Statins, Central Blood Pressure, and Blood Pressure Amplification

Safar, Michel E.; Protogerou, Athanase D.; Blacher, Jacques

doi:10.1161/circulationaha.108.824532

Cited by 29 publications

(15 citation statements)

References 22 publications

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“…30 However, the application of this principle needs further validation. (1) the morphological differences of the pulse wave (PW) between the aorta and the brachial artery in young healthy subjects (upper panel) and (2) the effect of heart rate (upper panel versus lower panel ) on systolic blood pressure (SBP) augmentation and PW amplification, for the same reflected pressure wave and similar pulse height of the forward ejected pressure wave (modified from Safar et al 74 ). Aortic S1 indicates 1st systolic peak attributed to the forward wave; Aortic S2, 2nd late systolic peak attributable to the augmentation by the reflected pressure wave; brachial S2, systolic peak attributable to the reflected wave from the upper limb; D, accentuated diastolic wave attributable to the delayed arrival of the reflected wave from the lower body; ED, ejection duration; T0, onset of the forward ejected wave; Tr, time to return at the aorta of the backward reflected wave from the T0.…”

Section: Assessment and Expression Of Pulse Pressure Amplification Inmentioning

confidence: 99%

Role of Pulse Pressure Amplification in Arterial Hypertension

et al. 2009

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Section: Assessment and Expression Of Pulse Pressure Amplification Inmentioning

confidence: 99%

Role of Pulse Pressure Amplification in Arterial Hypertension

et al. 2009

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“…The most widely accepted model used to explain the SBP amplification relies on retrograde wave reflection from resistant distal arterioles, which is additive to the antegrade wave. 15 Several lines of evidence indicate that reflected waves occur at various sites in the vascular bed, 16,17 with some attenuation along the arterial system. 18,19 However, the reflected wave is not the sole explanation for the changes in pressure wave morphology.…”

Section: Physiology Of the Abi Why Is Sbp Higher In The Ankles Than Imentioning

confidence: 99%

Measurement and Interpretation of the Ankle-Brachial Index

Aboyans

Criqui²,

Ábrahám³

et al. 2012

Circulation

1,345

827

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T he ankle-brachial index (ABI) is the ratio of the systolic blood pressure (SBP) measured at the ankle to that measured at the brachial artery. Originally described by Winsor 1 in 1950, this index was initially proposed for the noninvasive diagnosis of lower-extremity peripheral artery disease (PAD). 2,3 Later, it was shown that the ABI is an indicator of atherosclerosis at other vascular sites and can serve as a prognostic marker for cardiovascular events and functional impairment, even in the absence of symptoms of PAD. 4 -6 Rationale for Standardization of the ABIThe current lack of standards for measurement and calculation of the ABI leads to discrepant results with significant impact from clinical, public health, and economic standpoints. Indeed, the estimated prevalence of PAD may vary substantially according to the mode of ABI calculation. [7][8][9] In a review of 100 randomly selected reports using the ABI, multiple variations in technique were identified, including the position of the patient during measurement, the sizes of the arm and leg cuffs, the location of the cuff on the extremity, the method of pulse detection over the brachial artery and at the ankles, whether the arm and ankle pressures were measured bilaterally, which ankle pulses were used, and whether a single or replicate measures were obtained. 10 There is controversy about what ABI threshold should be used to diagnose PAD. The ABI threshold most commonly used is Յ0.90 based on studies reporting Ͼ90% sensitivity and specificity to detect PAD compared with angiography. 2,3 These studies were limited in that they included mostly older white men with PAD or who were at high risk for PAD and compared them with a younger healthy group. A recent metaanalysis of 8 studies of diverse populations, including diabetic patients, confirmed a high specificity but lower sensitivity (at best Ͻ80%) than that reported in earlier studies. 11 Similar to other vascular markers such as carotid intimamedia thickness 12 or coronary artery calcium score, 13 standardization of the techniques used to measure the ABI and the calculation and interpretation of its values is necessary. Aims and ScopeThe goals for this document are to provide a comprehensive review of the relevant literature on the measurement of the The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on September 10, 2012. A copy of the document is available at http://my.americanheart.org/statements by selecting either the "By Topic" link or the "By Publication Date" link. To purchase additional repri...

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“…The CAFE heart rate study focused on the importance of heart rate as a determinant of this effect and showed that a lower heart rate induced by beta-blockade was associated with higher aortic systolic pressure and pulse pressure, an effect that was primarily attributed to increased central pressure wave reflections at lower heart rates ( Fig. 2) (81). As possible mechanisms that account for the inverse relationship between heart rate and aortic pressure, the authors discuss an increase of central systolic pressure attributable to a shift of the reflected wave into late systole due to the reduction in ejection duration by heart rate reduction, and an increased stroke volume secondary to heart rate reduction and better diastolic filling (Frank-Starling mechanism), which is then ejected into the proximal aorta with its windkessel function.…”

Section: Pathophysiology Of Elevated Heart Ratementioning

confidence: 99%

“…ED ϭ ejection duration; T0 ϭ onset of the forward-ejected wave; Tr ϭ time to return at the aorta of the backward-reflected wave from T0. Adapted from Safar et al (81).…”

Section: Pathophysiology Of Elevated Heart Ratementioning

confidence: 99%

Vascular Pathophysiology in Response to Increased Heart Rate

Custodis

Schirmer

Baumhäkel

et al. 2010

Journal of the American College of Cardiology

221

156

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This review summarizes the current literature and the open questions regarding the physiology and pathophysiology of the mechanical effects of heart rate on the vessel wall and the associated molecular signaling that may have implications for patient care. Epidemiological evidence shows that resting heart rate is associated with cardiovascular morbidity and mortality in the general population and in patients with cardiovascular disease. As a consequence, increased resting heart rate has emerged as an independent risk factor both in primary prevention and in patients with hypertension, coronary artery disease, and myocardial infarction. Experimental and clinical data suggest that sustained elevation of heart rate-independent of the underlying trigger-contributes to the pathogenesis of vascular disease. In animal studies, accelerated heart rate is associated with cellular signaling events leading to vascular oxidative stress, endothelial dysfunction, and acceleration of atherogenesis. The underlying mechanisms are only partially understood and appear to involve alterations of mechanic properties such as reduction of vascular compliance. Clinical studies reported a positive correlation between increased resting heart rate and circulating markers of inflammation. In patients with coronary heart disease, increased resting heart rate may influence the clinical course of atherosclerotic disease by facilitation of plaque disruption and progression of coronary atherosclerosis. While a benefit of pharmacological or interventional heart rate reduction on different vascular outcomes was observed in experimental studies, prospective clinical data are limited, and prospective evidence determining whether modulation of heart rate can reduce cardiovascular events in different patient populations is needed.

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Statins, Central Blood Pressure, and Blood Pressure Amplification

Cited by 29 publications

References 22 publications

Role of Pulse Pressure Amplification in Arterial Hypertension

Role of Pulse Pressure Amplification in Arterial Hypertension

Measurement and Interpretation of the Ankle-Brachial Index

Vascular Pathophysiology in Response to Increased Heart Rate

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