Objective: Central and systemic arterial stiffness are major determinants of cardiovascular risk and play an important role in developing complications, particularly in hypertension. We evaluated the prevalence of structural, functional and mechanical alterations of heart and their association with arterial stiffness in patients with uncomplicated, mild essential hypertension. Methods: Two hundred thirty nine patients (51years; 63% male; BP 151/103 mmHg) were compared to 136 age and sex-matched normotensive controls (52years; 52% male; BP 114/79mmHg). Left ventricular (LV) hypertrophy (mass index; LVMI), systolic (ejection fraction; EF) and diastolic function (deceleration time of the early mitral filling; DT), and LV stiffness (棺-index) were measured by echocardiography. Systemic arterial (augmentation index; AI) and aortic (棺-index) stiffness were measured using radial pulse tonometry. Results: The hypertensives had significantly higher prevalence of cardiac hypertrophy (p>0.001), diastolic dysfunction (p>0.001), and increased LV stiffness (p>0.001) compared to the normotensives. Systolic function and coronary pressure gradient were similar in both groups. Aortic 棺-index and AI were increased in hypertensive patients (p>0.001). The prevalence of abnormal structure, diastolic dysfunction and altered mechanical properties of LV in hypertension was 59, 24, and 28% (greater than mean+1SD of controls), and 28, 3, and 10% (greater than mean+2SD of controls), respectively. The prevalence of increased stiffness in aorta and systemic artery was 23 and 35% (greater than mean+1SD of controls) and 13 and 6% (greater than mean+2SD of controls) in hypertension. No correlation was found between aortic or systemic arterial stiffness and the parameters of cardiac alterations after adjustment for sex, age, body mass index, blood pressure, and cholesterol. Conclusion: Arterial stiffness precedes clinically relevant manifestations of cardiac target organ damage in mild essential hypertension. The lack of association between arterial stiffness and cardiac alterations suggests that different mechanisms exist for target organ damage of heart and artery in hypertension and differential strategy is needed to reverse them.