Article
Is it the blood pressure or the blood vessel?

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Abstract

The physiologic link between vascular health and arterial pressure makes it difficult to separate the adverse effects of pressure and vascular functional and structural alterations in determining the adverse complications of hypertension. Since endothelial dysfunction and nitric oxide deficiency are characteristic features of hypertension and of other risk factors for morbid events, it is proposed that blood pressure elevation may be viewed in part as a complication of functional and structural changes in the microcirculation, and that structural changes in the conduit arteries leading to morbid events may be viewed as a complication of both pressure elevation and endothelial dysfunction. Improvement in endothelial dysfunction will relax the microcirculation and lower blood pressure. Thus pressure elevation and its lowering in resposne to treatment serves as a useful guide to the vascular abnormality and its amelioration, but vascular structural abnormalities are the proximate cause of vascular events and therapy aimed at the vasculature rather than the pressure may serve as a more sensitive and specific guide to treatment.

Section snippets

Risk Factors and Blood Pressure

Hypertension, as traditionally defined, is often accompanied by other risk factors for cardiovascular disease.10 Indeed, the presence of these risk factors, including elevated blood cholesterol, smoking, diabetes, and obesity, greatly increases the risk for hypertension-related morbid events.11 The prevalence of these risk factors in hypertensive patients often generates concerns about co-inheritance or common environmental factors. But one physiological mechanism seems clear. These risk

Mechanisms of Drug Effects

Vasodilation usually is accompanied by a reduction in diastolic and mean arterial pressure. Dilation of the microvasculature that controls vascular resistance may be a direct smooth muscle effect of a drug, may be a consequence of interference with an endogenous vasoconstrictor mechanism, or may result from local generation of a vasodilator such as nitric oxide. Although the initial fall in blood pressure induced by any of these mechanisms may be comparable, the long-term efficacy of such drugs

Cardiovascular Morbid Events

Hypertension contributes to a wide range of cardiovascular morbidity, including angina pectoris, myocardial infarction, stroke, heart failure, renal failure, peripheral vascular disease, dementia, and sudden death. Most of these events are a consequence of progressive structural change in the vasculature sometimes interrupted by a thrombotic event. These structural changes are often classified as atherosclerosis, but the mechanisms of these adverse events vary. Some are predominantly

Relationship Between Blood Pressure and Cardiovascular Disease

The apparent linear relationship between casual blood pressure in a population and risk of a cardiovascular morbid event has led some to the simple conclusion that blood pressure is the lethal risk factor.33 Although pressure itself exerts effects on the artery wall and the left ventricle that may contribute to morbidity, it is difficult to attribute to pressure itself the vascular events that occur in so-called pre-hypertensives with casual pressures below 130/85 mm Hg. Indeed, no guideline is

Effect of Drugs on Blood Pressure and Cardiovascular Events

There is now substantial trial evidence that antihypertensive drugs reduce the incidence of morbid events and prolong life in hypertensive patients. In the early trials that were placebo-controlled, baseline blood pressures were usually >160/100 mm Hg, likely indicative of co-existent structural abnormalities of the vasculature, and other risk factors were not treated.35, 36, 37, 38 The magnitude of therapeutic benefit in those populations cannot simply be extrapolated to contemporary cohorts

Specific Drug Effects

As noted in the preceding text, drugs exert their antihypertensive effects by a variety of mechanisms. When pressure is markedly elevated, the benefit of pressure reduction itself may overwhelm mechanistic differences in the prevention from cardiovascular disease events. When pressures are only modestly increased or within the so-called normal range, the mechanistic difference may become particularly important. Therapeutic benefit on the artery wall will, however, produce long-term reduction of

Prevention of Hypertension

The emphasis in cardiovascular health care in the next generation should shift from end-stage disease management to early detection and treatment to slow progression. Prevention of hypertension has, therefore, become a clinical goal.69 But the concept of prevention of hypertension suffers from the same semantic deficiency as the concept of pre-hypertension.34 Some, but not all, individuals with blood pressure <140/90 mm Hg harbor endothelial dysfunction likely to progress to structural

Clinical Implications

Resting blood pressure, despite its variability, should continue to serve as a useful and simple screening tool to stratify patients into risk categories. It must be recognized, however, that these risk categories based on blood pressure alone do not necessarily mandate therapeutic decisions for individual patients. Identifying vascular functional and structural abnormalities may in the future determine the need or lack of need for therapeutic interventions. One approach to this effort is

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