Arterial Stiffness: A New Cardiovascular Risk Factor?

Arnett, Donna K.; Evans, Gregory W.; Riley, Ward A.

doi:10.1093/oxfordjournals.aje.a117315

Cited by 437 publications

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“…Since carotid IMT is recognized as a marker of systemic atherosclerosis (38), our patients can be considered as having premature atherosclerosis, which was also confirmed by higher prevalence of atherosclerotic plaques compared with controls (40% vs 10%), although the difference did not reach significance due to the relatively small population under evaluation. Increased IMT indicates reduced diameter and significantly increased stiffness of carotid walls, the latter being recognized as an independent marker of cardiovascular risk (41,42). This result is in accordance with Smith et al, who have found significantly higher indices of vessel stiffness in PHPT patients compared with healthy controls, independently of systolic BP values (20).…”

Section: Discussionsupporting

confidence: 86%

Increased intima-media thickness of the carotid artery wall, normal blood pressure profile and normal left ventricular mass in subjects with primary hyperparathyroidism

Nuzzo

Tauchmanovà

Fonderico

et al. 2002

European Journal of Endocrinology

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Objective: Despite the increasing evidence that primary hyperparathyroidism (PHPT) contributes to greater risk of cardiovascular morbidity and mortality, its exact role in the development of cardiovascular changes and its clinical significance are still controversial. Given the multiple influence of PHPT on the cardiovascular system, this study aimed to assess the effects of PHPT on blood pressure profile, and on features of the heart and arterial vessels in normotensive symptomless patients. Design: Twenty patients (8 males and 12 females) with a median age of 51.5 years (range 44 to 65 years) were evaluated and the results were compared with those of 20 controls matched for age, gender and body mass index. Patients' parathyroid hormone levels ranged from 172 to 454 pg/ml and Ca levels ranged from 11.4 to 13.5 mg/dl. Fasting levels of glucose, insulin, total and high density lipoprotein cholesterol and triglycerides were within the normal range in all subjects recruited. Methods: Twenty-four-hour blood pressure profile, left ventricle (LV) dimension and carotid artery anatomy were investigated, the latter two by ultrasonography. Results: No difference was found between the patients and controls in blood pressure profile, when the following parameters were considered: supine systolic/diastolic pressure, average 24-h systolic, diastolic and mean arterial pressure, day-time mean arterial pressure and fall in nocturnal blood pressure (217% and 2 18% respectively). Heart rate and all parameters of LV mass were similar in patients and controls. The only alteration found in patients was in significantly greater carotid intimal-medial thickness (IMT) ðP , 0:001Þ: Atherosclerotic plaques were more frequent in patients than in controls, with a difference reaching a trend (40% vs 10%, x 2 ¼ 4:8; P ¼ 0:091). Considering that the carotid IMT is considered to be a marker of systemic atherosclerosis, our finding suggests early atherosclerotic changes in PHPT. No correlation was found between the severity and cardiovascular manifestation of PHPT. Conclusions: Vascular changes may occur due to a combination of structural and functional impairments in PHPT patients, likely as a result of altered calcium metabolism and impaired equilibrium of other factors regulating vascular function. Both extent and duration of PHPT can play a relative role in the development of cardiovascular complications. Considering that PHPT is now recognized as a quite common and often symptomless endocrine disorder, the evidence of cardiovascular manifestation in normotensive patients, found by this morphological study, suggests a possible implication for the management of such patients. In this light, screening for abnormalities in cardiovascular system function should be recommended in all PHPT subjects.

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Section: Discussionsupporting

confidence: 86%

Increased intima-media thickness of the carotid artery wall, normal blood pressure profile and normal left ventricular mass in subjects with primary hyperparathyroidism

Nuzzo

Tauchmanovà

Fonderico

et al. 2002

European Journal of Endocrinology

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“…Arterial stiffness is increasingly recognised as an independent risk factor for cardiovascular disease 1 and contributes to the development of hypertension 2 and left ventricular hypertrophy. 3 In young subjects, arterial wave reflection (AWR) is timed to return to the ascending aorta during diastole, after ventricular ejection has ceased.…”

Section: Introductionmentioning

confidence: 99%

Favourable effects on arterial wave reflection and pulse pressure amplification of adding angiotensin II receptor blockade in resistant hypertension

