nificance of a non-specific intraventricular conduction delay (IVCD) with normal QRS morphology is uncertain. However, marked nonspecific IVCD >140 ms is considered abnormal and should prompt further evaluation. Left axis deviation LAD, defined as −30° to −90°, is present in almost 12% of HCM patients but less than 1% of athletes (figure 7).9 23 25 LAD can be a secondary marker for pathological LV hypertrophy (LVH) and if present warrants additional evaluation. Left atrial enlargement ECG findings suggestive of LAE have been defined in different ways. Overall, LAE on ECG is present in approximately 10–21% of HCM patients but has been reported in up to 44% of black patients with HCM (figure 8).21–23 LAE is defined as a prolonged P wave duration of >120 ms in leads I or II with negative portion of the P wave ≥1 mm in depth and ≥40 ms in duration in lead V1. LAE on ECG is an uncommon finding in athletes and should prompt additional investigation. Increased QRS voltage in athletes and HCM The isolated presence of high QRS voltages fulfilling voltage criterion for LVH is regarded as a normal finding in athletes related to physiological increases in cardiac chamber size and/or wall thickness and does not in itself require additional evaluation. 5 6 As expected, voltage criteria for LVH also are commonly identified in individuals with HCM. However, the presence of isolated increased QRS voltage in the absence of other ECG abnormalities is uncommon and present in <2% of individuals with the disease.19 Several studies have evaluated athletes and young adults with isolated increased QRS voltage using echocardiography or cardiac MRI and none had HCM.24 26 31–33 Therefore, isolated increased QRS voltage on the ECG in the absence of other abnormalities in an asymptomatic athlete with a negative family history is not a reliable indicator of HCM and does not require further evaluation. Co-existing ECG abnormalities such as TWI, ST segment depression, pathological Q waves, IVCD, LAD or LAE should be investigated by additional testing. Evaluation of suspected HCM If HCM is suspected based on ECG abnormalities, evaluation of LV morphology and function is required.34 circumstances. HCM can be diagnosed when wall thickness is ≥1.5 cm with normal or small LV cavity size in the absence of other causes capable of causing myocardial hypertrophy. Diastolic dysfunction, mitral valve pathology and LVoutflow tracts obstruction are other findings that support the diagnosis of HCM. However, echocardiographic quality is variable based on numerous factors, including operator proficiency and patient acoustic windows, and may have limited ability to detect hypertrophy of the anterolateral LV wall and apex (figure 9).35 Echocardiography provides assessment of LV cavity size and wall thickness, systolic and diastolic function and valvular structure and function, and is the first test of choice under most Cardiac MRI provides superior assessment of myocardial hypertrophy and may demonstrate late gadolinium enhancement which is a non-specific marker suggesting myocardial fibrosis. Cardiac MRI should be considered when echocardiography is nummer 3 | juli 2013 | Sport & Geneeskunde 31 Figure 7. ECG demonstrates abnormal left-axis deviation defined as frontal plane QRS axis of less than −30°. The QRS is positive in lead I and negative in aVF and lead II. The QRS axis shown here is about −70°. Figure 8. Abnormal ECG in a patient with hypertrophic cardiomyopathy showing left atrial enlargement, defined as a prolonged P wave duration >120 ms in leads I or II with negative portion of the P wave≥1 mm in depth and ≥40 ms duration in lead V1. Pagina 30
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Sport & Geneeskunde nummer 3 | Juli 2013 Lees publicatie 24Home