A Review of Cardiac Contractility Indices during LVAD Support

2013 ◽  
pp. 103-106
Author(s):  
P. Naiyanetr
Keyword(s):  
Cardiac Contractility ◽  
Lvad Support ◽  
Contractility Indices

CARDIAC CONTRACTILITY MEASURES OF LEFT VENTRICULAR SYSTOLIC FUNCTIONAL ASSESSMENT OF NORMAL AND DISEASED HEARTS

2009 ◽  
Vol 09 (04) ◽  
pp. 555-578
Author(s):  
DHANJOO N. GHISTA ◽  
LIANG ZHONG ◽  
THU-THAO LE ◽  
RU-SAN TAN
Keyword(s):  
Heart Failure ◽  
Functional Assessment ◽  
Systolic Function ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Medical Applications ◽  
Pressure Distributions ◽  
Blood Flow Velocities ◽  
Lv Systolic Function ◽  
Contractility Indices

Left ventricular (LV) contraction is the basis of LV systolic function, impairment of which underlies heart failure pathophysiology. Its accurate quantification in the form of LV contractility indices is imperative for diagnostic and follow-up assessment of LV systolic function in heart failure. Herein, we analyze LV contractile performance by focusing on LV contractility indices at different physiological organizational levels: from sarcomere dynamics to LV myocardial properties (such as elastic modulus and elastance), and from LV wall contractile stress development to the generation of intra-LV blood flow velocities and pressure distributions. Further, we present the development analyses of these indices and their medical applications. Using improved development of invasive and noninvasive techniques for measuring ventricular pressure, geometry, and volume, we show how these indices have become more amenable for clinical usage to obtain better patient assessment. The purpose of this paper is to present a comprehensive coverage of LV contraction physiology, indices to qualify LV contraction, formulation, and medical applications of some major intrinsic LV contractility indices, so as to provide the basis of functional assessment of normal versus diseased hearts.

Heat shock protein (HSP)-47 decreases in myocardium under LVAD-support

2005 ◽  
Vol 53 (S 01) ◽  
Author(s):  
C Skrabal ◽  
G Noon ◽  
R Southard ◽  
K Youker ◽  
M Loebe
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Lvad Support

Prolonged Exposure to Microgravity Reduces Cardiac Contractility and Initiates Remodeling in Drosophila

2020 ◽  
Author(s):  
Stanley Mark Walls ◽  
Soda Diop ◽  
Ryan Birse ◽  
Lisa Elmen ◽  
Zhouhui Gan ◽  
...  
Keyword(s):  
Prolonged Exposure ◽  
Cardiac Contractility

Cardioprotective and Vasoprotective Effects of Corticotropin-Releasing Hormone and Urocortins: Receptors and Signaling

2021 ◽  
pp. 107424842098530
Author(s):  
Sergey V. Popov ◽  
Ekaterina S. Prokudina ◽  
Alexander V. Mukhomedzyanov ◽  
Natalia V. Naryzhnaya ◽  
Huijie Ma ◽  
...  
Keyword(s):  
Mitochondrial Permeability Transition ◽  
Vascular Endothelial Cells ◽  
Isolated Heart ◽  
Cardiac Contractility ◽  
Permeability Transition Pore ◽  
Chronic Administration ◽  
Permeability Transition ◽  
Janus Kinase ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Despite the recent progress in research and therapy, cardiovascular diseases are still the most common cause of death worldwide, thus new approaches are still needed. The aim of this review is to highlight the cardioprotective potential of urocortins and corticotropin-releasing hormone (CRH) and their signaling. It has been documented that urocortins and CRH reduce ischemic and reperfusion (I/R) injury, prevent reperfusion ventricular tachycardia and fibrillation, and improve cardiac contractility during reperfusion. Urocortin-induced increase in cardiac tolerance to I/R depends mainly on the activation of corticotropin-releasing hormone receptor-2 (CRHR2) and its downstream pathways including tyrosine kinase Src, protein kinase A and C (PKA, PKCε) and extracellular signal-regulated kinase (ERK1/2). It was discussed the possibility of the involvement of interleukin-6, Janus kinase-2 and signal transducer and activator of transcription 3 (STAT3) and microRNAs in the cardioprotective effect of urocortins. Additionally, phospholipase-A2 inhibition, mitochondrial permeability transition pore (MPT-pore) blockade and suppression of apoptosis are involved in urocortin-elicited cardioprotection. Chronic administration of urocortin-2 prevents the development of postinfarction cardiac remodeling. Urocortin possesses vasoprotective and vasodilator effect; the former is mediated by PKC activation and prevents an impairment of endothelium-dependent coronary vasodilation after I/R in the isolated heart, while the latter includes both cAMP and cGMP signaling and its downstream targets. As CRHR2 is expressed by both cardiomyocytes and vascular endothelial cells. Urocortins mediate both endothelium-dependent and -independent relaxation of coronary arteries.

