When SBP is elevated, both LV output impedance and intramyocardial wall tension increase, resulting in increased myocardial oxygen demand. The wide pulse pressure and systolic hypertension in older individuals are usually attributable to inappropriately high aortic impedance, which results from decreased aortic diameter or increased effective stiffness caused by aortic wall thickening and changes in wall composition. Aging is associ- ated with thinning and fragmentation of vascular elastin and increased collagen deposition, a degenerative process that causes increased arterial stiffness (reduction of elasticity) with an associated elevation in SBP and widening of the pulse Rosendorff et al Treatment of Hypertension in Patients With CAD 1379 Increased arterial stiffness elevates SBP by increasing pulse-wave velocity and altering wave reflection from the With each ejection of blood from the LV, a pressure (pulse) wave is generated and travels from the heart to the periphery at a pulse-wave velocity that depends on the elastic properties of the conduit arteries. The pulse wave is reflected at any point of discontinuity in the arterial tree and returns to the aorta and LV. The elastic properties and length of the conduit arteries determine the timing of the In younger people, the pulse-wave velocity is sufficiently slow ( 5 m/s) that the reflected wave reaches the aortic valve after closure, leading to a higher DBP and enhancing coronary perfusion by providing a boosting effect. In older people, particularly those who are hyper- tensive, pulse-wave velocity is greatly increased ( 20 m/s) because of central arterial stiffening. Thus, the reflective wave reaches the aortic valve before closure, leading to the higher SBP, pulse pressure, and afterload and a lower DBP. The increase in SBP increases cardiac metabolic require- ments and predisposes to the development of LV hypertro- phy and HF. 