Augmentation index and central aortic blood pressure in patients with abdominal aortic aneurysms

Ruegg, Gion; Mason, Rebecca H.; Hardinge, Maxine; Perkins, Jeremy; Husmann, Marc; Russi, Erich W.; Bloch, Konrad E.; Stradling, John; Kohler, Malcolm

doi:10.1097/hjh.0b013e32833e1187

Cited by 16 publications

(15 citation statements)

References 29 publications

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“…However, these data do not completely rule out a potential link between blood pressure and AAA in general or in different animal models. Recent studies have shown that, in humans with AAA, elevated aortic blood pressure is a considerable risk factor for AAA progression [6]. Therefore, it remains a clinically relevant question to examine the role blood pressure plays in AAA formation and progression.…”

Section: Introductionmentioning

confidence: 99%

Nifedipine attenuation of abdominal aortic aneurysm in hypertensive and non-hypertensive mice: Mechanisms and implications

Miao

Siu

Cai

2015

Journal of Molecular and Cellular Cardiology

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Rupture of abdominal aortic aneurysm (AAA) is a lethal event. No oral medicine has been available to prevent or treat AAA. We have recently identified a novel mechanism of eNOS uncoupling by which AAA develops, in Angiotensin II (Ang II) infused hyperphenylalaninemia 1 (hph-1) mice. Using this unique model we investigated effects on AAA formation of the L-type calcium channel blocker nifedipine, in view of the unclear relationship between hypertension and AAA, and unclear mechanisms of aneurysm protective effects of some blood pressure lowering drugs. Six-month old hph-1 mice were infused with Ang II (0.7 mg/kg/day) for 2 weeks, and fed nifedipine chow at two different doses (5 and 20 mg/kg/day). While the high dose of nifedipine reduced blood pressure, the lower dose had no effect. Interestingly, the incidence rate of AAA dropped from 71% to 7 and 12.5% for low and high dose nifedipine, respectively. Expansion of abdominal aorta, determined by ultrasound imaging, was abolished by both doses of nifedipine, which recoupled eNOS completely to improve NO bioavailability. Both also abrogated aortic superoxide production. Of note, Ang II activation of NADPH oxidase in vascular smooth muscle cells and endothelial cells, known to uncouple eNOS, was also attenuated by nifedipine. Although low dose was a sub-pressor while the high dose reduced blood pressure via inhibition of calcium channels, both doses were highly effective in preventing AAA by preserving eNOS coupling activity to eliminate sustained oxidative stress from uncoupled eNOS. These data demonstrate that oral treatment of nifedipine is highly effective in preserving eNOS function to attenuate AAA formation. Nifedipine may be used for AAA prevention either at low dose to AAA risk group, or at high dose to patients with co-existing hypertension.

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Section: Introductionmentioning

confidence: 99%

Nifedipine attenuation of abdominal aortic aneurysm in hypertensive and non-hypertensive mice: Mechanisms and implications

Miao

Siu

Cai

2015

Journal of Molecular and Cellular Cardiology

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“…The 17 studies included a total of 4873 patients. The definitions of AAA and PAD, cohort size (range 30–1658) and population characteristics varied between studies ( Table ; an expanded version is available as Table S2 , supporting information). Only one study was a specifically designed case–control study with the explicit aim of assessing the association between PAD and AAA growth.…”

Section: Resultsmentioning

confidence: 99%

“…Of the 17 identified studies, four were rated as high quality, nine as average quality and four as low quality ( Table S4 , supporting information). Four studies failed to report the exact AAA case definition and nine failed to report the exact PAD case definition used. Only five 10,21–23,27 studies adjusted their analyses to account for differences in initial AAA diameter, smoking and diabetes mellitus.…”

Section: Resultsmentioning

confidence: 99%

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Meta-analysis of the association between peripheral artery disease and growth of abdominal aortic aneurysms

Matthews¹,

Rowbotham

Moxon³

et al. 2017

British Journal of Surgery

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“…As for other case-control studies, the matching of the patients with controls is critical and its inherent limitations might explain the diversity of results. As far as indices of wave refl ection are concerned, augmentation index seems to be higher in aortic aneurysm (thoracic or abdominal) patients compared to controls [ 39 , 41 ]; however, it does not seem to be able to discriminate between patients with fast and slow progression of aortic aneurysm in their early phase [ 42 ] but rather in their late phase [ 43 ]. On the contrary, central BP shows a steady incremental value over peripheral BP in prediction of fast progression, dissection, and rupture of aortic aneurysm [ 43 ].…”

Section: Aortic Aneurysmsmentioning

confidence: 99%

Arterial Stiffness and Risk in Various Cardiovascular Diseases

Vlachopoulos

Terentes‐Printzios

Takazawa

et al. 2014

Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases

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Atherosclerotic disease comprises four major areas: coronary artery disease, cerebrovascular disease, peripheral arterial disease, and aortic aneurysm. Investigators have mainly focused on using arterial stiffness and central hemodynamics indices for primary prevention and prediction of risk in patients without cardiovascular disease. Their role in these patients is constantly evolving, and in some cases such as hypertensives and diabetics, their clinical signifi cance has been corroborated by recent guidelines and recommendations. Despite the overwhelming data for their predictive role in primary prevention, secondary prevention prognostic studies are lacking. Especially, data on the role of arterial stiffness in peripheral arterial disease patients, including patients with vasculogenic erectile dysfunction or aortic disease such as aortic aneurysm, Marfan syndrome, and coarctation of the aorta, emerge mostly from cross-sectional studies. Respectively, most prospective predictive studies of arterial stiffness have not used peripheral arterial disease or aortic disease endpoints as an exclusive outcome but preferably as a part of a composite cardiovascular endpoint. This chapter will focus on the link between arterial stiffness and risk of cardiovascular events and organ damage in other cardiovascular diseases such as peripheral arterial and aortic diseases.

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Augmentation index and central aortic blood pressure in patients with abdominal aortic aneurysms

Cited by 16 publications

References 29 publications

Nifedipine attenuation of abdominal aortic aneurysm in hypertensive and non-hypertensive mice: Mechanisms and implications

Nifedipine attenuation of abdominal aortic aneurysm in hypertensive and non-hypertensive mice: Mechanisms and implications

Meta-analysis of the association between peripheral artery disease and growth of abdominal aortic aneurysms

Arterial Stiffness and Risk in Various Cardiovascular Diseases

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