Gillian Gordon Perue, MBBS, DM
In the 65 years since the start of the Framingham Heart Study, our knowledge of atherosclerosis and its risk factors as expanded exponentially. We now understand that stroke is but one of the final clinical outcomes of a prolonged sub-clinical course of atherosclerosis and “hardening of the arteries”.
In a recent article from Stroke, Stein and colleagues present results from MESA; a large prospective Multi-Ethnic Study on Atherosclerosis. They evaluate the prevalence, cause and progression of subclinical cerebrovascular disease in a population based cohort of 6,814 men and women aged 45-84. They found that age and the use of antihypertensive medications at baseline, independently predicted arterial stiffness over time. Adding antihypertensive medications improved distensibility coefficient (DC) and the Young’s elastic modulus (YEM) of the right common carotid artery which was measured at baseline and follow up exam. For all ethnic groups, the rate of progression of YEM and DC showed no significant difference. It is noteworthy, that whites had a higher DC (better) at baseline than other ethnic groups and blacks had a higher YEM (worse) at baseline than other ethnic groups.
This observation is an important one, especially as it relates to the well known race-ethnic disparities in the effects of hypertension and stroke. The implication is that hypertensive effects on the vessels begin well before the age of 45 in our African American population. Encouraging us as medical Practitioners to screen this group at an earlier age for hypertension and start treatment earlier.
Beyond the effect of aging on the carotid artery, this paper provides insight into the biology of how our vessels respond to hypertension. One can see how YEM and DC can readily fit in a clinical module for management of our hypertensive patients. Imagine, your patient presenting to clinic; rather than making a decision on one blood pressure reading in your office we can measure the DC and YEM at baseline and follow its improvement over time. We can follow the response in the DC to the start of antihypertensive and anticipate the worsening of the DC if these agents are stopped or our patient has poor compliance. If these tools become clinically available (rather than as a research tool) YEM and DC could become to hypertension what HbA1c is to the management of diabetes.