Carotid and brachial blood pressure–measurements in hypertensive subjects

Physiologically, central pulse pressure is lower than peripheralpulse pressure for the same mean arterial pressure. Thissituation protects the heart from an increase in post load asa consequence of mechanisms related to wave reflectionsand/or arterial stiffness. Nowadays, non-invasive measurementsenable to evaluate this physiological particularity.One of the methods enabling to minor measurement errorsis to calculate the difference between brachial and carotidpulse pressure, so called amplification (mmHg). When thisprocedure is used, errors are limited to those of brachialblood pressure measurements. Amplification is reducedwith age, but augmented by tachycardia, mostly in women.Amplification is poorly modified by drug treatment, exceptthrough drug-induced changes in heart rate. Longitudinalstudies are needed to evaluate the role of amplification incardiovascular epidemiology and therapeutics.

Correlation between arterial mechanical properties, vascular biomaterial and tissue engineering.

This review presents some of the recent technological developments in biomaterials used for the construction of synthetic cardiovascular vessels that are capable of simulating specific biological responses. However, with respect to the problems of stiffness, a major hypertensive risk factor, it is necessary to underline the important role of mechanical properties, such as vessel strength and composition, in vascular reconstructive surgery. Biomaterials occupy a central place in many cardiovascular disease treatments and they depend on the chemical nature of the polymers, on the biotechnology used, and also on cellular and gene therapy. Several methodologies using animal or human cells have emerged for constructing blood vessel replacements. Tissue-engineered blood vessel (TEBV) substitutes begin to motivate much work and have contributed to the restoration, maintenance, and/or improvement in tissue and organ function. Each methodology has it benefits, its promises, and holds many challenges in future biological, biomaterial and clinical research.

Carotid arterial stiffness, elastic fibre network and vasoreactivity in semicarbazide-sensitive amine-oxidase null mouse.

OBJECTIVE: We examined the arterial phenotype of semicarbazide-sensitive amine-oxidase null mouse (SSAO -/-) using various techniques including high resolution echotracking. METHODS AND RESULTS: SSAO -/- mice showed no change in arterial pressure under anesthesia. The in vivo arterial diameter, only measured in the carotid artery (CA), was higher in SSAO -/- than in SSAO +/+ animals. Elastic modulus-wall stress curves and CA rupture pressure were similar between SSAO -/- and +/+ mice, indicating no change in arterial wall stiffness or mechanical strength. There was no significant difference in insoluble elastin, total collagen content and elastic lamellar morphology between the two genotypes. No alteration in vascular reactivity was observed in aortic rings and mesenteric arteries from SSAO -/- mice. Aortic lysyl oxidase (LO) activity remained unaltered, indicating that SSAO invalidation is not accompanied by a compensatory increase in LO activity. CONCLUSION: This is the first functional study of arteries lacking SSAO. Our results indicate that SSAO -/- mice present an increased arterial diameter associated with normal arterial mechanical properties, suggesting that SSAO deficiency might contribute to arterial wall remodeling. However, these results argue against the hypothesis that SSAO intervenes in elastic fibre organization, elastin cross-linking processes and vasoreactivity.