Showing papers by "Luc M. Van Bortel published in 2001"

Non-invasive assessment of local arterial pulse pressure: comparison of applanation tonometry and echo-tracking.

Abstract: ObjectivesPulse pressure is not constant throughout the arterial tree. Use of pulse pressure at one arterial site as surrogate for pulse pressure at another arterial site may be erroneous. The present study compares three non-invasive techniques to measure local pulse pressure: (i) internally calibr

Pulse Pressure, Arterial Stiffness, and Drug Treatment of Hypertension

Abstract: Epidemiological studies in the past decade have stressed the importance of pulse pressure as an independent risk factor for cardiovascular morbidity and mortality. We briefly review the epidemiological evidence and discuss in more detail the pathophysiological basis for this observation and the therapeutic consequences. We focus on the vascular determinants of increased pulse pressure. Both longitudinal and cross-sectional components of the vascular system contribute to the shape of the arterial pressure wave and, thereby, to pulse pressure. The primary longitudinal component is the architecture of the arterial tree, which determines the major reflection sites for the pressure wave. The cross-sectional architecture of the vascular system consists of a geometric (diameter) and a structural (composition vessel wall) component. Both diameter and composition of the vessel wall vary greatly when going from central to more peripheral arteries. We review the implications for the functional properties of various arterial segments. Finally, we discuss the therapeutic consequences of targeting pulse pressure rather than mean blood pressure with various drug classes. Among the antihypertensive agents, nitrates, NO donors, and drugs that interfere with the renin-angiotensin-aldosterone system may offer useful tools to lower pulse pressure, in addition to mean blood pressure. Future developments may include non-antihypertensive agents that target collagen or other components of the arterial wall matrix. However, large-scale clinical trials will have to confirm the therapeutic value of these agents in the treatment of increased pulse pressure and arterial stiffness.

Carotid and Femoral Artery Stiffness in Relation to Three Candidate Genes in a White Population

Abstract: Different genetic polymorphisms influence cardiovascular disease. We recently discovered a relationship between the intima-media thickness of the muscular femoral artery, but not the elastic common carotid artery, and the combined ACE ( ACE, I/D ), α-adducin ( Gly460Trp ),and aldosterone synthase ( AS , C−344T ) gene polymorphisms. To investigate the relationship between these polymorphisms and functional properties of the carotid artery and femoral artery, a sample of 756 subjects enrolled in a population study were genotyped for the presence of the ACE D, α-adducin 460Trp , and aldosterone synthase −344T alleles. Vessel wall properties were assessed using a vessel wall movement detector system in combination with applanation tonometry. Statistical analysis allowed for confounders and interaction among genes. Cross-sectional compliance of the common carotid artery was negatively associated with the ACE D allele. ACE II versus ACE DD homozygotes differed, expressed as a percentage of the population mean (7.0%; 95% confidence interval [CI], 1.6% to 12.4%; P =0.02). In multigene analysis, ACE DD subjects also deviated significantly from the population mean for the distensibility coefficient of the common carotid artery when carrying the AS/T allele (−5.5%; 95% CI, −9.3% to −1.7%; P ACE DD subjects, when homozygote for α-adducin Gly460 , had a lower femoral cross-sectional compliance (−10.4%; 95% CI, −1.9% to −18.9%; P P ACE I/D polymorphism. Cross-sectional compliance and distensibility coefficients are influenced by the ACE I/D genotype, but this influence depends on the vascular territory and genetic background.

Does B-mode common carotid artery intima-media thickness differ from M-model?

Abstract: An increased intima-media thickness of the common carotid artery is thought to be an early sign of atherosclerosis. Both B- and M-mode ultrasonographic techniques are used to measure the intima-media thickness of the common carotid artery (B-IMT and M-IMT, respectively). The present study compares intima-media thickness of the common carotid artery measured with the two techniques. Intima-media thickness was measured in a random population sample of 250 subjects. Comparison was made by mean and 95% confidence intervals of differences between B-IMT and M-IMT, by linear regression analysis, and by intraclass and concordance correlation coefficients. M-IMT was 0.011 0.091 mm (95% confidence intervals: 0.167 to 0.188 mm) larger than B-IMT, which was 0.661 0.136 mm (range: 0.380 to 1.120 mm). Intraclass and concordance correlation coefficients were 0.802 and 0.801, respectively. In conclusion, acceptable agreement exists between the two methods and there was no important systematic difference between B-IMT and M-IMT. (E-mail: luc.vanbortel@rug.ac.be) © 2001 World Federation for Ultrasound in Medicine & Biology.

Arterial structure and function and blockade of the renin-angiotensin system in hypertension

Abstract: Cardiovascular disease is a major cause of morbidity and mortality in patients with hypertension. Epidemiological and clinical studies have shown that damage of large conduit arteries is a major contributory factor [1]. Macrovascular disease develops slowly in hypertensive patients and is responsible for the high incidence of congestive heart failure, left ventricular hypertrophy (LVH), ischemic heart disease, sudden death, cerebrovascular accidents and peripheral artery diseases. Although the most frequent underlying cause of these complications is occlusive lesions due to atheromatous plaques, this aspect represents only one form of the structural response to metabolic and hemodynamic alterations which interfere with the hypertensive process. The spectrum of arterial alterations in hypertension is broader, including large artery hypertrophy associated with hemodynamic burden [2]. The consequences of these alterations may be different from those attributed to the presence of atherosclerotic plaques alone. In this chapter, the basic concepts on changes in arterial structure and function in hypertension are reviewed and their alterations in response to the blockade of the renin-angiotensin system are discussed in experimental and clinical situations.