We were very interested to read the article by Oxborough et al. in the March issue of JASE . The authors found that right ventricular (RV) chamber dimensions were larger in endurance athletes than those described by “normal ranges” and “frequently meet the major criteria for the diagnosis of arrhythmogenic RV cardiomyopathy.” They are correct in pointing out that this may lead to misdiagnosis of arrhythmogenic RV cardiomyopathy, and it is important to measure RV mechanics, although RV function assessment is not always straightforward, because of the shape of the right ventricle. One should always consider the clinical context: a healthy endurance athlete with excellent exercise tolerance and another young man with postviral cardiomyopathy might both have large ventricular dimensions, but the lack of symptoms of dyspnea on minimal exertion in the athlete will provide helpful clues to the meaning of his ventricular enlargement. Clinical echocardiographers are familiar with the differential diagnoses of short linear echogenic masses in association with the aortic valve. In a healthy person with no symptoms or fever, one might diagnose Lambl’s excrescence as a common cause, whereas an ill patient with fever, splinter hemorrhages, a heart murmur, arterial emboli, and positive blood cultures should prompt the echocardiographer to consider endocarditis. Thus, we must always remember to treat the patient, not just the echocardiographic images.

In addition to arrhythmogenic RV cardiomyopathy, there are numerous causes of pathologic RV dilatation. Cor pulmonale is very commonly seen (e.g., in chronic obstructive pulmonary disease). Perhaps more worryingly, failure to recognize the important observation of Oxborough et al. that RV enlargement per se can be normal might lead to the overdiagnosis of RV strain in acute pulmonary embolus (PE). Some would advocate thrombolysis in patients with PE and right-heart strain, even in the absence of hemodynamic compromise. Nevertheless, thrombolysis is associated with significant risks, in particular bleeding and occasionally hemorrhagic stroke. Consider a young and otherwise healthy patient, admitted to the hospital after a long flight with left-sided pleuritic chest pain and breathlessness on exertion but a normal heart rate and blood pressure and no signs of heart failure or electrocardiographic abnormalities. Mild hypoxia on blood gas analysis and increased d -dimer would lead the clinician to perform computed tomographic pulmonary angiography, which might confirm a small PE in the left lung. A dilated right ventricle that nevertheless appears to contract well with normal tricuspid annular plane systolic excursion may help avoid misdiagnosing RV strain. However, beware “McConnell’s sign”: patients with acute PE had a distinct regional pattern of RV dysfunction, with akinesia of the mid free wall but normal motion at the apex. The advent of computed tomographic pulmonary angiography performed with electrocardiographic gating permits new advances in the assessment of acute right-sided heart failure, such as measurement of the ventricular ejection fraction.

In conclusion, Oxborough et al. ‘s findings should certainly make clinicians think carefully about the role of thrombolysis in acute PE. Considering the clinical context plus lack of evidence of RV strain on electrocardiography and the absence of RV function abnormality will help avoid misinterpreting the meaning of RV enlargement.