Arnold P.G. Hoeks

Arterial Stiffness and Risk of Coronary Heart Disease and Stroke The Rotterdam Study

Background— Arterial stiffness has been associated with the risk of cardiovascular disease in selected groups of patients. We evaluated whether arterial stiffness is a predictor of coronary heart disease and stroke in a population-based study among apparently healthy subjects. Methods and Results— The present study included 2835 subjects participating in the third examination phase of the Rotterdam Study. Arterial stiffness was measured as aortic pulse wave velocity and carotid distensibility. Cox proportional hazards regression analysis was performed to compute hazard ratios. During follow-up, 101 subjects developed coronary heart disease (mean follow-up period, 4.1 years), and 63 subjects developed a stroke (mean follow-up period, 3.2 years). The risk of cardiovascular disease increased with increasing aortic pulse wave velocity index. Hazard ratios and corresponding 95% CIs of coronary heart disease for subjects in the second and third tertiles of the aortic pulse wave velocity index compared with subjects in the reference category were 1.72 (0.91 to 3.24) and 2.45 (1.29 to 4.66), respectively, after adjustment for age, gender, mean arterial pressure, and heart rate. Corresponding estimates for stroke were 1.22 (0.55 to 2.70) and 2.28 (1.05 to 4.96). Estimates decreased only slightly after adjustment for cardiovascular risk factors, carotid intima-media thickness, the ankle-arm index, and pulse pressure. The aortic pulse wave velocity index provided additional predictive value above cardiovascular risk factors, measures of atherosclerosis, and pulse pressure. Carotid distensibility as measured in this study was not independently associated with cardiovascular disease. Conclusions— Aortic pulse wave velocity is an independent predictor of coronary heart disease and stroke in apparently healthy subjects.

Association Between Arterial Stiffness and Atherosclerosis The Rotterdam Study

Background and Purpose — Studies of the association between arterial stiffness and atherosclerosis are contradictory. We studied stiffness of the aorta and the common carotid artery in relation to several indicators of atherosclerosis. Methods — This study was conducted within the Rotterdam Study in >3000 elderly subjects aged 60 to 101 years. Aortic stiffness was assessed by measuring carotid-femoral pulse wave velocity, and common carotid artery stiffness was assessed by measuring common carotid distensibility. Atherosclerosis was assessed by common carotid intima-media thickness, plaques in the carotid artery and in the aorta, and the presence of peripheral arterial disease. Data were analyzed by ANCOVA with adjustment for age, sex, mean arterial pressure, and heart rate. Results — Both aortic and common carotid artery stiffness were found to have a strong positive association with common carotid intima-media thickness, severity of plaques in the carotid artery, and severity of plaques in the aorta (P for trend <0.01 for all associations). Subjects with peripheral arterial disease had significantly increased aortic stiffness (P =0.001) and borderline significantly increased common carotid artery stiffness (P =0.08) compared with subjects without peripheral arterial disease. Results were similar after additional adjustment for cardiovascular risk factors and after exclusion of subjects with prevalent cardiovascular disease. Conclusions — This population-based study shows that arterial stiffness is strongly associated with atherosclerosis at various sites in the vascular tree.

Arterial alterations with aging and high blood pressure. A noninvasive study of carotid and femoral arteries.

Noninvasive in situ evaluations of pulsatile changes of blood pressure and arterial diameter were performed at the sites of the common carotid and femoral arteries in a population of 78 untreated normotensive and hypertensive subjects. Arterial segments were studied by using an original echo-tracking technique for internal diameter and validated applanation tonometry for local pulse pressure measurements. Whereas mean arterial pressure is known to be identical in all parts of the arterial tree, pulse pressure was significantly lower in the carotid (52.7 +/- 2.2 mm Hg) than in the brachial (62.0 +/- 2.0 mm Hg) or femoral (62.5 +/- 2.5 mm Hg) arteries. Despite a higher pulse pressure and diastolic diameter, the femoral artery had a lower pulsatile change in diameter (3.47 +/- 0.18% versus 6.07 +/- 0.28%; p < 0.0001) and distensibility coefficient (9.36 +/- 0.58 versus 21.60 +/- 1.75 x 10(-3) kPa-1) than the carotid artery. Local cross-sectional compliance of the carotid artery was higher than that of the femoral artery (7.42 +/- 0.46 versus 6.20 +/- 0.28 m2.kPa-1.10(-7); p < 0.05). Whereas age was strongly correlated with arterial parameters at the site of the carotid artery (pulse pressure: r = 0.54, p < 0.0001; pulsatile change in arterial diameter: r = -0.62, p < 0.0001; distensibility coefficient: r = -0.70, p < 0.0001), no significant correlation was observed at the femoral artery. Mean blood pressure was the second factor of carotid artery alterations: the higher the mean blood pressure, the lower the distensibility of this artery (r = -0.36, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of the distensibility of superficial arteries