Mahmud

Feely

2000

J Hum Hypertens

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Objective: Angiotensin-converting enzyme (ACE) inhibitors have beneficial effects on arterial compliance and distensibility and favourably modify the arterial pressure waveform in hypertensive patients. The objective of our study was to explore the possible effects of adding an ATII AT 1 receptor antagonist to an ACE inhibitor on augmentation pressure, a measure of arterial stiffness, and pulse pressure amplification in patients with poorly controlled essential hypertension. Design and methods: We studied a group of 18 patients with poorly controlled hypertension, despite at least three antihypertensive drugs including an ACE inhibitor, before, at 2 h and 2 weeks following the administration of 80 mg of valsartan, an ATII AT 1 receptor antagonist. Haemodynamic responses were measured by cuff sphygmomanometry, arterial pulse-wave analysis and the pulse pressure gradient was calculated as the difference between the brachial pulse pressure (cuff sphygmomanometry) and derived aortic pulse pressure (arterial pulse wave analysis). Results: Blood pressure decreased significantly (P Ͻ 0.001) and the effect was more pronounced on central

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“…The increase in stiffness of arteries represents an early risk factor for cardiovascular diseases (1,19). Specifically, increased stiffness is associated with aging (14), atherosclerosis (6), and heart failure (27).…”

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confidence: 99%

Right coronary artery becomes stiffer with increase in elastin and collagen in right ventricular hypertrophy

Garcia

Kassab²

2009

Journal of Applied Physiology

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Garcia M, Kassab GS. Right coronary artery becomes stiffer with increase in elastin and collagen in right ventricular hypertrophy. J Appl Physiol 106: 1338 -1346, 2009. First published January 29, 2009 doi:10.1152/japplphysiol.90592.2008.-Changes in blood flow influence the structure, function, mechanical properties, and remodeling of arteries. The objective of the present study was to investigate the role of increased blood flow on the biaxial incremental elastic moduli of the porcine right coronary artery (RCA) and to determine the microstructural basis for the changes in moduli. We hypothesized that an increase in RCA flow will lead to increased stiffness in conjunction with remodeling of elastin and collagen in the vessel wall. The control and experimental groups consisted of five RCA vessels each. The RCA of the experimental group was exposed to 4 wk of flow-overload in right ventricular hypertrophy induced by pulmonary artery banding. Stress-strain relationships were determined and the incremental elastic moduli were derived in the circumferential, axial, and cross directions. The results show a significant increase in the elastic moduli in the circumferential (262.7 Ϯ 15.7 vs. 120.2 Ϯ 12.4 kPa; P Ͻ 0.001), axial (177.8 Ϯ 25.5 vs. 100.3 Ϯ 11.9 kPa; P ϭ 0.025), and cross directions (104.8 Ϯ 8.2 vs. 68.2 Ϯ 8.6 kPa; P ϭ 0.016) of the experimental RCA compared with controls. Multiphoton microscopy was used to assess the changes in elastin and collagen content in the media and adventitia of the vessel wall. We found a significant increase in elastin and collagen area fraction particularly in the adventitial layer. These data suggest stiffening of the vessel wall as a result of increased elastin and more predominantly collagen. stress; strain; wall shear stress; constitutive equation BLOOD VESSELS ARE subjected to the mechanical loading of blood pressure and blood flow throughout the cardiac cycle. The vessels undergo structural and mechanical adaptations in response to changes in the local hemodynamic conditions. For example, changes in blood flow cause changes in fluid wall shear stress (WSS; the tractive frictional force exerted by flowing blood on the inner layer of the vessel wall) by eliciting a wide range of biochemical and physiological responses in experimental (46) and clinical studies (16,22). Studies have demonstrated that a sudden increase in blood flow initiates an enlargement of the arterial lumen that progresses for months as the WSS tends to a homeostatic or normal level (23,25). A gradual increase in blood flow has been reported by several groups to result in outward hypertrophic remodeling of resistance (4,41,44,45,47) and conductive arteries (25,36,39). The flow-induced remodeling may be an attempt to maintain mechanical homeostasis (24,25). When blood flow is elevated in a vessel, the endothelium responds to restore WSS toward homeostatic levels by changing vascular tone, increasing the lumen diameter (44), and potentially altering the function and mechanical properties of the vessel wall. ...

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Arterial Stiffness: A New Cardiovascular Risk Factor?

Cited by 437 publications

References 0 publications

Increased intima-media thickness of the carotid artery wall, normal blood pressure profile and normal left ventricular mass in subjects with primary hyperparathyroidism

Increased intima-media thickness of the carotid artery wall, normal blood pressure profile and normal left ventricular mass in subjects with primary hyperparathyroidism

Favourable effects on arterial wave reflection and pulse pressure amplification of adding angiotensin II receptor blockade in resistant hypertension

Right coronary artery becomes stiffer with increase in elastin and collagen in right ventricular hypertrophy

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