BP Components and Risk

The information conveyed by PP is fundamentally different from that conveyed by MAP, the product of cardiac output and systemic vascular resistance (SVR). While MAP is closely related to SVR, PP is determined principally by flow-impedance relations in large arteries, often called 'ventricular-vascular interactions'. When the aorta cannot optimally accommodate the degree of pulsatile flow, either due to an inappropriately small aortic diameter [19] or increased aortic wall stiffness [7, 8, 20], PP and systolic BP inevitably increase (fig. 2). Increased SVR can further exacerbate increased systolic BP (fig. 2) because PP and MAP have additive effects on systolic BP. In contrast, these two physiologically and anatomically distinct components of BP have opposing effects on diastolic BP. An increase in MAP is associated with higher DBP, while an increase in PP is generally associated with a lower DBP.

To make matters more confusing, higher MAP and higher PP are each independently associated with increased cardiovascular disease risk. The contrasting effects of MAP and PP on diastolic DBP contribute to the frequently described and often misunderstood non-linear (U- or J-shaped) relation between diastolic BP and cardiovascular events. For example, low diastolic BP and wide PP are associated with increased risk of mortality [21] yet high diastolic BP independently increases risk [22]. The problem is in the confounding caused by the use of diastolic BP as a risk surrogate. The situation becomes much clearer if risk is attributed to either elevated MAP or elevated PP. Hypertension as a clinical condition is thus intrinsically heterogeneous, and is perhaps best considered as an admixture of disordered large artery function (generating systolic hypertension) and disordered microcirculatory function (generating diastolic hypertension). Understanding which form of hypertension to treat and how to improve therapy begins with a discussion of normal and abnormal vascular function.

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