Traditional echocardiography is unable to detect neither the early stages of iron overload cardiomyopathy nor myocardial iron deposition. The aim of the study is to determine myocardial systolic strain indices in thalassemia major (TM), and assess their relationship with T2*, a cardiac magnetic resonance index of the severity of cardiac iron overload. 55 TM cases with recent cardiac magnetic resonance (CMR-T2*) underwent speckle tracking analysis to assess regional myocardial strains and rotation. The results were compared with a normal control group (n = 20), and were subsequently analyzed on the basis of the CMR-T2* values. Two TM groups were studied: TM with significant cardiac iron overload ("low" T2*, ≤20 ms; n = 21), and TM with normal T2* values ("normal" T2*, >20 ms; n = 34). TM patients show significant, uniform decrease in circumferential and radial strain (P < 0.05), and a remarkable reduction in end-systolic rotation, both global, and for all segments (P < 0.001). No significant differences were found between the low- and the normal T2* group either in regional strains and rotation or in standard echocardiographic and CMR parameters. Spearman's correlation coefficient shows no significant correlation between myocardial strains, rotation and cardiac T2* values. In conclusion, our results are in accordance with recent evidence that myocardial iron overload is not the only mechanism underlying iron cardiomyopathy in TM. Strain imaging can predict subclinical myocardial dysfunction irrespective of CMR-T2* values, although it cannot replace CMR-T2* in assessing cardiac iron overload. Finally, it might be useful to appropriately time cardioactive treatment.

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Abstract-Congestive heart failure is characterized by a sympathetic activation that is coupled with a baroreflex impairment. Whether these alterations are affected by clonidine is unknown. In 26 normotensive patients age 58.0Ϯ1.1 years (meanϮSEM) affected by congestive heart failure (New York Heart Association functional class II or III) and treated with furosemide and enalapril, we measured mean arterial pressure, heart rate, venous plasma norepinephrine, and muscle sympathetic nerve traffic (microneurography) at rest and during baroreceptor stimulation and deactivation caused by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were repeated after a 2-month administration of transdermal clonidine patch (14 patients) or placebo (12 patients) according to a double-blind, randomized sequence. Clonidine caused a slight, nonsignificant reduction in mean arterial pressure and heart rate without affecting exercise capacity and echocardiographically determined left ventricular ejection fraction. In contrast, both plasma norepinephrine and sympathetic nerve traffic were significantly reduced (Ϫ46.8% and Ϫ26.7%, respectively; PϽ0.01 for both). This reduction was coupled with no change in cardiac and sympathetic baroreflex responses. Transdermal placebo administration for a 2-month period did not affect any of the above-mentioned variables. Thus, in congestive heart failure patients who are undergoing conventional drug treatment, chronic clonidine administration exerts marked sympathoinhibitory effects without adversely affecting cardiac functions and clinical state.Whether this leads to further therapeutic benefits remains to be tested.

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