several functional and structural abnormalities are involved in the rise of systolic BP with aging and consequently the development of isolated systolic hypertension in the elderly. Endothelial dysfunction together with vascular remodeling and fibrosis will decrease arterial elasticity or increase arterial stiffness. Consequently there will be an increase of the arterial wave reflections leading to an increased second systolic peak and enhanced development of systolic hypertension.[3] The renin–angiotensin–aldosterone system plays a key role in sodium handling, vascular remodeling and inflammation.[4] Figure 1 illustrates the pathogenesis of systolic hypertension in the elderly and the clinical consequences. Aging is associated with increased arterial stiffness due to endothelial dysfunction, vascular remodeling and a change in the extracellular matrix. There is a decrease in elastin fibers and an increase in collagen fibers in the arterial wall. Increased arterial stiffness and arterial wave reflections will lead to a rise in systolic BP and, consequently, to the development of isolated systolic hypertension. The increased arterial load due to increased systolic BP and arterial wave reflections will promote left ventricular hypertrophy and consequently heart failure, atherosclerotic disease resulting in coronary heart disease, cerebrovascular disease and aortic aneurysms.