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Correspondence regarding: Distinct effects of losartan and atenolol on vascular stiffness in Marfan syndrome by Bhatt et al.

We compliment Bhatt et al.1 on their study of arterial hemodynamics in patients with Marfan syndrome, treated by losartan or atenolol, and suggest that additional information may be available from their study. The authors found a significant decrease in central aortic augmented pressure with losartan compared to atenolol (difference 3.2 mmHg, p = 0.009), and a significant decrease also in E′ septal velocity of the echocardiogram (difference 1.73 m/s, p = 0.03). Late systolic augmented pressure, E′ septal velocity and left ventricular ejection time are indices of diastolic left ventricular dysfunction,2,3 so that findings warrant consideration as a favourable effect of losartan over atenolol on the left ventricle in this condition. The authors suggest that reduction of AIx by losartan may be due to reduction in peripheral resistance, but there was no difference in mean pressure between the two drugs (cardiac output was not measured). Differences can be attributed to conduit arterial (rather than arteriolar) dilation. Conduit dilation can occur independently of arteriolar dilation with reduced peripheral resistance, and be apparent only as a reduction in pressure wave reflection. This has previously been described for ramipril compared with atenolol.4 We would appreciate the authors’ views on these issues.