scholarly journals Device interaction between Cardiac‐Contractility‐Modulation (CCM) und subcutaneus Defibrillator (S‐ICD)

2021 ◽  
Author(s):  
Luca Trolese ◽  
Thomas Faber ◽  
Alexander Gressler ◽  
Johannes Steinfurt ◽  
Judith Stuplich ◽  
...  
Keyword(s):  
Cardiac Contractility ◽  
Cardiac Contractility Modulation ◽  
Device Interaction

scholarly journals Regulation of Cardiac PKA Signaling by cAMP and Oxidants

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 663
Author(s):  
Friederike Cuello ◽  
Friedrich W. Herberg ◽  
Konstantina Stathopoulou ◽  
Philipp Henning ◽  
Simon Diering
Keyword(s):  
Contractile Function ◽  
Cardiac Contractility ◽  
Cellular Protein ◽  
Cardiac Contractile Function ◽  
Cardiac Contractile ◽  
Main Driver ◽  
Dependent Protein ◽  
Relevant Regulation ◽  
Protein Dysfunction ◽  
Substrate Proteins

Pathologies, such as cancer, inflammatory and cardiac diseases are commonly associated with long-term increased production and release of reactive oxygen species referred to as oxidative stress. Thereby, protein oxidation conveys protein dysfunction and contributes to disease progression. Importantly, trials to scavenge oxidants by systemic antioxidant therapy failed. This observation supports the notion that oxidants are indispensable physiological signaling molecules that induce oxidative post-translational modifications in target proteins. In cardiac myocytes, the main driver of cardiac contractility is the activation of the β-adrenoceptor-signaling cascade leading to increased cellular cAMP production and activation of its main effector, the cAMP-dependent protein kinase (PKA). PKA-mediated phosphorylation of substrate proteins that are involved in excitation-contraction coupling are responsible for the observed positive inotropic and lusitropic effects. PKA-actions are counteracted by cellular protein phosphatases (PP) that dephosphorylate substrate proteins and thus allow the termination of PKA-signaling. Both, kinase and phosphatase are redox-sensitive and susceptible to oxidation on critical cysteine residues. Thereby, oxidation of the regulatory PKA and PP subunits is considered to regulate subcellular kinase and phosphatase localization, while intradisulfide formation of the catalytic subunits negatively impacts on catalytic activity with direct consequences on substrate (de)phosphorylation and cardiac contractile function. This review article attempts to incorporate the current perception of the functionally relevant regulation of cardiac contractility by classical cAMP-dependent signaling with the contribution of oxidant modification.

Cardiac contractility assessment: A case study with clear impact and relevance of preclinical data

2012 ◽  
Vol 66 (2) ◽  
pp. 174 ◽  
Author(s):  
Pierre Lainée ◽  
Karen Philp ◽  
Alex Harmer ◽  
Matthew Bridgland-Taylor ◽  
Jackie Moors ◽  
...  
Keyword(s):  
Cardiac Contractility ◽  
Preclinical Data
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