addition echocardiography showed complete normalisation of left ventricular cavity size (LVEDD 5.2 cm, LVESD 3.3 cm) (figure 5). The only remaining abnormal finding was mild concentric hypertrophy (IVSd 1.2 cm, LVPWd 1.2 cm). This remission was mirrored by the repeat CMR (figure 6). The history of longstanding steroid use in conjunction with intensive body building, collective imaging data and reversibility of the condition favour the diagnosis of steroid-induced cardiomyopathy.

Figure 4.

ECG 3 years after discontinuation of steroids.

Figure 5.

Echocardiography 3 years after discontinuation of steroids. left: four chamber view, right: short axis view.

Figure 6.

Cardiac MRI 3 years after discontinuation of steroids.

Discussion

Importance of the present study

A surprisingly small number of case reports/series show only the tip of the iceberg of this widespread and unrecognised problem of steroid abuse in athletes.

Data quality is compromised by the large number of uncontrolled variables regarding these illicit substances which are self-administered and obtained without prescription. The effects appear to be dose and duration dependent,⁷ but the exact dose, substance, duration and concomitant physical training often remain poorly described. Interventional trial data are limited to animal studies. Here lies the importance of case reports such as the present study, which allows in-depth observation of drugs effects and reversibility.

Uncertainties over reversibility

Very few papers address the question of reversibility of LVH after steroid use. The degree of reversibility appears to be dependent on the interval after steroid cessation. Whereas no normalisation was detected at 9 weeks,⁸ some degree of normalisation can be seen in the majority of cases after 8 months⁹ or a mean of 24 months.¹⁰

In agreement with these findings, the present study demonstrates reversibility after steroid cessation at 3 years. In addition, this is the first published report on steroid abuse in an athlete that shows near normalisation of LVH and left ventricular cavity dimension.

Unusual feature of the present case

Complete reversibility of steroid-induced LVH has been detected in several paediatric patients. These patients received high doses of steroids for treatment of congenital adrenal hyperplasia (CAH)⁵ and bronchogenic dysplasia.⁶ In these patients, cardiac morphology appeared to mimic obstructive HCM with its typical findings of a small left ventricular cavity, LVH and LVOTO. This report is the first to document significant reduction in left ventricular cavity size in association with LVH secondary to steroid use in an adult. One might speculate that steroid-induced LVH associated with small cavity dimensions may have a greater degree of reversibility than steroid-induced cardiomyopathy with a dilated left ventricular cavity.

Importance of differential diagnosis

Differentiating steroid-induced cardiomyopathic changes from the other causes of LVH in an athlete may prove difficult, particularly as these conditions may occur in a similar subgroup of the population. However, it is of utmost importance to reach a diagnosis as the therapeutic interventions and clinical outcome differ greatly, with HCM being a common cause of death among athletes.¹¹ Interestingly, recent publications also attribute significant morbidity and mortality to steroid use at supra-therapeutic dosages, including myocardial infarction and sudden cardiac death.¹² In addition, LVH in itself is an important risk factor for sudden death and other causes of cardiovascular morbidity and mortality even after adjusting for blood pressure (reviewed by Levy¹³ and Gosse¹⁴).

The most important tools in identifying the aetiology of LVH are detailed history taking including anabolic steroid use, and prolonged observation following lifestyle modification including cessation of steroid use and physical training.

Learning points

• The differential diagnosis of left ventricular hypertrophy (LVH) in young athletes includes hypertrophic cardiomyopathy, athlete’s heart and steroid-induced cardiomyopathy.

• Steroid-induced cardiomyopathy is an under-reported condition.

• History taking, ECG, echocardiography and cardiac MRI may be helpful in identifying the aetiology of LVH.

• Distinguishing steroid-induced cardiomyopathy from other forms of cardiomyopathy is important as treatment by steroid withdrawal results in at least partial regression.

• The most important diagnostic and therapeutic tool is the withdrawal of steroids and physical de-conditioning in this population.