As discussed in their article,1RV involvement may have a different origin, including primary myocardial involvement, lung fibrosis, and/or pulmonary artery hypertension. Based on the absence of LV or RV systolic abnormalities and extensive lung fibrosis, they assumed that RV diastolic abnormalities are consistent solely with pulmonary artery hypertension; they also addressed a few limitations concerning the assessment of pulmonary artery pressure by resting echocardiography. However, to our knowledge, the absence of systolic abnormalities using conventional techniques does not rule out primary myocardial involvement.2Moreover, diastolic function may be altered very early in the course of SSc, and may be consistent with primary myocardial involvement.3 Even more intriguing may be the absence of LV systolic, LV diastolic, and RV systolic abnormalities. In fact, we and others have previously highlighted that patients with SSc often exhibit myocardium perfusion abnormalities in up to 100%2together with LV diastolic dysfunction,3–4 and also RV systolic dysfunction3; moreover, these alterations were demonstrated in both cutaneous subtypes of the disease and in patients with normal pulmonary artery pressure and early manifestations of SSc (duration of disease, < 5 years).3 The question is how to explain the absence of any alterations in both LV function and RV systolic function in the population investigated in the article by Lindqvist et al.1 What was the detailed therapeutic regimen? Did they explore patients with very recent manifestations of SSc, indicating that RV diastolic function is an early marker of heart involvement; one may therefore question the definition of disease duration (first symptom of Raynaud syndrome?). Were some patients with undifferentiated connective tissue disorder included in the study? Or does the study reflect the lack of sensitivity of their method of assessment?