Mechanism and Time Course of the Early Electrical Changes During Acute Coronary Artery Occlusion: An Attempt to Correlate the Early ECG Changes in Man to the Cellular Electrophysiology in the Pig

doi:10.1378/chest.77.4.499

Chest

Volume 77, Issue 4, April 1980, Pages 499-505

https://doi.org/10.1378/chest.77.4.499 Get rights and content

A comparison is made between precordial ECG leads recorded during the first minutes of acute myocardial infarction in man, and transmembrane potentials and local DC-extracellular electrograms recorded during the first minutes following coronary artery occlusion in isolated pig hearts. In the pig heart, the electrical changes are as follows: (1) a decrease in resting potential, resulting in depression of the TQ segment of the DC extracellular electrogram; (2) a decrease in amplitude of the action potential, leading to true ST elevation of the extracellular complex; (3) decrease in upstroke velocity, and thus a delayed activation of ischemic cells, giving rise to a late intrinsic deflection in the extracellular signal; (4) a transient period of alternation with respect to amplitude and duration of the transmembrane action potential leading to alternation in ST elevation and T wave; (5) unresponsiveness of ischemic cells after 5 to 10 minutes at a membrane potential around −65 mV, which produces a monophasic extracellular complex; and (6) a transient increase between 20 to 40 minutes in resting potential and reappearance of action potentials, resulting in decrease in TQ and ST deflection and reappearance of intrinsic deflection. In the precordial leads in the patient, the configuration of the complexes and the time course of the changes was very similar to the configuration of the extracellular signals in the pig, suggesting that cellular changes in man are similar to those in the pig.

Section snippets

Case Report

A 41-year-old diabetic man was admitted to the Ciudad Sanitaria de Barcelona because of two successive episodes of chest pain four hours previously. They were related to minimal exercise and lasted 2 and 20 minutes respectively. On admission, the ECG showed normal sinus rhythm with slight ST-segment depression (1 to 2 mm) in leads 2, 3, and aVF. The T waves were positive and symmetrical in leads V₃ to V₅. Serum glutamic oxaloacetic transaminase (SGOT) value was 32, creatine Phosphokinase (CPK)

Discussion

It has been established long ago that “injury” to the heart, usually by locally applying concentrated potassium chloride solutions to the epicardium, resulted in “elevation” of the ST segment, which in reality, was due to a depression of the baseline.5, 6, 7 More recent studies⁴ and the present report show that in acute myocardial ischemia, the ST elevation as recorded with AC-coupled amplifiers is, in fact, caused by a combination of depression of the TQ segment and true elevation of the ST

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There are more references available in the full text version of this article.

Cited by (71)

