Origin of the giant R wave in acute transmural myocardial infarction in the pig.

Chang, Winshih; Akiyama, Toshio; Richeson, J. Franklin; Faillace, Robert T.; Serrino, Peter

doi:10.1536/ihj.30.863

Cited by 4 publications

(4 citation statements)

References 38 publications

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“…As illustrated in figure 1, a giant R wave quickly developed during the first 4 min of coronary occlusion, and also later in time around 11-22 min. This particular finding has been reported in previous studies carried out in experiments with pigs (Chang et al 1989) and also in humans (Faillace et al 1985). However, those other studies did not focus their attention on the two different peaks in R a evolution.…”

Section: Ischemia-induced Ecg Changes In Depolarization and Repolarizsupporting

confidence: 70%

“…However, those other studies did not focus their attention on the two different peaks in R a evolution. Chang et al (1989) studied the presumable genesis for this giant R wave during transient transmural ischemia and hyperacute phase of transmural myocardial infarction by the analysis of different factors. They concluded that the origin of the giant R wave is the slowed conduction velocity into the ischemic tissue, which led to the formation of a homogeneous and discrete wavefront advancing toward the center of the ischemia from its lateral and subendocardial areas.…”

Section: Ischemia-induced Ecg Changes In Depolarization and Repolarizmentioning

confidence: 99%

“…A number of animal experiments have been carried out to investigate whether changes in the ECG, mostly in the ST-T interval, are related to the amount of ischemia assessed either by different image techniques or by histochemical analysis. In pigs, during regional ischemia produced by clamping one of the coronary arteries (mainly the left anterior descending (LAD) artery), changes were reflected as T-Q depression, decreased action potential amplitude and upstroke velocity (Chang et al 1989, Janse et al 1979, Morena et al 1980. Also, changes in QRS vector (magnitude and direction) (Näslund et al 1993a), and ST vector (Näslund et al 1993b) have been reported, and were also correlated with the myocardium at risk (MaR) during the initial minutes of ischemia.…”

Section: Introductionmentioning

confidence: 99%

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Characterization of ventricular depolarization and repolarization changes in a porcine model of myocardial infarction

Romero¹,

Ringborn²,

Demidova³

et al. 2012

Physiol. Meas.

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In this study, several electrocardiogram (ECG)-derived indices corresponding to both ventricular depolarization and repolarization were evaluated during acute myocardial ischemia in an experimental model of myocardial infarction produced by 40 min coronary balloon inflation in 13 pigs. Significant changes were rapidly observed from minute 4 after the start of coronary occlusion, achieving their maximum values between 11 and 22 min for depolarization and between 9 and 12 min for repolarization indices, respectively. Subsequently, these maximum changes started to decrease during the latter part of the occlusion. Depolarization changes associated with the second half of the QRS complex showed a significant but inverse correlation with the myocardium at risk (MaR) estimated by scintigraphic images. The correlation between MaR and changes of the downward slope of the QRS complex, [Formula: see text], evaluated at the two more relevant peaks observed during the occlusion, was r = -0.75, p < 0.01 and r = -0.79, p < 0.01 for the positive and negative deflections observed in [Formula: see text], temporal evolution, respectively. Repolarization changes, analyzed by evaluation of ST segment elevation at the main observed positive peak, also showed negative, however non-significant correlation with MaR: r = -0.34, p = 0.28. Our results suggest that changes evaluated in the latter part of the depolarization, such as those described by [Formula: see text], which are influenced by R-wave amplitude, QRS width and ST level variations simultaneously, correlate better with the amount of ischemia than other indices evaluated in the earlier part of depolarization or during the ST segment.

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Section: Ischemia-induced Ecg Changes In Depolarization and Repolarizsupporting

confidence: 70%

Section: Ischemia-induced Ecg Changes In Depolarization and Repolarizmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Characterization of ventricular depolarization and repolarization changes in a porcine model of myocardial infarction

Romero¹,

Ringborn²,

Demidova³

et al. 2012

Physiol. Meas.

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“…To simulate this most common anginal chest pain scenario, we reduced regional coronary blood flow and increased myocardial activity ( Downar et al., 1977 ; Janse et al., 1980 ; Safdar et al., 2018 ). Whereas many previous studies have replicated the scenario of a myocardial infarct, typically by ligating a coronary vessel completely, ( Holland and Arnsdorf, 1977 ; Holland and Brooks, 1977 ; Kleber et al., 1978 ; Cinca et al., 1980 ; Janse et al., 1980 ; Chang et al., 1989 ; MacLeod et al., 1995a ; MacLeod et al., 1997 ), we sought a more controlled and nuanced approach that also created ischemia typical of stable transient angina ( Penny, 1984 ; Shome et al., 2007 ; Aras et al., 2009 ; Aras et al., 2011a ; Aras et al., 2016 ; Zenger et al., 2020a ).…”

Section: Example: Closed Chest In Situ Model Of Ca...mentioning

confidence: 99%

Tipping the scales of understanding: An engineering approach to design and implement whole-body cardiac electrophysiology experimental models

Zenger

Bergquist²,

Busatto³

et al. 2023

Front. Physiol.

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The study of cardiac electrophysiology is built on experimental models that span all scales, from ion channels to whole-body preparations. Novel discoveries made at each scale have contributed to our fundamental understanding of human cardiac electrophysiology, which informs clinicians as they detect, diagnose, and treat complex cardiac pathologies. This expert review describes an engineering approach to developing experimental models that is applicable across scales. The review also outlines how we applied the approach to create a set of multiscale whole-body experimental models of cardiac electrophysiology, models that are driving new insights into the response of the myocardium to acute ischemia. Specifically, we propose that researchers must address three critical requirements to develop an effective experimental model: 1) how the experimental model replicates and maintains human physiological conditions, 2) how the interventions possible with the experimental model capture human pathophysiology, and 3) what signals need to be measured, at which levels of resolution and fidelity, and what are the resulting requirements of the measurement system and the access to the organs of interest. We will discuss these requirements in the context of two examples of whole-body experimental models, a closed chest in situ model of cardiac ischemia and an isolated-heart, torso-tank preparation, both of which we have developed over decades and used to gather valuable insights from hundreds of experiments.

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Direct minimally invasive intraoperative electrophysiological mapping of the heart

Ando

Kawashima

Kim

et al. 2013

Minimally Invasive Therapy & Allied Technologies

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Origin of the giant R wave in acute transmural myocardial infarction in the pig.

Cited by 4 publications

References 38 publications

Characterization of ventricular depolarization and repolarization changes in a porcine model of myocardial infarction

Characterization of ventricular depolarization and repolarization changes in a porcine model of myocardial infarction

Tipping the scales of understanding: An engineering approach to design and implement whole-body cardiac electrophysiology experimental models

Direct minimally invasive intraoperative electrophysiological mapping of the heart

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