结论

　　综上所述，是否意味着所有高血压患者都应将目标血压降至<120/80 mm Hg？就卒中预防而言，证据相对确凿，卒中高危患者可考虑选择较低的降压目标值。冠脉疾病高危患者（包括糖尿病患者）或冠脉疾病患者，可能也是积极强化降压治疗的适宜人群。其他患者可继续选用既往<140/90 mm Hg的降压目标值。

　　There is abundant evidence that lowering an elevated blood pressure (BP) reduces the risk of serious cardiovascular events. Most guidelines suggest lowering BP to <140/90 mm Hg. In many ways， this cut-off value is very arbitrary. Important questions are: Should we go lower than that? Are there benefits in lowering the BP to levels lower than those currently recommended? What are the risks?

　　The evidence for lower BP targets is epidemiologic studies， clinical trials with surrogate outcome measures， and clinical trials with hard outcome measures.

　　Epidemiologic Studies:

　　Two studies have shown that the lower the BP the less is the cumulative incidence of CV events. The Framingham research group [1] reported that even “pre-hypertension” levels of BP (120-139/80-89 mm Hg) had a higher CV event rate than “normal” BP (<120/<80 mm Hg) (Fig 1.). In a very large epidemiology study， Lewington et al. [2] showed that ischemic heart disease (and stroke) mortality declined with BPs right down to about 116/70 mm Hg. (Fig. 2)

　　Clinical Trials with Surrogate Outcome Measures:

　　As part of the CAMELOT study 274 patients had intravascular ultrasound measurement [3] of the volume of their coronary atheroma at the start of the study and again after 2 years on either enalapril or amlodipine for their hypertension. Those with a mean BP in the hypertension range (>14/90 mm Hg) had an increase in atheroma volume， those with a mean BP in the “pre-hypertension” range (120-129/80-89 mm Hg)  had no change in atheroma volume， while those with a BP lower than 120/80 showed significant regression of atheroma volume. (Fig. 3)

　　The question is then: Why not lower BP to <120/<80 mm Hg? Is there any potential harm in doing so? The key to answering this question lies in an understanding of the autoregulation of blood flow through vital organs， particularly the myocardium.

　　Organ blood flow is proportional to perfusion pressure and inversely proportional to resistance (FαP/R). (Fig. 4).  In the case of the myocardium P is the diastolic blood pressure (DBP) because nearly all of myocardial perfusion occurs during diastole.  If P falls (as would happen with lower and lower BPs)， then autoregulatory mechanisms are activated to dilate resistance vessels， thereby decreasing  R， so that flow remains constant. Obviously there is a limit to the degree to which vessels can dilate， so that further lowering beyond that limit of P results in a fall in F. It could therefore be predicted that， at DBPs below the lower limit of coronary autoregulaton， there will be myocardial ischemia or even infarction. The problem is that we do not know what that DBP value is in humans， who may also have coronary artery disease (which may decrease myocardial oxygen supply) or hypertension with left ventricular hypertrophy (which will increase myocardial oxygen demand). Therefore， lower BP targets needed to be tested by a prospective clinical trial.