scholarly journals Extracellular potassium dynamics in the border zone during acute myocardial ischemia in a canine model

1988 ◽  
Vol 11 (2) ◽  
pp. 422-430 ◽  
Author(s):  
Daniel David ◽  
Eric L. Michelson ◽  
Masahito Naito ◽  
Leonard S. Dreifus
Circulation ◽  
1988 ◽  
Vol 77 (5) ◽  
pp. 1125-1138 ◽  
Author(s):  
R Coronel ◽  
J W Fiolet ◽  
F J Wilms-Schopman ◽  
A F Schaapherder ◽  
T A Johnson ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hector Martinez-Navarro ◽  
Ana Mincholé ◽  
Alfonso Bueno-Orovio ◽  
Blanca Rodriguez

AbstractAcute myocardial ischemia is a precursor of sudden arrhythmic death. Variability in its manifestation hampers understanding of arrhythmia mechanisms and challenges risk stratification. Our aim is to unravel the mechanisms underlying how size, transmural extent and location of ischemia determine arrhythmia vulnerability and ECG alterations. High performance computing simulations using a human torso/biventricular biophysically-detailed model were conducted to quantify the impact of varying ischemic region properties, including location (LAD/LCX occlusion), transmural/subendocardial ischemia, size, and normal/slow myocardial propagation. ECG biomarkers and vulnerability window for reentry were computed in over 400 simulations for 18 cases evaluated. Two distinct mechanisms explained larger vulnerability to reentry in transmural versus subendocardial ischemia. Macro-reentry around the ischemic region was the primary mechanism increasing arrhythmic risk in transmural versus subendocardial ischemia, for both LAD and LCX occlusion. Transmural micro-reentry at the ischemic border zone explained arrhythmic vulnerability in subendocardial ischemia, especially in LAD occlusion, as reentries were favoured by the ischemic region intersecting the septo-apical region. ST elevation reflected ischemic extent in transmural ischemia for LCX and LAD occlusion but not in subendocardial ischemia (associated with mild ST depression). The technology and results presented can inform safety and efficacy evaluation of anti-arrhythmic therapy in acute myocardial ischemia.


1984 ◽  
Vol 48 (1) ◽  
pp. 18-31 ◽  
Author(s):  
KENICHI MITSUNAMI ◽  
TAKEHISA FUKUHARA ◽  
SHOTARO KATO ◽  
KEIZO BITO ◽  
MASAHIKO KINOSHITA ◽  
...  

2016 ◽  
Vol 40 (3-4) ◽  
pp. 770-780 ◽  
Author(s):  
Xu Liu ◽  
Xiuzhong Li ◽  
Songgang Ji ◽  
Xiaobo Cui ◽  
Mingchun Li

Background/Aims: To study the spectrum-effect relationship and effective components of Ligusticum Chuanxiong Hort. (LCH) on the protection of canine myocardial ischemia. Methods: Fingerprint spectrum of LCH extracts was developed using high performance liquid chromatography (HPLC), and a canine model of acute myocardial ischemia was established by ligating the coronary artery. Bivariate correlation analysis and multivariate regression analysis were used to correlate the pharmacodynamics of LCH extract and its common peaks in HPLC. Results: The bioactive components of LCH were ligustrazine, ferulic acid, cnidilide and ligustilide. Ligustrazine and ferulic acid could significantly reduce serum lactic acid in canine model of acute myocardial ischemia, while ligustilide could significantly reduce the elevation of serum free fatty acid. Conclusions: The spectrum-effect relationship study shows that the effective components of LCH are ligustrazine, ferulic acid, cnidilide and ligustilide, which have protective effect on myocardial ischemia.


1999 ◽  
Vol 07 (04) ◽  
pp. 553-574 ◽  
Author(s):  
MAHESH SHENAI ◽  
BORIS GRAMATIKOV ◽  
NITISH V. THAKOR

A two-dimensional modified Luo-Rudy model was created to represent a 40 mm by 40 mm slab of myocardial tissue. An inhomogeneity was introduced to simulate acute myocardial ischemia, with components of hyperkalemia, acidosis and anoxia. Simulations were carried out for various degrees of ischemia, to study both the interaction of the propagation front with the inhomogeneity, and the reconstructed signals. The simulations utilized a modified LR model, with a realistic anisotropy of myocardial tissue. Each cluster (.4 mm ×.4 mm) was given bulk electric properties, Rx and Ry (25Ω and 250Ω, respectively). The slab was stimulated and the 2D depolarization pattern was computed by numerical integration. To study ischemia, a circular inhomogeneity with concentric regions (ro=12.8 mm{border zone, BZ} , ri=11.2 mm{extreme zone, EZ} ) regions was introduced in the model. From the 2D simulations and the regional action potentials (AP), unipolar and bipolar lead potentials were reconstructed. Time-frequency decomposition was performed on the lead signals by wavelet analysis. Isochrone and (dV/dt) max maps were obtained to study depolarization. Our results indicate that spatial inhomogeneities yield dramatic spatial dispersion of the wavefront and are the origin of mid-frequency intra-QRS components in cardiac signals. Severe APD shortening and spatial distortion of the isochrone and upstroke maps are also observed.


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