High blood pressure: An obscuring misnomer?

Abstract

High blood pressure (BP) has been identified as a major risk factor for cardiovascular complications. Although two-way association between BP and hypertensive complications makes hypertension a near-ideal biomarker, BP as "the cause" for the complications of HT per se still needs more evidence. Another entirely possible hemodynamic candidate for causing hypertensive cardiovascular adverse events can be flow or its iterations, which might have escaped the attention because of its perfect correlation with pressure and harder technical measurement. In this article, we analyze the evidence in hand to compare flow- and pressure-related phenomena to delineate which of the two is the dominant mediator of complications related to hypertension and should be the target for therapy. A "flow-" rather than a "pressure-" based factor, as the causative or major driving mediator of common hypertensive complications, may change our understanding of hypertension pathophysiology.

Figure 1

Since autoregulation maintains the flow in a certain pressure range, but not other flow-related parameters (e.g., flow velocity, flow profile, and shear forces), flow, and wall stress may be mismatched after a critical threshold has exceeded (left panel). After a certain amount of decrease in luminal cross-sectional area (critical limit separates A from B), which may require a certain amount of structural change, faster flowing blood may create a tendency to turbulence and low shear stress at certain vascular segments, such as bifurcations, bends, and kinks (right panel, B). After protective changes to avoid hyperperfusion induced structural changes, flow-wall stress mismatch sustains in face of normalized or even reduced flow