1 – The totality of the blood pressure curve
Blood pressure is a powerful cardiovascular risk factor that acts on the arterial wall and is responsible in part for various cardiovascular events, such as heart failure, ischemic heart disease and cerebrovascular accidents (1).
In clinical practice, 2 specific and arbitrary points of the blood pressure curve, peak systolic blood pressure and end-diastolic blood pressure, are used to define the cardiovascular risk factor.
Because the goal of drug treatment in hypertension is to prevent cardiovascular complications, it appears likely that the totality of the blood pressure curve, not simply peak systolic blood pressure and end-diastolic blood pressure, should be considered to act mechanically on the arterial wall and therefore should be used to propose an adequate definition of high blood pressure (2).
2 - Arterial Stiffness
Structural and functional properties of the arterial wall are altered in hypertension even at the early stages of the disease (3). Arterial stiffness is the most important cause of increasing systolic and pulse pressure, and for increasing pulse pressure with aging.
Pulse pressure alone is inadequate to assess arterial stiffness accurately. Problems include the ‘normal’ amplification of the pressure wave as it travels from the aorta to the periphery. The arterial pressure wave has two principal components—the wave generated by the heart, which travels away from the heart, and the reflected wave, which returns to the heart from peripheral sites, predominantly in the lower part of the body.
Morbidity and mortality associated with hypertension are primarily related to arterial damage and may affect one or several organs. Considering the potential implications of arterial assessment in the prevention of cardiovascular disease, evaluation of the arterial effects of antihypertensive treatment is recommended (4).
Abnormalities of the arterial vasculature that precede cardiovascular morbid events are likely to occur in a temporal sequence (5). The initial abnormalities appear to be functional, in large part related to endothelial dysfunction associated with decreased bioavailability of nitric oxide (6). A decrease in constitutive release of nitric oxide, which maintains low small artery tone, may be the initial abnormality, but it is soon accompanied by a decrease in stimulated release of endothelial vasodilators, as manifested by a reduction in flow mediated dilation of conduit arteries. These functional abnormalities of the vasculature precede and are mechanistic precursors of the structural alterations that are responsible for thickening of the conduit artery wall, increases in pulse pressure, and atherosclerotic plaque development. These structural changes may also result in additional functional abnormalities.
Noninvasive measurement of arterial stiffness entails measurement of surrogate parameters that are intrinsically associated with stiffness. This involves three main methodologies:
- Pulse transit time of the arterial wave form between two points along the arterial tree (e.g. carotid-femoral pulse wave velocity);
- Analysis of the arterial pressure pulse and its wave contour; and
- Direct stiffness estimation using measurements of vessel diameter and distending pressure (7).
3 - The future
The hope for the future is that a practical noninvasive screening technique will be used to assess the function and structure of the arterial wall in subjects with hypertension or even subjects at risk of developing hypertension. The effect of antihypertensive therapy on the functional and structural vessel wall abnormality can then be monitored during therapeutic intervention (8). Thus, a drug regimen that does not favorably affect the arterial structure or function in a given patient would be replaced by another drug regimen that might be more effective. The correction of the arterial wall abnormality could then serve as a guide to therapeutic efficacy rather than the absolute level of blood pressure, which now serves as the surrogate marker. How the blood pressure changes and the arterial wall changes might relate needs to be intensively studied.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.