Pulse Pressure and Vascular Disease
September 1, 2000 3 minutes read
Pulse Pressure and Vascular Disease
Abstract & Commentary
Synopsis:Regression of carotid artery wall hypertrophy by antihypertensive therapy was related to reductions in local PP rather than reductions in mean blood pressure.
Source: Boutouyrie P. Circulation 2000;101:2601-2606.
Data from the framingham heart study showed that in individuals older than 50 years of age, increases in pulse pressure (systolic minus diastolic pressure) were associated with the highest risk for coronary heart disease as compared to systolic or diastolic blood pressure.1 However, this study could not determine if pulse pressure (PP) had a causal relationship to cardiac events or was just a marker for underlying vascular disease. Thus, the study of Boutouyrie et al is of interest. They hypothesized that local PP may be important in the development of medial hypertrophy in large elastic vessels vs. small muscular vessels since the former can expand more and the resultant increase in wall stress may cause medial hypertrophy. To test this hypothesis, they studied 98 essential hypertension patients randomized to either the beta blocker celiprolol or enalapril. Both drugs could be titrated and hydrochlorothiazide could be added to achieve blood pressure control. A tonometric device was used to measure common carotid and radial artery PP and Duplex echo was used to measure intimal-medial thickness (IMT) of the arteries. After nine months of therapy, both drugs significantly reduced mean blood pressure, PP, and IMT at both arterial sites. Celiprolol also reduced heart rate—otherwise there were no differences between the effects of the two drugs. Multivariate analysis showed that the change in carotid IMT correlated best with reductions in carotid PP, but this was not the case with the radial artery. Boutouyrie et al conclude that regression of carotid artery wall hypertrophy by antihypertensive therapy was related to reductions in local PP rather than reductions in mean blood pressure.
Comment by Michael H. Crawford, MD
These results suggest that PP may have a causal role in arterial wall thickening in large elastic arteries such as the common carotid. Unfortunately, Duplex echo imaging cannot distinguish between medial hypertrophy from increased pressure and increased intimal layer due to atherosclerosis. However, Boutouyrie et al claim that the common carotid artery is usually spared atherosclerosis as compared to the bifurcation and the internal carotid where it is common. Consequently, they reasoned that the reductions in IMT they observed were due to regression of medial hypertrophy. This makes sense, since one wouldn’t expect significant regression of atherosclerosis in nine months. This study suggests that PP can cause changes in DNA synthesis and smooth muscle growth, so it is not just a marker of vascular disease. Whether it is causally related to atherosclerosis is still unclear.
Despite the decrease in carotid IMT, wall stress was reduced because carotid internal diameter decreased more than expected based upon the reductions in mean blood pressure. Also, the reductions in carotid internal diameter were closely correlated with reductions in PP. Thus, PP may play an important role in other conditions such as large artery rupture in the Marfan syndrome where the diseased media cannot hypertrophy adequately. In such conditions, reducing PP may be more important than reducing mean blood pressure.
Since the beta blocker and the angiotensin-converting enzyme ACE inhibitor performed equally well in reducing PP and IMT, it is unclear if certain antihypertensive agents are better than others for reducing PP. Carotid artery internal diameter decreased more on beta blocker vs. ACE inhibitor therapy, but radial artery mass decreased more with ACE inhibitor. These results suggest that these drugs have other effects independent of their blood pressure lowering capabilities. It is known that ACE inhibitors can reduce the smooth muscle growth stimulating effects of angiotensin II, but the beta blockers role in this regard is still controversial.
PP can decrease because systolic pressure decreases or diastolic pressure increases. Thus, there has been considerable interest in which antihypertensives are most effective for reducing systolic pressure, since this would reduce PP unless there were equal reductions in diastolic pressures. Increasing diastolic pressure has not been considered a therapeutic option, because in studies where it alone is considered, it is associated with a higher incidence of cardiovascular disease. The Hypertension Optimal Treatment Study showed that systolic pressures below 145 mm Hg were associated with the lowest risk of events with no significant J-curve (increasing risk of events at lower pressures).2
References
1. Franklin SS, et al. Circulation 1999;100:354-360.
2. Hansson L. Lancet 1998;351:1755-1762.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content