Transient recovery of epicardial and torso ST-segment ischemic signals during cardiac stress tests: A possible physiological mechanism
2021, Journal of Electrocardiology
Acute myocardial ischemia has several characteristic ECG findings, including clinically detectable ST-segment deviations. However, the sensitivity and specificity of diagnosis based on ST-segment changes are low. Furthermore, ST-segment deviations have been shown to be transient and spontaneously recover without any indication the ischemic event has subsided.
Assess the transient recovery of ST-segment deviations on remote recording electrodes during a partial occlusion cardiac stress test and compare them to intramyocardial ST-segment deviations.
We used a previously validated porcine experimental model of acute myocardial ischemia with controllable ischemic load and simultaneous electrical measurements within the heart wall, on the epicardial surface, and on the torso surface. Simulated cardiac stress tests were induced by occluding a coronary artery while simultaneously pacing rapidly or infusing dobutamine to stimulate cardiac function. Postexperimental imaging created anatomical models for data visualization and quantification. Markers of ischemia were identified as deviations in the potentials measured at 40% of the ST-segment. Intramural cardiac conduction speed was also determined using the inverse gradient method. We assessed changes in intramyocardial ischemic volume proportion, conduction speed, clinical presence of ischemia on remote recording arrays, and regional changes to intramyocardial ischemia. We defined the peak deviation response time as the time interval after onset of ischemia at which maximum ST-segment deviation was achieved, and ST-recovery time was the interval when ST deviation returned to below thresholded of ST elevation.
In both epicardial and torso recordings, the peak ST-segment deviation response time was 4.9±1.1 min and the ST-recovery time was approximately 7.9±2.5 min, both well before the termination of the ischemic stress. At peak response time, conduction speed was reduced by 50% and returned to near baseline at ST-recovery. The overall ischemic volume proportion initially increased, on average, to 37% at peak response time; however, it recovered to only 30% at the ST-recovery time. By contrast, the subepicardial region of the myocardial wall showed 40% ischemic volume at peak response time and recovered much more strongly to 25% as epicardial ST-segment deviations returned to baseline.
Our data show that remote ischemic signal recovery correlates with a recovery of the subepicardial myocardium, whereas subendocardial ischemic development persists.
Clinical Significance of Reciprocal ST-segment Changes in Patients With STEMI: A Cardiac Magnetic Resonance Imaging Study
2019, Revista Espanola de Cardiologia
Se trató de determinar la asociación de los cambios recíprocos en el segmento ST con el daño miocardio evaluado mediante imagen con resonancia magnética cardiaca (RMC) en pacientes con infarto agudo de miocardio con elevación del segmento ST (IAMCEST) que recibieron intervención coronaria percutánea (ICP).
Se realizó estudio de imagen con RMC a 244 pacientes tratados con ICP primaria durante el primer IAMCEST. El estudio con RMC se realizó de media 3 días después de la ICP primaria. Se analizó el primer electrocardiograma y los pacientes se estratificaron de acuerdo a la presencia de cambios recíprocos. El objetivo primario fue el tamaño del infarto medido por RMC y los secundarios el área en riesgo y el índice de miocardio rescatado.
Los pacientes con cambios recíprocos (133 pacientes, 54,5%) tuvieron una menor incidencia de infarto de miocardio anterior (27,8 frente al 71,2%; p < 0,001) y un tiempo más corto desde el inicio de los síntomas hasta la restauración del flujo coronario (221,5 ± 169,8 frente a 289,7 ± 337,3 min; p = 0,042). Usando un modelo de regresión lineal múltiple, se encontró que los pacientes con cambios recíprocos tuvieron una mayor área en riesgo (p = 0,002) y un mayor índice de miocardio rescatado (p = 0,04) comparado con los pacientes sin cambios recíprocos. Consecuentemente, el tamaño del infarto de miocardio no fue significantemente diferente entre los 2 grupos (p = 0,14). La tasa de eventos adversos cardiovasculares mayores, incluyendo muerte por todas las causas, infarto de miocardio, y nueva revascularización coronaria, fue similar entre los 2 grupos después de 2 años de seguimiento (p = 0,92).
Los cambios recíprocos del segmento ST se asociaron a una mayor extensión de miocardio isquémico en riesgo y a un mayor índice de miocardio rescatado, pero no a un mayor tamaño del infarto o eventos clínicos adversos en pacientes con IAMCEST tratados con ICP primaria.
We sought to determine the association of reciprocal change in the ST-segment with myocardial injury assessed by cardiac magnetic resonance (CMR) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).
