Transmural Heterogeneity of Cellular Level Power Output Is Reduced in Human Heart Failure

Haynes, Paul A.; Nava, Kristofer E.; Lawson, Benjamin A.; Chung, Charles S.; Mitov, Mihail I.; Campbell, Stuart G.; Stromberg, Arnold J.; Sadayappan, Sakthivel; Bonnell, Mark R.; Hoopes, Charles W.; Campbell, Kenneth S.

doi:10.1016/j.healun.2014.01.456

Cited by 9 publications

(10 citation statements)

References 38 publications

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“…Decay time of the Ca 2+ transient and the time required for 50% length relaxation increased with age, but not uniformly across the EPI, MID, and ENDO rat ventricular myocytes (Haynes et al. ). Mathematical modeling suggests that the prolonged action potential duration in ENDO myocytes is consistent with an enhanced amplitude of the sustained K + current ( I ss ) and larger influx of Ca 2+ ions via L‐type Ca 2+ channels, the latter resulting in increased loading of the SR (Pandit et al.…”

Section: Introductionmentioning

confidence: 99%

Regional effects of streptozotocin-induced diabetes on shortening and calcium transport in epicardial and endocardial myocytes from rat left ventricle

et al. 2016

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In the heart, the left ventricle pumps blood at higher pressure than the right ventricle. Within the left ventricle, the electromechanical properties of ventricular cardiac myocytes vary transmurally and this may be related to the gradients of stress and strain experienced in vivo across the ventricular wall. Diabetes is also associated with alterations in hemodynamic function. The aim of this study was to investigate shortening and Ca2+ transport in epicardial (EPI) and endocardial (ENDO) left ventricular myocytes in the streptozotocin (STZ)‐induced diabetic rat. Shortening, intracellular Ca2+ and L‐type Ca2+ current (I Ca,L) were measured by video detection, fura‐2 microfluorimetry, and whole‐cell patch clamp techniques, respectively. Time to peak (TPK) shortening was prolonged to similar extents in ENDO and EPI myocytes from STZ‐treated rats compared to ENDO and EPI myocytes from controls. Time to half (THALF) relaxation of shortening was prolonged in ENDO myocytes from STZ‐treated rats compared to ENDO controls. TPK Ca2+ transient was prolonged in ENDO myocytes from STZ‐treated rats compared to ENDO controls. THALF decay of the Ca2+ transient was prolonged in ENDO myocytes from STZ‐treated rats compared to ENDO controls. Sarcoplasmic reticulum (SR) fractional release of Ca2+ was reduced in EPI myocytes from STZ‐treated rats compared to EPI controls. IC a,L activation, inactivation, and recovery from inactivation were not significantly altered in EPI and ENDO myocytes from STZ‐treated rats or controls. Regional differences in Ca2+ transport may partly underlie differences in ventricular myocyte shortening across the wall of the healthy and the STZ‐treated rat left ventricle.

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Section: Introductionmentioning

confidence: 99%

Regional effects of streptozotocin-induced diabetes on shortening and calcium transport in epicardial and endocardial myocytes from rat left ventricle

et al. 2016

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“…However, in vivo measurements of electrical activity and transmural myofibre mechanics in adult mongrel dogs during normal sinus rhythm or atrial pacing showed a surprisingly significant transmural gradient in the onset of myofibre shortening; the mean propagation velocity of myofibre shortening from endocardium to epicardium was 0.25 m/s [ 54 ]. In addition, the recent study on preparations from nonfailing human hearts indicated that shortening velocity of myocytes from different regions of LV does not exhibit significant differences [ 55 ]. Reasons of these contradictions are unclear.…”

Section: Discussionmentioning

confidence: 99%

Effect of Transmural Differences in Excitation-Contraction Delay and Contraction Velocity on Left Ventricle Isovolumic Contraction: A Simulation Study