Doppler signal processing cannot only be employed to detect the local blood velocity as function of time, but also to assess transcutaneously the displacement of the arterial walls during the cardiac cycle (distension waveform) and, hence, the time-dependent changes in arterial diameter relative to its initial diameter at the start of a cardiac cycle. The distension waveform normalized with respect to the local pulse pressure provides useful information about the local elasticity of the arterial wall. The displacement of the arterial wall can be obtained by processing the RF-signals within a sample volume coinciding with the arterial wall. To evaluate this method a dedicated high-speed memory system has been developed storing the RF-signal, as obtained with a conventional echo-imager in M-mode, over a number of successive sweeps covering a selected depth range. The data are transferred line after line to a personal computer (PC) and processed on the fly, thereby relieving the memory requirements of the PC. It can be concluded that a RF-signal memory in combination with a PC provides a useful tool to extract detailed diameter waveforms from the RF-signals obtained. Although the system does not process the signals in real-time the process can be considered to be on-line since the results become available within one minute after the acquisition of the data is completed.

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

Objectives Pulse 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 calibrated readings from applanation tonometry, (ii) alternative calibration of pressure waves obtained with applanation tonometry and (iii) alternative calibration of arterial distension waves obtained with echo-tracking. Alternative calibration assumes mean and diastolic blood pressure constant throughout the large artery tree. Design and methods Study 1 used invasive measurements in the ascending aorta as a reference method and internally calibrated tonometer readings and alternatively calibrated pressure waves at the common carotid artery as test methods. Study 2 used alternatively calibrated pressure waves as a reference method and alternatively calibrated distension waves and internally calibrated applanation tonometer readings as test methods. Results In study 1, pulse pressure from internally calibrated tonometer readings was 10.2 ± 14.3 mmHg lower and pulse pressure from alternatively calibrated pressure waves was 1.8 ± 5.2 mmHg higher than invasive pulse pressure. Pulse pressure from calibrated distension waves was 3.4 ± 6.9 mmHg lower than pulse pressure from alternatively calibrated pressure waves. According to British Hypertension Society criteria, pulse pressure from the internally calibrated tonometer achieved grade D and pulse pressure from alternatively calibrated pressure waves achieved grade A. Pulse pressure from calibrated distension waves achieved grade B when alternatively calibrated pressure waves were used as a reference method. Conclusions Pulse pressure obtained from alternatively calibrated tonometer-derived pressure waves and echo-tracking-derived distension waves demonstrates good accuracy. Accuracy of pulse pressure from internally calibrated applanation tonometer readings at the carotid artery is poor.

Wall Shear Stress – an Important Determinant of Endothelial Cell Function and Structure – in the Arterial System in vivo

It has been well established that wall shear stress is an important determinant of endothelial cell function and gene expression as well as of its structure. There is increasing evidence that low wall shear stress, as pres- ent in artery bifurcations opposite to the flow divider where atherosclerotic lesions preferentially originate, expresses an atherogenic endothelial gene profile. Besides, wall shear stress regulates arterial diameter by modifying the release of vasoactive mediators by endothelial cells. Most of the studies on the influence of wall shear stress on endothelial cell function and structure have been performed in vitro, generally exposing endothelial cells from different vascular regions to an average wall shear stress level calculated according to Poiseuille’s law, which does not hold for the in vivo situation, assuming wall shear stress to be constant along the arterial tree. Also in vivo wall shear stress has been determined based upon theory, assuming the velocity profile in arteries to be parabolic, which is generally not the case. Wall shear stress has been calculated, because of the lack of techniques to assess wall shear stress in vivo. In recent years, techniques have been developed to accurately assess velocity profiles in arterioles, using fluorescently labeled particles as flow tracers, and non-invasively in large arteries by means of ultrasound or magnetic resonance imaging. Wall shear rate is derived from the in vivo recorded velocity profiles and wall shear stress is estimated as the product of wall shear rate and plasma viscosity in arterioles and whole blood viscosity in large arteries. In this review, we will discuss wall shear stress in vivo, paying attention to its assessment and especially to the results obtained in both arterioles and large arteries. The limitations of the methods currently in use are discussed as well. The data obtained in the arterial system in vivo are compared with the theoretically predicted ones, and the consequences of values deviating from theory for in vitro studies are considered. Applications of wall shear stress as in flow-mediated arterial dilation, clinically in use to assess endothelial cell (dys)function, are also addressed. This review starts with some background considerations and some theoretical aspects.

Methods and devices for measuring arterial compliance in humans

This review analyses methods and devices used worldwide to evaluate the arterial stiffness. Three main methodologies are based upon analysis of pulse transit time, of wave contour of the arterial pulse, and of direct measurement of arterial geometry and pressure, corresponding to regional, systemic and local determination of stiffness. They are used in clinical laboratory and/or in clinical departments. Particular attention is given to the reproducibility data in literature for each device. This article summarizes the discussion of the dedicated Task Force during the first Conference of Consensus on Arterial Stiffness held in June 2000 (Paris, France).

