The manuscript by Canepa and associates in this issue of the Journal, “Relationship Between Inter-Arm Difference in Systolic Blood Pressure and Arterial Stiffness in Community-Dwelling Old Adults,” is a prime example of how clinical investigators may provide valuable insights into physiology and pathophysiology by keen observation and use of simple techniques. As these investigators, and other astute clinicians, already knew, a significant inter-arm difference in systolic blood pressure (BP) exists for a sizable portion of the population, ranging from 5 mm Hg to 20 mm Hg or even higher. Moreover, evidence has been steadily accumulating that a significant difference in inter-arm systolic BP is associated with increased cardiovascular morbidity and mortality. However, the underlying basis for this relatively common inter-arm difference in systolic BP has not been at all clear.
Explanations for the inter-arm difference between the systolic BP recorded from the two arms have included both anatomical and hemodynamic reasons. Pathological causes of inter-arm BP differences include atherosclerosis, vasculitis, fibromuscular hyperplasia, connective tissue disorders, radiation arteritis, thoracic outlet compression, dissecting aortic aneurysm, and congenital abnormalities. However, in the absence of anatomic obstruction, it has been speculated that the inter-arm differences in systolic BP were related to some intrinsic property of the cardiovascular system.
Using carotid-femoral pulse wave velocity (cf-PWV) as a measure of arterial stiffness, Canepa and colleagues demonstrated that cf-PWV was higher in individuals with inter-arm BP ≥10 mm Hg and therefore concluded that significant inter-arm difference in systolic BP is associated with increased arterial stiffness. It is not surprising that female sex and Caucasian race also correlated with increased arterial stiffness in their population.
Alterations in arterial stiffness can explain the inter-arm difference in systolic BP. When arterial flow is primarily under the control of resistance vessels, as resistance is increased there is an increase in mean pressure with an equal incremental increase in systolic and diastolic BP. Nevertheless, the pulse wave form undergoes amplification as it travels from the heart to the periphery, accounting for the increase in systolic pressure in the arms and legs compared with the aorta. However, when there is increased arterial stiffness, ie, a loss of compliance, pressure oscillations increase resulting in a disproportionate increase in systolic BP and little change in diastolic BP. Because the elastic properties of conduit arteries vary along the arterial tree, it is easy to see how pressure oscillations would vary between the arms resulting in different recorded systolic BP.
Increased arterial stiffness is associated with an increase in cardiovascular morbidity and mortality. Canepa and colleagues utilized cf-PWV as the “gold standard” means of determining systemic compliance. Other means of assessment include regional pulse wave velocity and augmentation index. The latter is a quantification of reflected arterial waves resulting from areas of impedance mismatch, eg, arterial branches.
Kaaess and colleagues reported that measures of aortic stiffness correlated with progression of increased BP and incident hypertension. In particular, these findings are related to the development of systolic hypertension. Kaess and colleagues did not discuss the various hypertension hemodynamic phenotypes, ie, diastolic hypertension, isolated systolic hypertension, or mixed hypertension (diastolic hypertension with an increased pulse pressure). However, the increase in pulse wave magnitude produced by increased aortic stiffness imposes an increased burden on small resistance vessels with resultant increase in myogenic activity and remodeling and an increase in peripheral vascular resistance. Also, the baroceptor reflex responds to strain, not pressure, and therefore increased arterial stiffness will result in baroceptor dysfunction. Thus, a pathway for the development of diastolic hypertension caused by increased arterial stiffness exists.