Study of the Early Electrophysiological Changes Resulting from Subendocardial Ischemia Using an Intracavitary Electrode Catheter

1984 ◽  
pp. 117-130
Author(s):  
Robert M. Donaldson ◽  
Peter Taggart ◽  
Anthony F. Rickards
Keyword(s):  
Subendocardial Ischemia

scholarly journals Cardioprotective effects of compound ALM-802 on subendocardial ischemia models

2021 ◽  
pp. 18-22
Author(s):  
I. B. Tsorin ◽  
V. V. Barchukov ◽  
M. B. Vititnova ◽  
A. M. Likhosherstov ◽  
G. V. Mokrov ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Cardioprotective Effect ◽  
Rat Models ◽  
Subendocardial Ischemia ◽  
Anesthetized Rats ◽  
St Segment ◽  
Cardioprotective Effects

The investigation purpose. N1-(2,3,4-trimethoxybenzyl)-N2-{2-[(2,3,4-trimethoxybenzyl)amino]ethyl}-1,2-ethanediamine (ALM-802 compounds) cardioprotective effect has been studied in rat models of subendocardial ischemia caused by isoproterenol and dobutamine. Material and methods. Acute subendocardial myocardial ischemia in anesthetized rats (urethane 1300 mg/kg, i.p.) was caused by infusion of isoproterenol (20 µg/kg/min i.v.) or dobutamine (80 µg/kg/min i.v.). Results. It was shown that in anesthetized rats, isoproterenol and dobutamine caused almost the same ST-segment depression in the II standard ECG lead. The compound ALM-802 (2 mg/kg i.v.), administered 2 minutes before the infusion start of isoproterenol or dobutamine, equally prevented the occurrence of ischemic changes on the ECG. Conclusion. The non-selective beta-adrenomimetic isoproterenol and the selective β1-adrenomimetic dobutamine cause subendocardial ischemia of the same intensity in anesthetized rats. The compound ALM-802 has a pronounced anti-ischemic effect on both models.

scholarly journals A clinical method for detecting subendocardial ischemia after cardiopulmonary bypass

1975 ◽  
Vol 69 (1) ◽  
pp. 30-39 ◽  
Author(s):  
Peter A. Philips ◽  
Alan T. Marty ◽  
Alfonso M. Miyamoto ◽  
Martin D. McCurdy ◽  
Judith A. White ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Clinical Method ◽  
Subendocardial Ischemia

Mechanism for ST Depression Associated with Contiguous Subendocardial Ischemia

2004 ◽  
Vol 15 (10) ◽  
pp. 1200-1206 ◽  
Author(s):  
BRUCE HOPENFELD ◽  
JEROEN G. STINSTRA ◽  
ROB S. MACLEOD
Keyword(s):  
Subendocardial Ischemia ◽  
St Depression

scholarly journals Subendocardial ischemia after cardiopulmonary bypass

1972 ◽  
Vol 64 (5) ◽  
pp. 669-684 ◽  
Author(s):  
Gerald D. Buckberg ◽  
Bernard Towers ◽  
Donald E. Paglia ◽  
Donald G. Mulder ◽  
James V. Maloney
Keyword(s):  
Cardiopulmonary Bypass ◽  
Subendocardial Ischemia

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.

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