BJSM Figure 16. Echocardiographic (left panel) and cardiac MRI (right panel) of isolated left ventricular non-compaction. Note the prominent trabeculations in the left ventricular apex (red arrow), with a thin layer of compact myocardium (blue arrow) and prominent intertrabecular recesses. ces. Contrast echocardiography or cardiac MRI should be considered when image resolution is reduced. Athletes may have LV chamber enlargement as a part of physiological adaptation to exercise.64 This is most often seen in athletes participating in endurance sports such as cycling, crosscountry skiing or rowing. Mild reduction in LV contractility (EF 40–50%) is seen in a minority of athletes with LV cavity dilation, but is not an invariable component of physiological adaptation to exercise.64 65 Stress echocardiography can assess myocardial performance at submaximal or peak exercise which may help differentiate those with low normal or borderline systolic function, as systolic function is more likely to normalised in athlete’s heart than in DCM. Thus, LV dilatation and measures of systolic function should be interpreted carefully and in the context of the athlete’s level and amount of endurance training. All patients with DCM should be referred to a cardiologist for further aetiological evaluation, including assessment for myocardial ischaemia and infiltrative disorders. Figure 17. ECG from a patient with isolated left ventricular non-compaction. Note the ST segment depression in the inferolateral leads (II, III, aVF and V5–V6). LV non-compaction LVNC is a heart muscle disorder in which loosely organised myocardial fibres fail to condense into a compact layer resulting in increased myocardial trabeculations and thinning of the compact myocardium (figure 16).66 67 LVNC can occur along with other congenital or embryological abnormalities, or can be found in isolation, and can be due to underlying gene mutations. However, the majority of LVNC remains genetically elusive. This disturbance of myocardial structure leads to progressive weakening of heart muscle contraction (lower EF) with ventricular dilation. Therefore, LVNC should be distinguished from DCM. Blood clots may also form within the trabecular recesses, increasing the risk for embolic strokes. Figure 18. ECG from a patient with isolated left ventricular non-compaction, demonstrating left atrial enlargement with a left bundle branch block. An isolated premature ventricular complex is also present. These findings warrant further testing to evaluate for cardiomyopathy. nal evaluation to rule out an underlying cardiomyopathy are listed in table 1. Evaluation of suspected DCM When DCM is suspected, further evaluation of LV size and function is required. Echocardiography provides assessment of cardiac structure and function, including FS and/ or EF, and is the first test of choice under most circumstan34 Sport & Geneeskunde | september 2013 | nummer 4 Prevalence The exact prevalence of isolated LVNC is unknown, but is thought to be <0.1–0.2%. Reasons for the uncertainty in prevalence include challenges in imaging the non-compaction and disagreement regarding diagnostic criteria. Contribution as a cause of SCD LVNC is associated with an increased risk of abnormal heart rhythms and sudden cardiac arrest.68 LVNC is a rare (<1%) cause of SCD in a series of young athletes.2 Diagnostic criteria Several sets of diagnostic criteria for isolated LVNC exist, Pagina 33
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Sport & Geneeskunde nummer 4 | September 2013 Lees publicatie 25Home