Short and long-term effects of smoking on arterial wall properties in habitual smokers

OBJECTIVES This study investigated the short-term effects of smoking on hemodynamic function and distensibility and compliance of large arteries in habitual smokers. In addition, the effect of smoking was not measured in nonsmokers, but vessel wall properties were compared between smokers and nonsmokers (basal state). BACKGROUND Smoking is a well known risk factor for atherosclerosis. Loss of distensibility and compliance of large arteries may play a role in the onset of atherosclerosis. METHODS The distensibility and compliance coefficients of the common carotid and brachial arteries were determined from the arterial wall displacement during systole and the end-diastolic diameter by using a vessel wall movement detector and from the pulse pressure as assessed in the upper arm. Cardiac function (cardiac output, stroke volume) was measured with Doppler echocardiography. Systemic vascular resistance was calculated as mean arterial pressure divided by cardiac output. RESULTS In habitual smokers, smoking one cigarette caused a sharp increase in blood pressure (6%) and heart rate (14%). Cardiac index increased (16%), mainly because of the marked increase in heart rate. Stroke and systemic vascular resistance indexes did not change significantly. Smoking enhanced forearm blood flow after wrist occlusion (17%), but total forearm blood flow was unchanged, suggesting an increase in muscle blood flow and a decrease in skin flow. Because of higher blood pressure, the diameter of the elastic common carotid artery increased by 3% (passive phenomenon). Distensibility of the carotid artery decreased (7%), and as a result, carotid compliance was preserved. In contrast, despite higher blood pressure, the diameter of the muscular brachial artery did not change, suggesting an increased vascular tone. Brachial distensibility and compliance decreased (18% and 19%, respectively). Habitual smokers were comparable to nonsmokers with regard to blood pressure, cardiac function, vascular resistance and vessel wall properties of large arteries. Heart rate was higher in habitual smokers (14%). CONCLUSIONS These data indicate that in habitual smokers, smoking one cigarette causes short-term increases in arterial wall stiffness that might be harmful to the artery and increase the risk for plaque rupture. Except for a higher heart rate, no obvious long-term effect of smoking was observed on hemodynamic variables and arterial stiffness. Because acute cardiovascular events are mainly due to plaque rupture, the short-term effects of smoking might be a more important risk than long-term effects for these acute ischemic events.

Age-related changes in carotid artery wall properties in men

Changes in distensibility and cross-sectional compliance of the common carotid artery with age were studied in 80 presumed healthy volunteers, varying in age between 20 and 69 y. The distensibility was assessed from the relative increase in arterial diameter during systole normalized with respect to the arterial pulse pressure. The cross-sectional compliance was obtained by multiplying the distensibility by the arterial diameter. The relative diameter changes of the common carotid artery during the cardiac cycle were recorded on-line with a high resolution multigate pulsed Doppler system. The arterial diameter was assessed from the width of the velocity profiles which can also be recorded on-line with this system. Arterial pulse pressure was determined from brachial artery cuff blood pressure measurements. Both distensibility and cross-sectional compliance of the common carotid artery decreased linearly with age, starting in the third age decade. The reduction in the latter parameter was less pronounced, probably as a consequence of an increase in arterial diameter with age.

Carotid artery distensibility and distending pressure in hypertensive humans.

Whether the decrease in large-artery distensibility observed in hypertensive patients is due primarily to an increase in distending pressure or to hypertension-induced changes in structural properties has been much debated. We determined noninvasively the diameter-pressure curve of the common carotid artery over the systolic-diastolic range by continuously recording both the pulsatile changes in internal diameter (high-resolution echo-tracking system) and, simultaneously on the contralateral artery, the pressure waveform (high-fidelity applanation tonometry). We then derived the distensibility/pressure curve and compared arterial distensibility in 14 normotensive subjects and 15 age- and sex-matched hypertensive subjects at their respective mean arterial pressures (MAP) and at a common distending pressure: 100 mm Hg. Distensibility decreased as blood pressure increased, and distensibility at MAP was significantly lower in hypertensive than in normotensive subjects (7.8 +/- 0.7 versus 11.7 +/- 1.7 kPa-1.10(-3), mean +/- SEM; P < .05). In hypertensive subjects, the distensibility-pressure curve was shifted toward higher levels of blood pressure, and a large part of the curve overlapped that of normotensive subjects. No significant downward shift of the distensibility-pressure curve was observed in hypertensive subjects, and distensibility at 100 mm Hg was not significantly different from that of normotensive subjects (10.0 +/- 1.0 versus 9.0 +/- 1.1 kPa-1.10(-3)). Distensibility at 100 mm Hg decreased with aging (P < .05) and was not reduced in hypertensive subjects compared with normotensive subjects after adjustment for age.(ABSTRACT TRUNCATED AT 250 WORDS)