Vaverka¹,

Burša²,

Sumbera

et al. 2018

BioMed Research International

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Recent studies have shown that left ventricle (LV) exhibits considerable transmural differences in active mechanical properties induced by transmural differences in electrical activity, excitation-contraction coupling, and contractile properties of individual myocytes. It was shown that the time between electrical and mechanical activation of myocytes (electromechanical delay: EMD) decreases from subendocardium to subepicardium and, on the contrary, the myocyte shortening velocity (MSV) increases in the same direction. To investigate the physiological importance of this inhomogeneity, we developed a new finite element model of LV incorporating the observed transmural gradients in EMD and MSV. Comparative simulations with the model showed that when EMD or MSV or both were set constant across the LV wall, the LV contractility during isovolumic contraction (IVC) decreased significantly ((dp/dt)max⁡ was reduced by 2 to 38% and IVC was prolonged by 18 to 73%). This was accompanied by an increase of transmural differences in wall stress. These results suggest that the transmural differences in EMD and MSV play an important role in physiological contractility of LV by synchronising the contraction of individual layers of ventricular wall during the systole. Reduction or enhancement of these differences may therefore impair the function of LV and contribute to heart failure.

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“…Ageing also seems to play a role in the variability of results. The decay time of the Ca 2+ transient and the time required for 50% length relaxation increased with age, but not uniformly across the EPI, MID and ENDO rat ventricular myocytes (Haynes et al., ).…”

Section: Introductionmentioning

confidence: 99%

Cell shortening and calcium dynamics in epicardial and endocardial myocytes from the left ventricle of Goto‐Kakizaki type 2 diabetic rats

Smail

Kury

Qureshi

et al. 2018

Experimental Physiology

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Diabetic cardiomyopathy is considered to be one of the major diabetes-associated complications, and the pathogenesis of cardiac dysfunction is not well understood. The electromechanical properties of cardiac myocytes vary across the walls of the chambers. The aim of this study was to investigate shortening and Ca transport in epicardial (EPI) and endocardial (ENDO) left ventricular myocytes in the Goto-Kakizaki (GK) type 2 diabetic rat heart. Shortening and intracellular Ca transients were measured by video edge detection and fluorescence photometry. Myocyte surface area was increased in EPI-GK and ENDO-GK compared with control EPI-CON and ENDO-CON myocytes. Time to peak shortening was prolonged in EPI-GK compared with EPI-CON and in ENDO-CON compared with EPI-CON myocytes. Time to half-relaxation of shortening and time to peak Ca transient were prolonged in EPI-GK compared with EPI-CON myocytes. Time to half-decay of the Ca transient was prolonged in EPI-CON compared with EPI-GK and in EPI-CON compared with ENDO-CON myocytes. The amplitude of shortening and the Ca transient were unaltered in EPI-GK and ENDO-GK compared with their respective controls. Sarcoplasmic reticulum Ca and myofilament sensitivity to Ca were unaltered in EPI-GK and ENDO-GK compared with their respective controls. Regional differences in Ca signalling in healthy and diabetic myocytes might account for variation in the dynamics of myocyte shortening. Further studies will be required to clarify the mechanisms underlying regional differences in the time course of shortening and the Ca transient in EPI and ENDO myocytes from diabetic and control hearts.

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Transmural Heterogeneity of Cellular Level Power Output Is Reduced in Human Heart Failure

Cited by 9 publications

References 38 publications

Regional effects of streptozotocin-induced diabetes on shortening and calcium transport in epicardial and endocardial myocytes from rat left ventricle

Regional effects of streptozotocin-induced diabetes on shortening and calcium transport in epicardial and endocardial myocytes from rat left ventricle

Effect of Transmural Differences in Excitation-Contraction Delay and Contraction Velocity on Left Ventricle Isovolumic Contraction: A Simulation Study

Cell shortening and calcium dynamics in epicardial and endocardial myocytes from the left ventricle of Goto‐Kakizaki type 2 diabetic rats

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