We performed CMR imaging in 244 patients who underwent primary PCI for their first STEMI; CMR was performed a median 3 days after primary PCI. The first electrocardiogram was analyzed, and patients were stratified according to the presence of reciprocal change. The primary outcome was infarct size measured by CMR. Secondary outcomes were area at risk and myocardial salvage index.
Patients with reciprocal change (n = 133, 54.5%) had a lower incidence of anterior infarction (27.8% vs 71.2%, P < .001) and shorter symptom onset to balloon time (221.5 ± 169.8 vs 289.7 ± 337.3 min, P = .042). Using a multiple linear regression model, we found that patients with reciprocal change had a larger area at risk (P = .002) and a greater myocardial salvage index (P = .04) than patients without reciprocal change. Consequently, myocardial infarct size was not significantly different between the 2 groups (P = .14). The rate of major adverse cardiovascular events, including all-cause death, myocardial infarction, and repeat coronary revascularization, was similar between the 2 groups after 2 years of follow-up (P = .92).
Reciprocal ST-segment change was associated with larger extent of ischemic myocardium at risk and more myocardial salvage but not with final infarct size or adverse clinical outcomes in STEMI patients undergoing primary PCI.
Full English text available from: www.revespcardiol.org/en
Endocardial infarct scar recognition by myocardial electrical impedance is not influenced by changes in cardiac activation sequence
2018, Heart Rhythm
Measurement of myocardial electrical impedance can allow recognition of infarct scar and is theoretically not influenced by changes in cardiac activation sequence, but this is not known.
The objectives of this study were to evaluate the ability of endocardial electrical impedance measurements to recognize areas of infarct scar and to assess the stability of the impedance data under changes in cardiac activation sequence.
One-month-old myocardial infarction confirmed by cardiac magnetic resonance imaging was induced in 5 pigs submitted to coronary artery catheter balloon occlusion. Electroanatomic data and local electrical impedance (magnitude, phase angle, and amplitude of the systolic-diastolic impedance curve) were recorded at multiple endocardial sites in sinus rhythm and during right ventricular pacing. By merging the cardiac magnetic resonance and electroanatomic data, we classified each impedance measurement site either as healthy (bipolar amplitude ≥1.5 mV and maximum pixel intensity <40%) or scar (bipolar amplitude <1.5 mV and maximum pixel intensity ≥40%).
A total of 137 endocardial sites were studied. Compared to healthy tissue, areas of infarct scar showed 37.4% reduction in impedance magnitude (P < .001) and 21.5% decrease in phase angle (P < .001). The best predictive ability to detect infarct scar was achieved by the combination of the 4 impedance parameters (area under the receiver operating characteristic curve 0.96; 95% confidence interval 0.92–1.00). In contrast to voltage mapping, right ventricular pacing did not significantly modify the impedance data.
Endocardial catheter measurement of electrical impedance can identify infarct scar regions, and in contrast to voltage mapping, the impedance data are not affected by changes in cardiac activation sequence.
ST-segment deviation behavior during acute myocardial ischemia in opposite ventricular regions: Observations in the intact and perfused heart
2014, Heart Rhythm
Acute myocardial ischemia in opposite regions may attenuate ST-segment changes, but whether this effect is expressed differently in extracardiac compared to direct intramyocardial recordings is not well known.
The purpose of this study was to characterize ST-segment changes induced by opposite ischemic regions in intact and isolated perfused pig hearts.
Left anterior descending (LAD) and right coronary arteries (RCA) were occluded in 7 closed chest pigs and in 5 isolated pig hearts. ST-segment changes were analyzed in 12-lead ECG and in local extracellular electrograms.
Isolated LAD or RCA occlusion induced maximal ST-segment elevation in leads V₄ (0.84 ± 0.30 mV, P = .003) and III (0.16 ± 0.11 mV, P = .04), respectively. RCA occlusion also induced reciprocal ST-segment depression maximal in lead V₄ (–0.40 ± 0.16 mV, P = .005). Simultaneous LAD and RCA occlusion reduced ST-segment elevation by about 60% and blunted reciprocal ST-segment changes. Reperfusion of 1 of the 2 occluded arteries induced immediate regional reversion of ST-segment elevation with concurrent beat-to-beat re-elevation in the opposite ischemic region and reappearance of reciprocal ST-segment changes. In the isolated heart, single LAD or RCA ligature induced regional transmural ST-segment elevation that was maximal in endocardial electrograms with no appreciable reciprocal ST-segment depression. Simultaneous LAD and RCA ligature reduced ST-segment elevation by about 30% with no appreciable re-elevation after 1-vessel selective reperfusion.
