Heart Disease is the leading cause of death in the United States contributing to one in every four deaths 1 There is a need for novel treatments to strengthen and prevent the degradation of myocardium ID: 931565
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Positive Inotropic Response to (-)-Epigallocatechin-3-Gallate in Isolated Human Myocardium
Heart Disease is the leading cause of death in the United States, contributing to one in every four deaths[1]There is a need for novel treatments to strengthen and prevent the degradation of myocardium
The consumption of green tea has been linked to decreased risk of cardiovascular disease[2]Epigallocatechin gallate (EGCG) has been shown to increase the contractility of murine myocardium[3]The effect of EGCG on human myocardium is not known
EGCG’s positive effects on the contractility on failing human cardiac muscle opens the door for EGCG to be investigated as a potential therapy or preventative recommendation for cardiovascular diseasesIf the trend in non-failing muscle continues, investigation into why only atrophied myocardium responds to EGCG may be necessary
1. “Heart Disease Facts & Statistics.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention2. Kuriyama S, Shimazu T, Ohmori K, et al. Green Tea Consumption and Mortality Due to Cardiovascular Disease, Cancer, and All Causes in Japan: The Ohsaki Study. JAMA. 3. Feng, Wei et al. “Coordinated regulation of murine cardiomyocyte contractility by nanomolar (-)-epigallocatechin-3-gallate, the major green tea catechin.” Molecular pharmacology vol. 82,5 (2012): 993-1000.
Figure 2: EGCG’s effects on developed tension in failing (n=4) and non-failing (n=2) muscles
BACKGROUND
METHODS
RESULTS
Austin Hare, Kyra K.
Peczkowski
, Farbod
Fazlollahi
, Mohammed A.
Mashali
, Amanda W. Huang, Salome A.
Kiduko
, Nancy S. Saad, Mohammad T.
Elnakish, Courtney M. Campbell, Paul M.L. JanssenDepartment of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States
To determine if EGCG has a significant effect on the contractility of failing and non-failing human myocardium.
Tissue Acquisition
Human hearts were acquired through Columbus-area hospital transplant programsTwo categories of heartsFailing: Replaced heart from transplantNon-Failing: Instances of organ donation where the heart could not be usedExperimental SetupSmall linear multicellular ventricular preparations were excised and suspended between two hooksThe muscle was stimulated to contraction under physiological conditions (37 ◦C, 1 Hz)Dose Response ProtocolEGCG was gradually introduced into the system through a dose response protocol (1.0 μM – 150 μM)
Figure 1: EGCG, a catecholamine, is a component of green tea
BIBLIOGRAPHY
CONCLUSIONS
FUTURE DIRECTIONS
So far, EGCG has had a positive dose dependent effect (EC
50
~22
±
~11 μM) on the force of contraction of failing human myocardium (Figure 2)
Currently, EGCG has not made an impact on the contraction of non-failing tissue (Figure 2)
Relatively consistent TTP and RT50 measurements support that EGCG is not changing the kinetics of the muscles
Figure 3:
EGCG’s effects on TTP and RT50 in failing (n=4) and non-failing (n=2) muscles
0
EPIGALLOCATECHIN GALLATE
AIM