Dynamic Changes in Aortic Vascular Stiffness in Patients Bridged to Transplant With Continuous-Flow Left Ventricular Assist Devices

Patel, Amit; Dodson, R. Blair; Cornwell, William K.; Hunter, Kendall S.; Cleveland, Joseph C.; Brieke, Andreas; Lindenfeld, JoAnn; Ambardekar, Amrut V.

doi:10.1016/j.jchf.2016.12.009

Cited by 31 publications

(22 citation statements)

References 23 publications

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“…Mechanical unloading of the heart with the use of CF-LVAD alters normal hemodynamic forces due to the nonphysiologic, nonpulsatile flow patterns. Our previous work demonstrated that aortas from CF-LVAD patients exhibited marked decreases in distensibility and increased vessel stiffness that was associated with increased collagen deposition ( 14 , 15 ). Additionally, we showed that SMC-specific PTEN depletion in mice promotes spontaneous vascular fibrosis ( 31 ).…”

Section: Resultsmentioning

confidence: 99%

PTEN deficiency promotes pathological vascular remodeling of human coronary arteries

Moulton¹,

Li²,

Strand³

et al. 2018

JCI Insight

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Phosphatase and tensin homolog (PTEN) is an essential regulator of the differentiated vascular smooth muscle cell (SMC) phenotype. Our goal was to establish that PTEN loss promotes SMC dedifferentiation and pathological vascular remodeling in human atherosclerotic coronary arteries and nonatherosclerotic coronary arteries exposed to continuous-flow left ventricular assist devices (CF-LVADs). Arteries were categorized as nonatherosclerotic hyperplasia (NAH), atherosclerotic hyperplasia (AH), or complex plaque (CP). NAH coronary arteries from CF-LVAD patients were compared to NAH coronaries from non-LVAD patients. Intimal PTEN and SMC contractile protein expression was reduced compared with the media in arteries with NAH, AH, or CP. Compared with NAH, PTEN and SMC contractile protein expression was reduced in the media and intima of arteries with AH and CP. NAH arteries from CF-LVAD patients showed marked vascular remodeling and reduced PTEN and α-smooth muscle actin (αSMA) in medial SMCs compared with arteries from non-LVAD patients; this correlated with increased medial collagen deposition. Mechanistically, compared with ApoE–/– mice, SMC-specific PTEN-null/ApoE–/– double-knockout mice exhibited accelerated atherosclerosis progression and increased vascular fibrosis. By microarray and validated quantitative RT-PCR analysis, SMC PTEN deficiency promotes a global upregulation of proinflammatory and profibrotic genes. We propose that PTEN is an antiinflammatory, antifibrotic target that functions to maintain SMC differentiation. SMC loss of PTEN results in pathological vascular remodeling of human arteries.

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Section: Resultsmentioning

confidence: 99%

PTEN deficiency promotes pathological vascular remodeling of human coronary arteries

Moulton¹,

Li²,

Strand³

et al. 2018

JCI Insight

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“…It appears pulsatile volume unloading that may be more important than pressure unloading. Prior researches suggest that reduced pulsatility may contribute to ischemic and hemorrhagic stroke [ 39 ] and oxidative stress [ 40 ], as well as increased aortic stiffness [ 41 ]. Therefore, many studies improving volume unloading performance focus on designing pulsatile control strategies for CF-LVAD [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Computational analysis of the hemodynamic characteristics under interaction influence of β-blocker and LVAD

Zhang

Chang

et al. 2018

BioMed Eng OnLine

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BackgroundHemodynamic characteristics of the interaction influence among support level and model of LVAD, and coupling β-blocker has not been reported.MethodsIn this study, the effect of support level and model of LVAD on cardiovascular hemodynamic characteristics is investigated. In addition, the effect of β-blocker on unloading with LVAD is analyzed to elucidate the mechanism of LVAD coupling β-blocker. A multi-scale model from cell level to system level is proposed. Moreover, LVAD coupling β-blocker has been researching to explain the hemodynamics of cardiovascular system.ResultsMyocardial force was decreased along with the increase of support level of LVAD, and co-pulse mode was the lowest among the three support modes. Additionally, the β-blocker combined with LVAD significantly reduced the left ventricular volume compared with LVAD support without β-blocker. However, the left ventricular pressure under both cases has no significant difference. External work of right ventricular was increased along with the growth of support level of only LVAD. The LVAD under co-pulse mode achieved the lowest right-ventricular EW among the three support modes.ConclusionsCo-pulse mode with β-blocker could be an optimal strategy for promoting cardiac structure and function recovery.

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“…; Patel et al . ). It is important to underline that in pulsatile circulations, aortic stiffness increases the transmission of pulsatility to the periphery, and, if exceeding normal pulsatility, is detrimental to the brain and other end‐organs (Webb et al .…”

Section: Schematic Of the Device Location And Components And Typical mentioning

confidence: 97%

CrossTalk proposal: Blood flow pulsatility in left ventricular assist device patients is essential to maintain normal brain physiology

Stöhr

McDonnell

Colombo

et al. 2018

The Journal of Physiology

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Dynamic Changes in Aortic Vascular Stiffness in Patients Bridged to Transplant With Continuous-Flow Left Ventricular Assist Devices

Cited by 31 publications

References 23 publications

PTEN deficiency promotes pathological vascular remodeling of human coronary arteries

PTEN deficiency promotes pathological vascular remodeling of human coronary arteries

Computational analysis of the hemodynamic characteristics under interaction influence of β-blocker and LVAD

CrossTalk proposal: Blood flow pulsatility in left ventricular assist device patients is essential to maintain normal brain physiology

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