Background—
Increased iron store has been linked to risk of cardiovascular disease. Structural alterations of arteries in β-thalassemia major patients and in vitro functional disturbance of vascular endothelial cells by thalassemic serum have been described. We sought to determine whether arterial stiffness and endothelial function are altered in vivo.
Methods and Results—
Thirty thalassemia patients (16 male) aged 22.2±7.4 years were recruited. Left ventricular (LV) mass and function were assessed echocardiographically. Carotid and brachioradial artery stiffness was assessed by stiffness index and pulse-wave velocity (PWV), respectively. Brachial artery endothelial function was assessed by vascular response to reactive hyperemia (flow-mediated dilation [FMD]) and sublingual glyceryl trinitrate. These indexes were compared with those of 30 age- and sex-matched controls. None of the patients had LV systolic or diastolic dysfunction. When compared with controls, patients had greater absolute (113.8±38.0 versus 109.0± 32.6 g,
P
=0.04) and indexed (82.4±17.5 versus 66.7±12.7 g/m
2
,
P
<0.001) LV mass, carotid artery stiffness index (8.1±3.5 versus 5.5±1.6,
P
<0.001), and brachioradial PWV (8.9±2.4 versus 7.9±1.7 m/s,
P
= 0.03). Their FMD was impaired (3.5±3.3% versus 8.8±3.9%,
P
<0.001), whereas glyceryl trinitrate– mediated dilation was preserved (17.9±7.6% versus 16.3±6.1%,
P
=0.40). Both stiffness index and PWV correlated inversely with magnitude of FMD (
r
=−0.40,
P
=0.03;
r
=−0.41,
P
=0.03) and positively with indexed LV mass (
r
=0.50,
P
=0.005;
r
=0.40,
P
=0.027). Nonetheless, no significant correlation existed between ferritin level and carotid stiffness, PWV, or FMD.
Conclusions—
Increased arterial stiffness, endothelial dysfunction, and LV hypertrophy occur in patients with β-thalassemia major, which may result in reduction of mechanical efficiency of the heart.
