Relationship between changes in left ventricular bipolar electrograms and regional myocardial blood flow during acute coronary artery occlusion in the dog.

Ruffy, Rodolphe; Lovelace, D. Eugene; Mueller, Timothy I.; Knoebel, Suzanne B.; Zipes, Douglas P.

doi:10.1161/01.res.45.6.764

Cited by 78 publications

(35 citation statements)

References 34 publications

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“…Consistent with the study of Ruffy et al, 10 we observed no significant delay in subendocardial electrical activation during short-term ischemia. Therefore, electrical delay could not account for the observed dyssynchrony during ischemia.…”

Section: Relationship Between Regional Electrical and Mechanical Actisupporting

confidence: 93%

“…Possibly, more severe and longer lasting ischemia could induce conduction delays. 10,11 The aim of the present study, however, was to determine if onset AFG could identify mechanical activation in segments with decreased regional contraction, and we therefore used ischemia to depress myocardial function. Furthermore, the principle of onset AFG is such that it should identify delay in electrical activation regardless of etiology.…”

Section: Relationship Between Regional Electrical and Mechanical Actimentioning

confidence: 99%

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Evaluation of Left Ventricular Dyssynchrony by Onset of Active Myocardial Force Generation

Russell

Opdahl

Remme

et al. 2010

Circ: Cardiovascular Imaging

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Background-Better clinical tools for measuring left ventricular electrical dyssynchrony are needed. The present study investigates if onset of active myocardial force generation (AFG) may serve as a measure of electrical dyssynchrony. Methods and Results-In anesthetized dogs, we evaluated left ventricular mechanical dyssynchrony by 2 different approaches. First, we measured timing of peak myocardial shortening velocity and strain. Second, we measured the first sign of tension development by onset AFG as defined by the myocardial pressure-segment length loop upward shift from its passive-elastic state. Electrical dyssynchrony was measured by intramyocardial electromyograms (IM-EMG). Dyssynchrony was quantified as peak intersegment time difference and as standard deviation of timing for 6 to 8 myocardial segments. During baseline, reduced preload and myocardial ischemia shortening velocity and strain indicated segmental mechanical heterogeneity, whereas onset AFG and onset R in IM-EMG indicated synchronous activation of all segments. After induction of left bundle-branch block, all methods indicated dyssynchrony. Peak intersegment time difference for shortening velocity and strain showed weak correlations (rϭ0.17 and 0.16) and weak agreements (mean differences, Ϫ48Ϯ27 ms and Ϫ28Ϯ27 ms, respectively) with IM-EMG. Onset AFG by pressuresegment length loops, however, correlated well with IM-EMG (rϭ0.93), and agreement was good (mean difference, Ϫ0.6Ϯ6.8 ms). Results were similar for standard deviation of timing. Onset AFG from pressure-strain analysis by echocardiography showed accuracy similar to sonomicrometry. Conclusions-Onset AFG was an accurate marker of myocardial electrical activation and was superior to shortening velocity and strain. Identification of electrical dyssynchrony by onset AFG may be feasible clinically using left ventricular pressure-strain analysis. (Circ Cardiovasc Imaging. 2010;3:405-414.)

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Section: Relationship Between Regional Electrical and Mechanical Actisupporting

confidence: 93%

Section: Relationship Between Regional Electrical and Mechanical Actimentioning

confidence: 99%

Evaluation of Left Ventricular Dyssynchrony by Onset of Active Myocardial Force Generation

Russell

Opdahl

Remme

et al. 2010

Circ: Cardiovascular Imaging

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“…This site spares the septum, so our mapping array covers and surrounds the risk zone (1). Ischemia was defined as a Ն45% decrease in bipolar electrogram voltage (1,2,28,36); all data in vivo or in vitro are reported as "ischemia" when this definition in vivo was met. We waited 60 min because infarct size in the open-chest dog is then ϳ75% of the risk zone (2).…”

Section: Methodsmentioning

confidence: 99%

Triggered activity due to delayed afterdepolarizations in sites of focal origin of ischemic ventricular tachycardia

