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Abstract Back ground: SCD is a chronic inflammatory state with extensive oxidative stress involving several enzyme systems and ischemia /reperfusion injury, with nitric oxide (NO) dysregulation playing a central role. Another model of SCD pathophysiology has therefore been proposed that involves the interaction of hemolysis and the endothelium (Hagar et al., 2008). Cardiac complications are a common, often unrecognized, cause of morbidity and mortality in SCD, and are a major cause of death in adult patients (Voskaridou et al., 2007). Cardiovascular complications are increasingly evident, with the notable development of a progressive proliferative systemic vasculopathy, pulmonary hypertension (PH), and left ventricular diastolic dysfunction.Chronic anemia in SCD results in cardiac chamber dilation and a compensatory increase in left ventricular mass. This is often accompanied by left ventricular diastolic dysfunction that has also been a strong independent predictor of mortality in patients with SCD (Hagar et al., 2008). Objectives: The aim of study is early detection of subtle myocardial dysfunction in SCD patients and to examine the potential deficiency of circulating nitric oxide as sign of endothelial dysfunction |