Negative displacement of the RS-T segment in the electrocardiogram and its relationships to positive displacement; an experimental study

Wolferth, Charles C.; Bellet, Samuel; Livezey, Mary M.; Murphy, Franklin D.

doi:10.1016/0002-8703(45)90519-9

Cited by 122 publications

(15 citation statements)

References 25 publications

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“…9 duration, Hellerstein and Katz" demonstrated that "pressure injury," resulting from pressure applied to the endocardial surface with a rigid probe sufficient to deform the left ventricular wall, produced S-T depression in the electrogram recorded from the overlying epicardial surface, and that this S-T depression was reversible, the S-T segment returning to normal within seconds to minutes after the pressure was removed. Because these experimental studies indicated that injury confined to the subendocardial myocardium produced S-T depression in the electrogram recorded from the overlying surface, it was deduced that the S-T depression occurring during exercise in patients with coronary artery stenosis resulted from ischemia localized to the subendocardial myocardium.…”

Section: Discussionmentioning

confidence: 99%

Distribution of myocardial blood flow in the exercising dog with restricted coronary artery inflow.

Ball¹,

Bache²

1976

Circulation Research

106

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SUMMARY The effect of a proximal coronary artery stenosis on transmural myocardial blood flow during exercise was studied in nine dogs with electromagnetic flowmeter probes and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow at rest and during treadmill exercise was estimated with radioactive microspheres 7-10 j»m in diameter. Exercise studies were performed during unrestricted coronary artery inflow (control exercise) and during partial inflation of the occluder to a level which did not reduce flow at rest but which limited the increase in flow during exercise to 66 ± 6% (mild restriction) or 44 ± 3% (severe restriction) of the value during control exercise. Mean myocardial blood flow at rest was 0.94 ± 0.06 rnl/min per g of myocardium and increased to 2.45 ± 0.15 ml/min per g during control exercise, with uniform distribution across the wall of the left ventricle. Flow to the subepicardial myocardium was significantly greater during exercise in the presence of a mild restriction than during control exercise, whereas flow to deeper layers of myocardium was progressively decreased below the control level. A similar pattern of redistribution of flow occurred during exercise in the presence of a severe restriction, but flow to all transmural layers was below that during mild restriction, resulting in more marked subendocardial underperfusion. Thus, exercise in the presence of stenosis resulted in transmural redistribution of myocardial blood flow with subendocardial underperfusion in proportion to the degree of restriction of coronary artery inflow.IN THE presence of occlusive coronary artery disease patients who have normal electrocardiograms at rest may develop S-T segment depression during exercise, often in association with chest pain. This electrocardiographic change suggests that in these patients exercise may result in selective ischemia of the subendocardial myocardium.1 Previous experimental studies in animals have demonstrated that in contrast to the uniform left ventricular perfusion that exists during unimpeded coronary artery inflow, transmural redistribution of flow may occur during restricted inflow. Thus, in open-chest dogs reduction of coronary inflow below the metabolic requirements of the myocardium resulted in transmural redistribution of myocardial blood flow with preferential underperfusion of the subendocardial myocardium.2 " 6In patients with occlusive coronary artery disease, arterial inflow at rest may be adequate and transmural distribution uniform, but because arterial inflow is unable to increase adequately during exercise a similar redistribution of myocardial blood flow may occur with preferential underperfusion of the subendocardial myocardium. The present study was an attempt to determine whether, in an experimental model with a flow-limiting proximal coronary artery stenosis, exercise could result in the proposed redistribution of myocardial blood flow. MethodsNine adult mongrel dogs weighing 22-34 kg were anesthetized with sodium thiamyl...

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Section: Discussionmentioning

confidence: 99%

Distribution of myocardial blood flow in the exercising dog with restricted coronary artery inflow.

Ball¹,

Bache²

1976

Circulation Research

106

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“…With ST depression, there is no satisfactory explanation of the cardiac electrophysiological changes. Early work 1,2,33 in isolated hearts suggested that the ST-segment response to myocardial injury was elevation and that the ST-segment depression recorded at the epicardium was the reciprocal of ST elevation in the underlying subendocardium. This amplified the dipole theory, which was developed by Wilson and coworkers in 1930s.…”

Section: The Origin Of Ischemic St Depressionmentioning

confidence: 99%

“…[3][4][5][6] Much of the current opinion regarding the genesis of ST-segment depression is derived from interpretations based on certain theoretical considerations 7,8 and indirect evidence from animal experiments. 1,2 Ischemic muscle generates intracellular currents, which effectively cause TQ depression and ST elevation over the ischemic area 9,10 and which conventional electrocardiography with AC-coupled amplifiers reflects as ST elevation. ST-segment depression recorded at the epicardium has been considered to be secondary to an injury current in the underlying subendocardium.…”

