Conduit arteries become stiffer with age due to alterations in their morphology and the composition of the their major structural proteins, elastin and collagen. The elastic lamellae undergo fragmentation and thinning, leading to ectasia and a gradual transfer of mechanical load to collagen, which is 100-1000 times stiffer than elastin. Possible causes of this fragmentation are mechanical (fatigue failure) or enzymatic (driven by matrix metallo proteinases (MMP) activity), both of which may have genetic or environmental origins (fetal programming). Furthermore, the remaining elastin itself becomes stiffer, owing to calcification and the formation of cross-links due to advanced glycation end-products (AGEs), a process that affects collagen even more strongly. These changes are accelerated in the presence of disease such as hypertension, diabetes and uraemia and may be exacerbated locally by atherosclerosis. Raised MMP activity, calcification and impaired endothelial function are also associated with a high level of plasma homocysteine, which itself increases with age. Impaired endothelial function leads to increased resting vascular smooth muscle tone and further increases in vascular stiffness and mean and/or pulse pressure. The effect of increased stiffness, whatever its underlying causes, is to reduce the reservoir/buffering function of the conduit arteries near the heart and to increase pulse wave velocity, both of which increase systolic and pulse pressure. These determine the peak load on the heart and the vascular system as a whole, the breakdown of which, like that of any machine, depends more on the maximum loads they must bear than on their average. Reversing or stabilising the increased arterial stiffness associated with age and disease by targeting any or all of its causes provides a number of promising new approaches to the treatment of systolic hypertension and its sequelae, the main causes of mortality and morbidity in the developed world.

Objectives-To examine the relation between disproportionate fetal growth and adult blood pressure and to investigate whether arterial compliance in adult life is related to early development. Design-A follow up study of a group of men and women whose birth weights and other measurements of body size had been recorded at birth. Setting-Home and outpatient study. Subjects-337 men and women born in the Jessop Hospital, Sheffield, between 1939 and 1940. Main outcome-Adult systolic and diastolic blood pressures and arterial compliance as measured by pulse wave velocity in two arterial segments. Results-Both systolic and diastolic blood pressures were higher in people whose birth weight was low, who were short or who had small abdominal or head circumferences at birth. Systolic blood pressure decreased by 2f7 mm Hg (95% CI 0f8 to 4.6) for each pound (454 g) gain in birth weight and by 3'4 mm Hg (95% CI 1P4 to 5.4) for each inch (2.54 cm) increase in crown-heel length. Diastolic pressure fell by 1 9 mm Hg (95% CI 0 9 to 2.9) for each pound (454 g) gain in birth weight and by 2-4 mm Hg (95% CI 1.4 to 3.5) for each inch (2.54 cm) increase in length. Systolic blood pressure was also higher in individuals whose mother's intercristal pelvic diameter was small or whose mother's blood pressure had been raised during pregnancy but these effects were statistically independent ofthe effects of low birth weight and other measurements that indicate fetal growth retardation. Arterial compliance was lower in those who had been small at birth. Conclusion-Impairment of fetal growthis associated with raised blood pressure in adult life and decreased compliance in the conduit arteries of the trunk and legs. (Br Heart J 1995;73:116-121)

To determine the response of the small intestinal mucosa to environmental conditions, we studied changes in mucosal architecture and function in a longitudinal cohort study in African adults. Over three consecutive years, 238 adults submitted monthly stool samples for parasitologic and bacteriologic analysis and underwent an annual endoscopic jejunal biopsy for mucosal morphometry. Absorption and permeability assays were performed on the same day as the enteroscopy. Variation in mucosal architecture and function was correlated with environmental factors and stool microbiology. The whole cohort had structural and functional evidence of tropical enteropathy, but structure and function were only weakly correlated. There were marked changes over time, and seasonal variation was observed in villous height (16%), xylose recovery (16%), and permeability (28%). Asymptomatic intestinal infections were common. Enteropathy was more severe in participants with Citrobacter rodentium or hookworm ova in the stool sample taken one month before the investigations were performed.

In the last 40 years, as techniques and materials have improved, the success rate of vascular prostheses with a diameter greater than 6mm has risen steadily, 5‐year survival rates exceeding 95% in most centres. With smaller grafts no comparable improvement has occurred, the majority failing within 5 years, usually as a result of intimal hyperplasia and, ultimately atherosclerosis, in and around the downstream anastomosis. Clinical evidence suggests that the patency rates of small grafts are improved by matching the elastic properties of the graft to that of the artery into which it is placed. Although there is little reliable evidence that ‘elastic mismatch’ per se is the cause of intimal hyperplasia, it is generally accepted that mechanical factors are important in its genesis. These include disturbed flow at the anastomosis leading to fluctuations in shear stress at the endothelium (a known cause of intimal hyperplasia in normal arteries), injury due to suturing and stress concentration at the anastomosis. Few suitable materials or techniques have yet been developed to improve the long‐term survival rates of small grafts. Recent advances in tissue engineering in which prostheses are manufactured by culturing vascular smooth muscle cells on a tubular scaffold of biodegradable polymer may ultimately make it possible to manufacture biologically and haemodynamically compatible grafts with diameters as small as 1mm. Copyright © 2000 John Wiley & Sons, Ltd.

Abstract. With the advance of computer and photonics technology, imaging photoplethysmography [(PPG), iPPG] can provide comfortable and comprehensive assessment over a wide range of anatomical locations. However, motion artifact is a major drawback in current iPPG systems, particularly in the context of clinical assessment. To overcome this issue, a new artifact-reduction method consisting of planar motion compensation and blind source separation is introduced in this study. The performance of the iPPG system was evaluated through the measurement of cardiac pulse in the hand from 12 subjects before and after 5 min of cycling exercise. Also, a 12-min continuous recording protocol consisting of repeated exercises was taken from a single volunteer. The physiological parameters (i.e., heart rate, respiration rate), derived from the images captured by the iPPG system, exhibit functional characteristics comparable to conventional contact PPG sensors. Continuous recordings from the iPPG system reveal that heart and respiration rates can be successfully tracked with the artifact reduction method even in high-intensity physical exercise situations. The outcome from this study thereby leads to a new avenue for noncontact sensing of vital signs and remote physiological assessment, with clear applications in triage and sports training. C 2011 Society of Photo-Optical Instrumentation Engineers (SPIE).

Arterial wall stresses are thought to be a major determinant of vascular remodeling both during normal growth and throughout the development of occlusive vascular disease. A completely physiologic mechanical model of the arterial wall should account not only for its residual strains but also for its structural nonhomogeneity. It is known that each layer of the artery wall possesses different mechanical properties, but the distribution of residual strain among the different mechanical components, and thus the true zero stress state, remain unknown. In this study, two different sets of experiments were carried out in order to determine the distribution of residual strains in artery walls, and thus the true zero stress state. In the first, collagen and elastin were selectively eliminated by chemical methods and smooth muscle cells were destroyed by freezing. Dissolving elastin provoked a decrease in the opening angle, while dissolving collagen and destroying smooth muscle cells had no effect. In the second, different wall layers of bovine carotid arteries were removed from the exterior or luminal surfaces by lathing or drilling frozen specimens, and then allowing the frozen material to thaw before measuring residual strain. Lathing material away from the outer surface caused the opening angle of the remaining inner layers to increase. Drilling material from the inside caused the opening angle of the remaining outer layers to decrease. Mechanical nonhomogeneity, including the distribution of residual strains, should thus be considered as an important factor in determining the distribution of stress in the artery wall and the configuration of the true zero stress state.

No abstract

No abstract