Left Ventricular Trabeculations in Athletes
Left ventricular noncompaction (LVNC) cardiomyopathy is characterized by prominent myocardial trabeculations and deep recesses.1-3 The clinical spectrum of the disorder ranges from being completely asymptomatic to progressive left ventricular (LV) systolic impairment, a tendency to fatal arrhythmias and systemic thromboembolic events.3 The clinical diagnosis is predominantly reliant on three proposed echocardiographic criteria and based on an increased ratio of the noncompacted inner layer to the compacted outer layer of the LV myocardium (Figure 1).3
The past two decades have witnessed significant advances in tissue harmonics and image resolution in echocardiography, which has enabled detailed assessment of the ventricular myocardium. Coinciding with these developments has been an increasing number of reports of athletes with LVNC.4-7
In a large study4 of over 1,000 asymptomatic athletes, 18% showed increased LV trabeculation and 76 (8%) fulfilled echocardiographic criteria for LVNC. These findings suggest that in most athletes, increased LV trabeculation, which may fulfill criteria for LVNC represents a non-specific epiphenomenon in response to a chronic increase in preload and afterload associated with exercise. However, 10 (0.9%) athletes had T-wave inversion and reduced resting indices of systolic function that may be considered diagnostic of LVNC. This gray zone is smaller than that observed in hypertrophic cardiomyopathy (2%)8 but conversely greater than that for ARVC (0.3%).9 The distinction between cardiac remodeling from athletic training and LVNC is important given that the primary cardiomyopathies are the most common cause of exercise related sudden cardiac death in young athletes.10
The dilemma in differentiating benign myocardial trabeculations from LVNC arises because the current LVNC criteria1,2,11,12,13 are derived from small cohorts and lack specificity particularly in asymptomatic, low-risk populations. Although the criteria rely on the presence of increased LV trabeculations and the presence of a double myocardial layer, an outer compacted area and an inner noncompacted layer, they differ from each other with respect to the precise area and timing in the cardiac cycle for the measurement of the compacted and noncompacted layers.
The authors of this Expert Analysis article propose the following guidance, which requires utilizing several diagnostic modalities, for the assessment of athletes with a triad of echocardiographic features fulfilling criteria for LVNC, impaired resting LV function and T-wave inversion on the electrocardiogram (Figure 2). The proposal is based on experience of comparing athletes with features of LVNC and actual patients diagnosed with the condition.4
Patients with LVNC frequently (75%) express symptoms of LV dysfunction whereas athletes are asymptomatic. These individuals also frequently (66%) demonstrate a LV cavity >64 mm, an ejection fraction <45%, suppressed longitudinal LV function (Sa <9 cm/sec), and impaired LV filling (E' <9 cm/sec). In contrast, athletes with increased LV trabeculation and reduced EF usually show an EF range of 45-50% and normal indices of longitudinal LV function and normal diastolic function. Other echocardiographic parameters, including speckle tracking and strain, may be helpful in borderline cases.
The pattern of T-wave inversion is different between the two groups; patients with noncompaction show T-wave inversion in the inferolateral leads, whereas the majority of athletes showed T-wave inversion in V1-V3. Left bundle branch block (LBBB) is most unusual in athletes but is common in patients with LVNC. In the authors' experience, a cardiopulmonary exercise stress test followed by a peak exercise echocardiography is useful in the differentiation between the two groups. Athletes reveal a high peak VO2 (>120% predicted for age and size) and dynamic LV contraction, whereas patients with LVNC show low peak VO2 and exercise echocardiogram reveals poor LV contractile reserve on exercise. The identification of non-sustained ventricular tachycardia during exercise in athletes with criteria for LVNC would support pathology. In situations in which image quality is poor on transthoracic echocardiography, cardiac MRI may support a myopathic process by revealing fibrosis following gadolinium.
Long-term follow-up is crucial for athletes with a family history of premature sudden cardiac death and heart failure. We would also recommend screening of first-degree relatives for features of LVNC; the detection of another member with a similar phenotype would favor a diagnosis of LVNC.
Current imaging criteria for LVNC are non-specific in athletes and prone to an erroneous diagnosis. Increased cardiac preload is the most probable mechanism for increased trabeculation in the majority of athletes. A minority of athletes reveal the triad of increased LV trabeculations fulfilling LVNC criteria, T-wave inversion and LV systolic dysfunction. This group requires more detailed investigation and long-term follow-up.
- Chin TK, Perloff JK, Williams RG, Jue K, Mohrmann R. Isolated noncompaction of left ventricular myocardium. A study of eight cases. Circulation 1990;82:507-13.
- Jenni R, Oechslin E, Schneider J, Attenhofer Jost C, Kaufmann PA. Echocardiographic and pathoanatomical characteristics of isolated left ventricular non-compaction: A step towards classification as a distinct cardiomyopathy. Heart 2001;86:666-71.
- Oechslin E, Jenni R. Left ventricular non-compaction revisited: A distinct phenotype with genetic heterogeneity? Eur Heart J 2011;32:1446-56.
- Gati S, Chandra N, Bennett RL, et al. Increased left ventricular trabeculation in highly trained athletes: Do we need more stringent criteria for the diagnosis of left ventricular non-compaction in athletes? Heart 2013;99:401-8.
- Luijkx T, Cramer MJ, Zaidi A, et al. Ethnic differences in ventricular hypertrabeculation on cardiac mri in elite football players. Neth Heart J 2012;20:389-95.
- Martinoli R, Papetti F, Dofcaci A, et al. Isolated left ventricular non compaction as possible cause of athletic training suspension: A preliminary study on screened athletes. J Sports Med Phys Fitness 2013;53:240-7.
- Ganga HV, Thompson PD. Sports participation in non-compaction cardiomyopathy: A systematic review. Br J Sports Med 2014;48:1466-71.
- Basavarajaiah S, Wilson M, Whyte G, Shah A, McKenna W, Sharma S. Prevalence of hypertrophic cardiomyopathy in highly trained athletes: Relevance to pre-participation screening. J Am Coll Cardiol 2008;51:1033-9.
- Zaidi A, Ghani S, Sharma R, et al. Physiologic right ventricular adaptation in elite athletes of african and afro-caribbean origin. Circulation 2013;127:1783-92.
- Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Sudden deaths in young competitive athletes: Analysis of 1866 deaths in the united states, 1980-2006. Circulation 2009;119:1085-92.
- Stollberger C, Finsterer J. Left ventricular hypertrabeculation/noncompaction. J Am Soc Echocardiogr 2004;17:91-100.
- Petersen SE, Selvanayagam JB, Wiesmann F, et al. Left ventricular non-compaction: Insights from cardiovascular magnetic resonance imaging. J Am Coll Cardiol 2005;46:101-5.
- Jacquier A, Thuny F, Jop B, et al. Measurement of trabeculated left ventricular mass using cardiac magnetic resonance imaging in the diagnosis of left ventricular non-compaction. Eur Heart J 2010;31:1098-104.
Clinical Topics: Arrhythmias and Clinical EP, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Sports and Exercise Cardiology, EP Basic Science, SCD/Ventricular Arrhythmias, Acute Heart Failure, Echocardiography/Ultrasound, Sports & Exercise and ECG & Stress Testing, Sports & Exercise and Imaging
Keywords: Athletes, Bundle-Branch Block, Cardiomyopathies, Cardiomyopathy, Hypertrophic, Death, Sudden, Cardiac, Diastole, Echocardiography, Electrocardiography, Exercise Test, Follow-Up Studies, Gadolinium, Heart Failure, Humans, Myocardium, Phenotype, Sports, Tachycardia, Ventricular
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