Effect of a
            <i>COL1A1</i>
            Sp1 Binding Site Polymorphism on Arterial Pulse Wave Velocity

Brull, David; Murray, Liam; Boreham, Colin; Ralston, Stuart H.; Montgomery, Hugh; Gallagher, Alison M.; McGuigan, Fiona; Smith, George Davey; Savage, Maurice; Humphries, Steve E.

doi:10.1161/01.hyp.38.3.444

Cited by 40 publications

(32 citation statements)

References 44 publications

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“…59 The complex interplay between hypertension-induced aortic distension, which reduces characteristic impedance, and passive stiffening due to recruitment of collagen fibres could thus provide contrasting results when aortic stiffness and ventricular load are assessed with different parameters. 109,110 Elasticity of large arteries is influenced by polymorphisms of genes coding for elastin, 111 collagen, 112,113 fibrillin 114 and the renin-angiotensin system. 115,116 All these genetic variants can affect the structural and functional characteristics of the arterial tree and have significant impact on arterial load.…”

Section: Impact Of Arterial Structure and Function On Ventricular Loamentioning

confidence: 99%

Ventricular–vascular coupling in hypertension

Saba

Cameli

Casalnuovo

et al. 2014

Journal of Cardiovascular Medicine

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The present review is addressed to analyse the complex interplay between left ventricle and arterial tree in hypertension. The different methodological approaches to the analysis of ventricular-vascular coupling in the time and frequency domain are discussed. Moreover, the role of hypertension-related changes of arterial structure and function (stiffness and wave reflection) on arterial load and how ventricular-vascular coupling modulates the process of left ventricular adaptation to hypertension are analysed.The different interplay between vascular bed and left ventricle emerges as the pathophysiological basis for the development of the multiple patterns of ventricular structural adaptation in hypertension and provides a pathway for the interpretation of systolic and diastolic functional abnormalities observed in hypertensive patients. Targeting the therapeutic approach to improve ventricularvascular coupling may have relevant impact on reversing left ventricular hypertrophy and improving systolic and diastolic dysfunction. J Cardiovasc Med 2014, 15:773-787

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Section: Impact Of Arterial Structure and Function On Ventricular Loamentioning

confidence: 99%

Ventricular–vascular coupling in hypertension

Saba

Cameli

Casalnuovo

et al. 2014

Journal of Cardiovascular Medicine

View full text Add to dashboard Cite

show abstract

“…They may be divided into 2 categories: those related to the pathophysiology of high BP, such as the renin-angiotensin-aldosterone system, the endothelial NO synthase system, and the ␣-adducin systems, [43][44][45][46] and those related to CV aging, particularly those related to elastin, collagen, and telomere length. [47][48][49] However, results regarding the association of individual gene polymorphisms with arterial behavior are still controversial. Recent research suggests that combinations of 2 or 3 specific polymorphisms acting on the same BP control mechanism can affect vessel wall properties profoundly.…”

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confidence: 99%

Current Perspectives on Arterial Stiffness and Pulse Pressure in Hypertension and Cardiovascular Diseases

2003

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Blood pressure (BP) is a powerful cardiovascular (CV) risk factor that acts on the arterial wall and is responsible in part for various CV events, such as cerebrovascular accidents and ischemic heart disease. In clinical practice, 2 specific and arbitrary points of the BP curve, peak systolic BP (SBP) and end-diastolic BP (DBP), are used to define the CV risk factor. Because the goal of drug treatment of hypertension is to prevent CV complications, it appears likely that the totality of the BP curve, not simply 2 specific and arbitrary points, should be considered to act mechanically on the arterial wall and therefore should be used to propose an adequate definition of high BP.A current approach consists of considering the BP curve as the summation of a steady component, mean blood pressure (MBP), and a pulsatile component, pulse pressure (PP). 1 MBP, the product of cardiac output multiplied by total peripheral resistance, is the pressure for the steady flow of blood and oxygen to peripheral tissues and organs. The pulsatile component, PP, is the consequence of intermittent ventricular ejection from the heart. PP is influenced by several cardiac and vascular factors, but it is the role of large conduit arteries, mainly the aorta, to minimize pulsatility. In addition to the pattern of left ventricular ejection, the determinants of PP (and SBP) are the cushioning capacity of arteries and the timing and intensity of wave reflections. 1 The former is influenced by arterial stiffness, usually expressed in the quantitative terms of compliance and distensibility. 1 The latter result from the summation of a forward wave coming from the heart and propagating at a given speed (pulse wave velocity, or PWV) toward the origin of resistance vessels and a backward wave returning toward the heart from particular sites characterized by specific reflection coefficients. 1 Over the past few years, arterial stiffness and wave reflections have been widely investigated in old and/or hypertensive subjects for several reasons. First, whereas DBP was considered in the past as the better guide to determine disease severity, epidemiological studies have directed attention to SBP as a more informative CV risk factor, particularly in patients older than 50 years of age, and it has been shown that PP is an independent marker of CV risk, mainly for myocardial infarction. 2 Second, in subjects Ͼ50 years of age, ventricular ejection tends to be reduced, so that arterial stiffness and amplitude and timing of wave reflections become the main determinants of increased SBP and PP. Third, whereas drug control of DBP is consistently obtained in large populations of hypertensive patients, the ability to control SBP is observed much less frequently. 3 Finally, increased PP is also a predictor of CV risk in subjects with recurrent myocardial infarction and congestive heart failure. 2,4,5 From the hemodynamic factors that influence PP, 2 have been shown to independently predict CV risk: aortic stiffness, measured from aortic PWV, 6,7 and early return of...

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“…8 Dysregulation of their expression, degradation, and protein cross-links may lead to alterations in the elastin/collagen ratio with subsequent arterial stiffening. 9 The mineralocorticoid hormone aldosterone is a potent and blood pressure-independent inducer of both, elastin and collagen expression, 10 pointing to the direct implication of aldosterone in vascular elasticity. Most recently, the involvement of the vascular endothelium has been discussed extensively as an important regulator of vascular elasticity.…”

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confidence: 99%