Xing

Martins

2004

American Journal of Physiology-Heart and Circulatory Physiology

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Xing, Dezhi, and James B. Martins. Triggered activity due to delayed afterdepolarizations in sites of focal origin of ischemic ventricular tachycardia. Am J Physiol Heart Circ Physiol 287: H2078 -H2084, 2004. doi:10.1152/ajpheart.00027.2004.-This study for the first time systematically evaluated the site of origin of focal ventricular tachycardia (VT) induced 1-3 h after acute coronary artery ligation in dogs. We determined whether delayed afterdepolarizations (DADs) and triggered activity (TA) are more often recorded from ischemic endocardium excised from focal sites of VT origin. A total of 145 ␣-chloralose-anesthetized dogs were studied: in 54 dogs without inducible VT, normal or ischemic endocardium was investigated in vitro; in 91 dogs, inducible VT was studied by threedimensional activation mapping, with in vitro study of 51 endocardial foci compared with 40 endocardial ischemic sites not of VT origin. Incidence of DADs (71% vs. 33%, P Ͻ 0.05) and TA (32% vs. 11%, P Ͻ 0.05) was greater in ischemic than in normal Purkinje tissues. Purkinje sites of origin of focal VT demonstrated the greatest frequency of DADs (92%, P Ͻ 0.05) and TA (75%, P Ͻ 0.05), with repetitive TA predominating. Similar results were obtained in endocardial sites of origin. Action potentials were mildly depolarized and prolonged in the focal sites of origin. These abnormalities were stable up to 2.5 h of recording. This study demonstrated that DADs and TA may underlie a majority of focal VTs in ischemic endocardium and Purkinje tissue.ventricles; myocardial infarction; endocardium SUDDEN CARDIAC DEATH is a major public health problem. Ventricular tachycardia (VT) and fibrillation (VF) are responsible for most cases of sudden cardiac death (22). The understanding of mechanisms of VT and VF in early myocardial ischemia and infarction is hampered in humans by rapidly changing substrate over the first hours, which are rarely observed in the hospital. Animal models have been studied instead (31). Although reentry has been thought to underlie early VT (25, 36) and VF, some studies have implicated focal mechanisms (1, 2, 10, 11, 25) in endocardial and Purkinje tissue (1, 2, 10). In vitro models of acute ischemia (3,20,27,32) involving Purkinje tissue have suggested that triggered activity (TA) due to delayed afterdepolarizations (DADs) may explain these focal VTs. Abnormalities that may contribute to the occurrence of these mechanisms in acute ischemia include increased free fatty acids, oxygen free radials, acidosis, and catecholamines (22). We studied our model of inducible VT (2) after acute coronary artery occlusion employing three-dimensional activation mapping to investigate the hypothesis that TA due to DADs may be found more frequently in endocardial and Purkinje tissues that were excised from sites of origin (SOOs) of focal VT. METHODSAnimal preparation. A total of 145 dogs of either gender, weighing 8 -20 kg, were studied. The protocol was approved by the University of Iowa Animal Use and Care Committee and adhered to the standards of...

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“…Previous in vivo studies have shown that, during AMI, endocardial (Endo) conduction remains comparatively preserved at a time when epicardial (Epi) conduction is delayed and fractionated [1][2][3][4][5]. Other studies have demonstrated that, despite similar changes in resting membrane potential, ischemia induces a greater depression of the action potentials of ventricular Epi vs Endo tissues [6,7].…”

Section: Introductionmentioning

confidence: 99%

Brugada syndrome and ischemia-induced ST-segment elevation. Similarities and differences

Diego

Fish

Antzelevitch

2005

Journal of Electrocardiology

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Introduction-ST-Segment elevation is a common electrocardiogram (ECG) manifestation of acute transmural myocardial ischemia in leads facing the injury. Acute myocardial ischemia involving the right-ventricular (RV) outflow tract is known to induce a Brugada-like ECG. In this paper, we examined the electrophysiological bases for the similarities between the ECG characteristics of the Brugada syndrome model induced by terfenadine (5 μmol/L) and the ECG manifestations of the acute transmural no-flow ischemia model.Methods-For both experimental simulations, we used isolated arterially perfused canine RV wedge preparations to record transmembrane action potentials (AP) from endocardium and epicardium together with a transmural pseudo-ECG (ECG); basic cycle length = 400 to 2000 ms.Results-In the presence of a prominent I to -mediated AP notch, no-flow ischemia causes true STsegment elevation because of selective depression and loss of the AP dome at some epicardial sites. In the absence of a prominent AP notch, ischemia ultimately produces an apparent ST-segment elevation, which is secondary to a prolongation of the R wave caused by marked transmural conduction delays. Similarly, in the Brugada syndrome model generated in preparations displaying a large epicardial I to , ST-segment elevation was due to loss of the epicardial AP dome at some sites but not at others. Transmural conduction delay giving the appearance of ST-segment elevation is also observed in the Brugada model in preparations exhibiting smaller AP notch. In both models, propagation of the dome from the site at which it is maintained to a site at which it is lost may result in closely coupled phase 2 reentrant extrasystoles.Conclusion-Our results suggest that I to can modulate the electrocardiographic manifestation of acute ischemia as well as that of the Brugada syndrome, and that both clinical entities are the result of a similar electrophysiological substrate.

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Relationship between changes in left ventricular bipolar electrograms and regional myocardial blood flow during acute coronary artery occlusion in the dog.

Cited by 78 publications

References 34 publications

Evaluation of Left Ventricular Dyssynchrony by Onset of Active Myocardial Force Generation

Evaluation of Left Ventricular Dyssynchrony by Onset of Active Myocardial Force Generation

Triggered activity due to delayed afterdepolarizations in sites of focal origin of ischemic ventricular tachycardia

Brugada syndrome and ischemia-induced ST-segment elevation. Similarities and differences

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