The ?border zone? in acute myocardial ischemia ? A histochemical, biochemical and ultrastructural study in the canine heart T. Fukuhara, K. Mitsunami, K. Bito, M. Kinoshita, S. Kawakita. The First Dept. of Internal Medicine, Shiga University of Medical Science, Otsu, Japan

1981 ◽  
Vol 13 ◽  
pp. 45
Keyword(s):  
Internal Medicine ◽  
Myocardial Ischemia ◽  
Ultrastructural Study ◽  
Medical Science ◽  
Acute Myocardial Ischemia ◽  
Border Zone ◽  
Canine Heart

scholarly journals The border zone in acute myocardial ischemia in the dog. A histochemical, biochemical and ultrastructural study.

1984 ◽  
Vol 48 (1) ◽  
pp. 18-31 ◽  
Author(s):  
KENICHI MITSUNAMI ◽  
TAKEHISA FUKUHARA ◽  
SHOTARO KATO ◽  
KEIZO BITO ◽  
MASAHIKO KINOSHITA ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ultrastructural Study ◽  
Acute Myocardial Ischemia ◽  
Border Zone

scholarly journals High arrhythmic risk in antero-septal acute myocardial ischemia is explained by increased transmural reentry occurrence

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hector Martinez-Navarro ◽  
Ana Mincholé ◽  
Alfonso Bueno-Orovio ◽  
Blanca Rodriguez
Keyword(s):  
Myocardial Ischemia ◽  
High Performance ◽  
Acute Myocardial Ischemia ◽  
Border Zone ◽  
Apical Region ◽  
Efficacy Evaluation ◽  
Detailed Model ◽  
Subendocardial Ischemia ◽  
Ischemic Region ◽  
The Impact

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.

COMPUTER MODELS OF DEPOLARIZATION ALTERATIONS INDUCED BY MYOCARDIAL ISCHEMIA: THE EFFECT OF SUPERIMPOSED ISCHEMIC INHOMOGENEITIES ON PROPAGATION IN SPACE AND TIME-FREQUENCY DOMAINS

1999 ◽  
Vol 07 (04) ◽  
pp. 553-574 ◽  
Author(s):  
MAHESH SHENAI ◽  
BORIS GRAMATIKOV ◽  
NITISH V. THAKOR
Keyword(s):  
Myocardial Ischemia ◽  
Action Potentials ◽  
Spatial Dispersion ◽  
Acute Myocardial Ischemia ◽  
Border Zone ◽  
Myocardial Tissue ◽  
Time Frequency ◽  
Frequency Decomposition ◽  
Propagation Front ◽  
Frequency Domains

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.

Heparin from Intestine and Lung Source Administered in Large Dose to Dogs with Acute Myocardial Ischemia

1978 ◽  
Vol 40 (02) ◽  
pp. 407-417
Author(s):  
Michael J Saliba ◽  
Richard J Pavalec
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Adenosine Triphosphate ◽  
Intestinal Mucosa ◽  
Large Dose ◽  
Acute Myocardial Ischemia ◽  
Ischemic Myocardium ◽  
Atp Levels ◽  
Initial Control ◽  
The Difference

SummaryIntestinal mucosa heparin (IMH) and beef lung heparin (BLH) were infused into dogs subjected to myocardial ischemia by intermittent coronary artery occlusions. The IMH was from a mixture of beef, sheep, and pig intestinal mucosa. Initial control occlusion and recovery was followed by a second occlusion with 60,000 units of IMH or BLH added. Electrocardiographic S-T segment elevations (ST) were measured acutely. There were no significant differences in ST in non-ischemic myocardium before occlusions or with occlusions. In ischemic myocardium, IMH significantly lowered control ST 84% in amount (t = 6.1 p <0.00005), and 76% in number (t = 11.6 p <0.00001). BLH lowered control ST a significant, lesser, 36% in amount (t = 3.6 p <0.008), and 35% in number (t = 3.2 p <0.01). The difference between IMH and BLH in ischemic myocardium was a significant 48% in amount (t = 4.0 p <0.0007), and 41% in number (t = 2.0 p <0.06). Myocardial adenosine triphosphate (ATP) levels were assayed after 90 min. ATP levels were 31% higher in both ischemic and non-ischemic myocardium in IMH-treated dogs than in BLH- treated. It was concluded that IMH and BLH are functionally different, and IMH was significantly more effective.

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