Acute myocardial ischemia in opposite ventricular regions attenuated ST-segment elevation and blunted reciprocal depression in conventional ECG leads but not in direct local myocardial electrograms.
New electrocardiographic criteria to differentiate acute pericarditis and myocardial infarction
2014, American Journal of Medicine
Transmural myocardial ischemia induces changes in QRS complex and QT interval duration but, theoretically, these changes might not occur in acute pericarditis provided that the injury is not transmural. This study aims to assess whether QRS and QT duration permit distinguishing acute pericarditis and acute transmural myocardial ischemia.
Clinical records and 12-lead electrocardiogram (ECG) at ×2 magnification were analyzed in 79 patients with acute pericarditis and in 71 with acute ST-segment elevation myocardial infarction (STEMI).
ECG leads with maximal ST-segment elevation showed longer QRS complex and shorter QT interval than leads with isoelectric ST segment in patients with STEMI (QRS: 85.9 ± 13.6 ms vs 81.3 ± 10.4 ms, P = .01; QT: 364.4 ± 38.6 vs 370.9 ± 37.0 ms, P = .04), but not in patients with pericarditis (QRS: 81.5 ± 12.5 ms vs 81.0 ± 7.9 ms, P = .69; QT: 347.9 ± 32.4 vs 347.3 ± 35.1 ms, P = .83). QT interval dispersion among the 12-ECG leads was greater in STEMI than in patients with pericarditis (69.8 ± 20.8 ms vs 50.6 ± 20.2 ms, P <.001). The diagnostic yield of classical ECG criteria (PR deviation and J point level in lead aVR and the number of leads with ST-segment elevation, ST-segment depression, and PR-segment depression) increased significantly (P = .012) when the QRS and QT changes were added to the diagnostic algorithm.
Patients with acute STEMI, but not those with acute pericarditis, show prolongation of QRS complex and shortening of QT interval in ECG leads with ST-segment elevation. These new findings may improve the differential diagnostic yield of the classical ECG criteria.
Influence of the extent of coronary atherosclerotic disease on ST-segment changes induced by ST elevation myocardial infarction
2014, American Journal of Cardiology
The accuracy of the admission electrocardiogram (ECG) in predicting the site of acute coronary artery occlusion in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel disease is not well known. This study aimed to assess whether the presence of multivessel coronary artery disease (CAD) modifies the artery-related ST-segment changes in patients with acute coronary artery occlusion. We reviewed the admission ECG, clinical records, and coronary angiography of 289 patients with STEMI caused by acute occlusion of left anterior descending (LAD; n = 140), right (n = 118), or left circumflex (LCx; n = 31) coronary arteries. All patients underwent primary percutaneous coronary reperfusion during the first 12 hours. The magnitude and distribution of artery-related ST-segment patterns were comparable in patients with single (n = 149) and multivessel (n = 140) CAD. Occlusion of proximal (n = 55) or mid-distal (n = 85) LAD artery induced ST-segment elevation in leads V₁ to V₅, but only the proximal occlusion induced reciprocal ST-segment depression in leads II, III, and aVF (p <0.001). Proximal and mid-distal occlusion of right (n = 45 and 73, respectively) or LCx (n = 15 and 16) coronary artery always induced ST-segment elevation in leads II, III, and aVF and reciprocal ST-segment depression in leads V₂ and V₃. ST-segment elevation in lead V₆ >0.1 mV predicted LCx artery occlusion. In conclusion, patients with STEMI with single or multivessel CAD have concordant artery-related ST-segment patterns on the admission ECG; in both groups, reciprocal ST-segment depression in LAD artery occlusion predicts a large infarct. Subendocardial ischemia at a distance is not a requisite for the genesis of reciprocal ST-segment changes.

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: Manuscript received February 15; revision accepted July 2.

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Chest

CommentaryMechanism and Time Course of the Early Electrical Changes During Acute Coronary Artery Occlusion: An Attempt to Correlate the Early ECG Changes in Man to the Cellular Electrophysiology in the Pig

Section snippets

Case Report

Discussion

J Electrocardiol

An electrocardiographic sign of coronary artery obstruction

Arch Intern Med

ST-segment mapping: realistic and unrealistic expectations

Circulation

The effect of coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart

Circulation

Mechanism and time course of S-T and T-Q segment changes during acute regional myocardial ischemia in the pig heart determined by extracellular and intracellular recordings

Circ Res

Observations on the genesis of the electrical currents established by injury to the heart

Am J Physiol

The injury current in the electrogram

Am J Physiol

Commentary
Mechanism and Time Course of the Early Electrical Changes During Acute Coronary Artery Occlusion: An Attempt to Correlate the Early ECG Changes in Man to the Cellular Electrophysiology in the Pig