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Representativeness of peripheral blood pressure values: the pulsatile component of blood pressure in hypertension
1Department of Internal Medicine 1, Hôpital Broussais, Paris, France.
Whereas mean arterial pressure remains practically unmodified along the arterial tree, pulse pressure increases markedly from central to peripheral arteries, principally due to an increase in systolic blood pressure and a small lowering of diastolic blood pressure. This hemodynamic pattern, due to the progressive increase in arterial stiffness and to the summation between the incident and the backward pressure wave along the arterial tree, has several implications, in that: i) the pulse pressure amplification increases with the effective length of the arterial tree (and therefore with the body height of subjects), but decreases with aging, due to a significant age-induced increase in aortic wave reflections and pulse pressure, ii) the magnitude of the pulse pressure amplification is strongly influenced by the status of the autonomic nervous system, so that carotid pulse pressure decreases more than brachial pulse pressure following sympathetic stimulation using lower body negative pressure, and iii) the pulse pressure amplification may be restored following administration of pharmacological agents as converting enzyme inhibitors and calcium entry-blockers but not dihydralazine. These particularities of pressure wave transmission may have fundamental consequences for: the diagnosis of hypertension, whether in humans or in animal; the evaluation of cardiac afterload and the effectiveness of antihypertensive agents; and finally, the interpretation of cardiovascular epidemiology. Indeed increased brachial pulse pressure is known to be an independent cardiovascular risk factor, particularly for myocardial infarction, but not for cerebrovascular complications.
Whereas mean arterial pressure remains practically unmodified along the arterial tree, pulse pressure increases markedly from central to peripheral arteries, principally due to an increase in systolic blood pressure and a small lowering of diastolic blood pressure. This hemodynamic pattern, due to the progressive increase in arterial stiffness and to the summation between the incident and the backward pressure wave along the arterial tree, has several implications, in that: i) the pulse pressure amplification increases with the effective length of the arterial tree (and therefore with the body height of subjects), but decreases with aging, due to a significant age-induced increase in aortic wave reflections and pulse pressure, ii) the magnitude of the pulse pressure amplification is strongly influenced by the status of the autonomic nervous system, so that carotid pulse pressure decreases more than brachial pulse pressure following sympathetic stimulation using lower body negative pressure, and iii) the pulse pressure amplification may be restored following administration of pharmacological agents as converting enzyme inhibitors and calcium entry-blockers but not dihydralazine. These particularities of pressure wave transmission may have fundamental consequences for: the diagnosis of hypertension, whether in humans or in animal; the evaluation of cardiac afterload and the effectiveness of antihypertensive agents; and finally, the interpretation of cardiovascular epidemiology. Indeed increased brachial pulse pressure is known to be an independent cardiovascular risk factor, particularly for myocardial infarction, but not for cerebrovascular complications.