Artery Research

Editorial Board

2010-06-01

Editorial

John R. Cockcroft — 2010-06-01

Welcome to the latest addition of Artery Research. This issue sees the first in a series of ARTERY Society guidelines for validation of non-invasive haemodynamic measurement devices. As pulse wave velocity is the current ‘gold standard’ for assessing arterial stiffness in clinical practice, the first set of guidelines appropriately focuses on validation of devices to measure this parameter. Future issues will carry validation guidelines for other important parameters such as central aortic blood pressure.

ARTERY Society guidelines for validation of non-invasive haemodynamic measurement devices: Part 1, arterial pulse wave velocity

2010-04-01

Abstract: The last 15 years have seen an explosion of interest in large artery haemodynamics, and arterial stiffness in particular. A number of devices are now available to assess arterial stiffness, and although many are in routine use, they do not necessarily provide identical information. The aim of this statement is to provide guidelines for the process of validating new devices. The focus of the article is aortic pulse wave velocity. We hope that equipment manufacturers, and researchers will both find these guidelines helpful, and that they will allow greater standardization of aortic pulse wave velocity measurements.

Shear stress, inflammation and Atherosclerosis

Rob Krams, Simon Cuhlmann, Nicolas Foin, Paul Evans — 2010-04-30

Summary: Background: Atherosclerosis is the disease with one of the largest mortalities of the Western world. An important cause of this high mortality rate is rupture of atherosclerotic plaques and subsequent total blockage of the vessel by thrombus. Because, plaque rupture has been associated with a distinct plaque phenotype there is a growing need for understanding the pathogenesis of plaque composition. In this manuscript, we will discuss the new hypothesis that blood flow and lipid driven inflammation are intimately related to each other and that shear stress induced expression of chemokines and the resulting coordinated homing of inflammatory cells influence plaque composition in such a way that vulnerable plaque may be induced. As vulnerable plaques are intimately related to the high mortality of atherosclerosis, it re-emphasis the important role blood flow has in atherosclerosis.

The effects of weight loss using dietary manipulation and rimonabant therapy on arterial stiffness in type 2 diabetes

A. Chakera, S. Bunce, C. Heppenstall, J.C. Smith — 2010-04-30

Abstract: Background: Obesity is considered an important factor contributing to premature arterial stiffening in type 2 diabetes but it is uncertain whether weight loss through dietary modification leads to a reduction in arterial stiffness. Rimonabant is an anti-obesity drug which, through its pharmacological action of cannabinoid receptor blockade, could exert effects on central haemodynamics.Methods: In an open design, 29 obese subjects with type 2 diabetes were studied. Subjects were studied before, during and after 6 months dietary intervention with (20 subjects), or without (9 subjects) rimonabant. Arterial stiffness (aortic and brachial pulse wave velocity), central aortic pressure and wave reflection were assessed non-invasively (Sphygmocor).Results: After 6 months (in comparison with baseline), there were reductions in weight (104 ± 21 versus 107 ± 21 Kg, p < 0.001), and improvements in HbA1c (7.3 ± 1.4 at 3 months, p < 0.01 and 7.4 ± 1.5 at 6 months, p = 0.06 versus 7.7 ± 1.5% at baseline) and HDL cholesterol (1.3 ± 0.2 versus 1.2 ± 0.3 mmol/L, p < 0.001). Aortic diastolic pressure (82 ± 10 versus 85 ± 8 mmHg, p < 0.05) was lowered despite unchanged peripheral mean arterial pressure. No reductions in aortic stiffness or wave reflection were observed.Conclusion: Dietary manipulation led to significant weight loss and favourable metabolic effects. These beneficial changes did not lead to a reduction in aortic stiffness or pressure wave reflection despite a fall in central aortic blood pressure.

Oxidative stress and arterial stiffness in strength- and endurance-trained athletes

2010-06-01

Abstract: Background: Endurance exercise training decreases arterial stiffness, whereas high-intensity strength exercise training increases arterial stiffness. However, the mechanisms underlying the adaptations to the 2 types of exercise training remain unclear. Increased oxidative stress induces vasoconstriction and endothelial dysfunction. Plasma advanced oxidation protein products (AOPP)—a novel marker of oxidative stress—have recently been reported to be positively associated with arterial stiffness in healthy subjects. We hypothesized that AOPP are involved in the adaptation of arterial stiffness in different types of exercise training.Methods: We investigated plasma AOPP concentration and arterial stiffness in strength- and endurance-trained athletes. The subjects included young strength-trained athletes (SA group) (shot put, hammer, or javelin throwers; n=12), endurance-trained athletes (EA group) (long- or middle-distance runners; n=10), and sedentary individuals (Control group) (n=12). We measured aortic pulse-wave velocity (PWV), systemic arterial compliance (SAC), and plasma AOPP concentrations.Results: PWV was higher in the SA than in the EA or control groups (SA: 6.48±0.47, EA: 6.00±0.67, Control: 5.65±0.52m/s, mean±SD), and SAC was lower in the SA than in the EA or control groups (SA: 1.04±0.24, EA: 1.56±0.44, Control: 1.38±0.35ml/mmHg); thus, arterial stiffness was higher in the SA group. Plasma AOPP concentrations were higher in the SA group than in the EA group (SA: 31.7±8.5, EA: 23.9±6.9, Control: 27.2±3.9μmol/l). We found that plasma AOPP levels tended to be related to SAC (P=0.073, r=−0.31).Conclusions: The present study provides a possibility that exercise training-induced oxidative stress may be partly involved in the mechanism underlying the adaptation of arterial stiffness in strength- and endurance-trained athletes.

Combined imaging, computational and histological analysis of a ruptured carotid plaque: A patient-specific analysis

2010-06-25

Abstract: Background: Rupture of carotid plaques is an important cause of cerebrovascular events. Several factors, including wall shear stress (WSS), plaque morphology and peak cap stress, have been associated with plaque vulnerability. The aim of this study was to investigate the relationship between these factors in an in vivo human ruptured carotid plaque.Methods: A 74-year-old male presenting with a transient ischemic attack underwent carotid magnetic resonance imaging (MRI), which indicated a ruptured plaque, followed by carotid endarterectomy, from which plaque histology was assessed. The carotid bifurcation was reconstructed from the MRI data, and three-dimensional flow simulations were performed using computational fluid dynamics to determine WSS and related parameters. Plaque vulnerability was assessed using a biomechanical method based on modified Glagov criteria.Results: The plaque rupture was just distal to the site of maximum stenosis in a region of low WSS, where MRI and histology both demonstrated fibrous cap thinning, a large lipid pool and calcification in the shoulder region. Plaque vulnerability analysis indicated critically vulnerable plaque at the rupture site by a wide margin.Conclusions: Both low and high WSS have been associated with plaque vulnerability, and high mechanical stress in the cap has been linked to plaque rupture, but these parameters are not routinely assessed clinically. This study demonstrates a complete analysis by combining imaging, histology and bio-fluid and biomechanical modelling.