AbstractPurpose of review
This review is intended to provide the background for a new comprehensive hemodynamic view of the syndrome of systolic or wide pulse pressure hypertension and its hallmark abnormality: increased central arterial stiffness.Recent findings
Studies of the pathogenesis of systolic hypertension have lagged. This review describes the systolic hypertension syndrome as a complex set of hemodynamic maladaptations that include stiff central arteries, normal peripheral arteries with variable pressure amplification characteristics, arteriolar constriction, microcirculatory rarefaction, metabolic abnormalities, cardiac hypertrophy, and increased blood pressure variability. Because the structural and functional properties of arteries of different caliber are highly heterogeneous and vary with aging and disease, simple measurements such as standard brachial artery blood pressure, brachial pulse pressure, or mean arterial pressure are inadequate to provide meaningful insight into the pathophysiology of the syndrome. Additional parameters developed to describe changes in arterial mechanics (arterial compliance or stiffness, elastic modulus, impedance, pulse wave velocity, augmentation index, and pulse pressure amplification) are intrinsically limited and are directly or indirectly pressure-dependent. Quantitation of central arterial stiffness provides a modest increment in cardiovascular and renal risk stratification.Summary
Better clinical management of systolic hypertension depends on greater insight into the syndrome as a whole, more critical analysis of existing techniques, and the development of new approaches.