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confidence: 99%

Source of Electrocardiographic ST Changes in Subendocardial Ischemia

Yong

et al. 1998

Circulation Research

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Abstract-To clarify the source of electrocardiographic ST depression associated with ischemia, a sheep model of subendocardial ischemia was developed in which simultaneous epicardial and endocardial ST potentials were mapped, and a computer model using the bidomain technique was developed to explain the results. To produce ischemia in different territories of the myocardium in the same animal, the left anterior descending coronary artery and left circumflex coronary artery were partially constricted in sequence. Results from 36 sheep and the computer simulation are reported. The distributions of epicardial potentials from either ischemic source were very similar (rϭ0.77Ϯ0.14, PϽ0.0001), with both showing ST depression on the free wall of the left ventricle and no association between the ST depression and the ischemic region. However, endocardial potentials showed that ST elevation was directly associated with the region of reduced blood flow. Insulating the heart from the surrounding tissue with plastic increased the magnitude of epicardial ST potentials, which was consistent with an intramyocardial source. Increasing the percent stenosis of a coronary artery increased epicardial ST depression at the lateral boundary and resulted in ST elevation starting from the ischemic center as ischemia became transmural. Computer simulation using the bidomain model reproduced the epicardial ST patterns and suggested that the ST depression was generated at the lateral boundary between ischemic and normal territories. ST depression on the epicardium reflected the position of this lateral boundary. The boundaries of ischemic territories are shared, and only those appearing on the free wall contribute to external ST potential fields. These effects explain why body surface ST depression does not localize cardiac ischemia in humans.(Circ Res. 1998;82;957-970.)Key Words: ST depression Ⅲ potential mapping Ⅲ bidomain model Ⅲ subendocardial ischemia Ⅲ regional myocardial blood flow E lectrocardiographic ST-segment depression has long been recognized as a sign of ischemia, 1,2 but the explanations of the responsible mechanisms have been controversial. [3][4][5][6] Much of the current opinion regarding the genesis of ST-segment depression is derived from interpretations based on certain theoretical considerations 7,8 and indirect evidence from animal experiments. 1,2 Ischemic muscle generates intracellular currents, which effectively cause TQ depression and ST elevation over the ischemic area 9,10 and which conventional electrocardiography with AC-coupled amplifiers reflects as ST elevation. ST-segment depression recorded at the epicardium has been considered to be secondary to an injury current in the underlying subendocardium. [11][12][13][14] In conventional stress testing, as myocardial demand exceeds the ability of the narrowed coronary arterial bed to increase blood flow, the ischemic threshold is exceeded, and reversible ST-segment depression is produced. However, the location of this ST depression does not enable us to localize...

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“…E LECTROCARDIOGRAPHIC (ECG) ST segment depression has long been recognized as a sign of ischaemia [1], but the explanations of the responsible mechanisms have been controversial [2]. In this paper, we present a simple mathematical model of a slab of cardiac tissue in an attempt to further our understanding of the relationship between subendocardial ischaemia and the resulting epicardial potential distributions.…”

Section: Introductionmentioning

confidence: 99%

The importance of anisotropy in modeling ST segment shift in subendocardial ischaemia

Johnston

Kilpatrick

2001

IEEE Trans. Biomed. Eng.

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Abstract-In this paper, a simple mathematical model of a slab of cardiac tissue is presented in an attempt to better understand the relationship between subendocardial ischaemia and the resulting epicardial potential distributions. The cardiac tissue is represented by the bidomain model where tissue anisotropy and fiber rotation have been incorporated with a view to predicting the epicardial surface potential distribution. The source of electric potential in this steady-state problem is the difference between plateau potentials in normal and ischaemic tissue, where it is assumed that ischaemic tissue has a lower plateau potential. Simulations with tissue anisotropy and no fiber rotation are also considered.Simulations are performed for various thicknesses of the transition region between normal and ischaemic tissue and for various sizes of the ischaemic region. The simulated epicardial potential distributions, based on an anisotropic model of the cardiac tissue, show that there are large potential gradients above the border of the ischaemic region and that there are dips in the potential distribution above the region of ischaemia. It could be concluded from the simulations that it would be possible to predict the region of subendocardial ischaemia from the epicardial potential distribution, a conclusion contrary to observed experimental data. Possible reasons for this discrepancy are discussed.In the interests of mathematical simplicity, isotropic models of the cardiac tissue are also considered, but results from these simulations predict epicardial potential distributions vastly different from experimental observations. A major conclusion from this work is that tissue anisotropy and fiber rotation must be included to obtain meaningful and realistic epicardial potential distributions.

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Negative displacement of the RS-T segment in the electrocardiogram and its relationships to positive displacement; an experimental study

Cited by 122 publications

References 25 publications

Distribution of myocardial blood flow in the exercising dog with restricted coronary artery inflow.

Distribution of myocardial blood flow in the exercising dog with restricted coronary artery inflow.

Source of Electrocardiographic ST Changes in Subendocardial Ischemia

The importance of anisotropy in modeling ST segment shift in subendocardial ischaemia

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