The Polarizing Treatment in Cardiovascular Conditions Experimental Basis and Clinical Applications

Sodi‐Pallares, Demetrio; Bisteni, A; Medrano, Gustavo A.; Alessio, Micheli; León, J. Ponce de; Calva, E.; Fishleder, B; Testelli, M. R.; Miller, Ben

doi:10.1159/000388598

Cited by 15 publications

(9 citation statements)

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“…The finding that changes in the TQ-ST segment were similar at either nonischemic or ischemic regions on the epicardium and precordium suggests that potassium exerts a primarily nonspatial influence on the TQ-ST segment and thus is not dependent upon either electrode location or ischemic geometry. This nonspatial influence of potassium may help to account for any previously observed absences of TQ-ST deflections in the ECG from the acute myocardial infarction patient who is also in renal failure (85), as well as suggest an alternate mechanism by which glucose-insulin-potassium improves the ECG picture of patients with an acute myocardial infarction (86).…”

Section: +++mentioning

confidence: 74%

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

Holland¹,

Brooks²,

Lidl³

1977

J. Clin. Invest.

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A B S T R A C T Spatial and nonspatial aspects ofTQ-ST segment mapping were studied with the solid angle theorem and randomly coded data from 15,000 electrograms of 160 anterior descending artery occlusions each of 100-s duration performed in 18 pigs. Factors analyzed included electrode location, ischemic area and shape, wall thickness, and increases in plasma potassium (K+). Change from control in the TQ-ST recorded at 60 s (ATQ-ST) was measured at 22 ischemic (IS) and nonischemic (NIS) epicardial sites overlying right (RV) and left (LV) ventricles. In IS regions, ATQ-ST decreased according to LV > septum > RV and LV base > LV apex. In NIS regions, LV sites had negative (Neg) ATQ-ST which increased as LV IS border was approached. However, RV NIS had positive (Pos) ATQ-ST which again increased as RV IS border was approached. With large artery occlusion IS area increased 123+18%, ATQ-ST at IS sites decreased (-38.1+3.6%), and sum of ATQ-ST at IS sites increased by only 67.3±10.3%. In RV NIS Pos ATQ-ST became Neg. With increased K+, ATQ-ST decreased proportionately to log K+ (r = 0.97±0.01) at IS and NIS sites on the epicardium and precordium. TQ-ST at 60 s was obliterated when K+ = 8.7+0.2 mM. All findings were significant (P < 0.005) and agreed with the solid angle theorem. Thus, a transmembrane potential difference and current flow at the IS boundary alone are responsible for the TQ-ST. Nonspatial factors affect the magnitude of transmembrane potential difference, while spatial factors alter the position of the boundary to the electrode site.

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Section: +++mentioning

confidence: 74%

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

Holland¹,

Brooks²,

Lidl³

1977

J. Clin. Invest.

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“…In all other instances LVEDP during pacing in the GKI state was equal to or greater than that recorded in the control paced state. LVEDP in the postpace control state was abnormally elevated in six patients (1,3,4,6,7,8). In all instances the postpace LVEDP during GKI was equal to or greater than that recorded in the postpace control state.…”

Section: Glucose-insulin Relationshipsmentioning

confidence: 78%

Ineffectiveness of Glucose, Potassium, and Insulin Infusion During Pacing Stress in Chronic Ischemic Heart Disease

et al. 1974

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“…1, were determined by their relationship to the epicardial vessels so that electrode positions were at measured distances from the junction of the diagonal branches with the main LAD coronary artery. Four of these positions (normal zone: 1-4) were above the level of the LAD ligature, four (border zone: [5][6][7][8] were at the level of the ligature bordering the cyanotic area, and six (center zone: 9-14) were over the center of the evolving infarct. The center of each electrode position was measured at 1 cm from that of its neighbor.…”

Section: Methodsmentioning

confidence: 99%

“…Its electrophysiological correlates were established by Samson and Scher (4) who showed that acute epicardial STsegment shifts in ischemia were due to accelerated repolarization when surface and intracellular cardiac potentials were recorded simultaneously. The possibility that a reduction in the magnitude of this electrophysiologic change may be associated with less ischemic injury was raised by the work of SodiPallares et al (5). They reported a reduction in the extent of ST-segment alterations by the use of "polarizThe Journal of Clinical Investigation Volume 58 December 1976 1317- 1326 1317…”

mentioning

confidence: 99%

“…ing" solutions (5) and subsequently by the coronarv vasodilator drug, verapamil (6). More recently, Maroko and his colleagues (7,8) have demonstrated that after experimental coronary occlusion, interventions which autgment myocardial oxygen consumption (MVO2) tend to aggravate epicardial and precordial ST-segment elevation, whereas those which diminish MVO2 lead to a reduction in ST-segment elevation.'…”

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confidence: 99%

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Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs.

Heng¹,

Singh²,

Norris³

et al. 1976

J. Clin. Invest.

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A B S T R A C T The relationship between early and late epicardial electrocardiographic changes as well as those in regional myocardial blood flow (MBF) and the severity of myocardial damage was determined in 12 anesthetized dogs with left anterior descending coronary artery ligation. Radioactive microspheres (15 ,um) were used to measure regional MBF at 15 min (early) and 24h (late) after coronary occlusion. Severity of myocardial damage was assessed by the extent of myocardial creatine phosphokinase depletion 24 h after coronary ligation. There was a close linear correlation between myocardial creatine phosphokinase activity and regional MBF both early (r = 0.93, 2P < 0.001) and late (r = 0.88, 2P < 0.001). An inverse but less precise relationship existed between acute epicardial ST-segment elevation and early (r = -0.41, 2P < 0.001), or late (r = -0.35, 2P < 0.05) regional MBF. Similarly, a weak correlation was found between myocardial creatine phosphokinase (IU/mg protein) at 24 h and early epicardial ST (millivolt) elevation (r = -0.36, 2P < 0.02). In the center zones of the infarct with MBF 1/10 of normal, about 35% of the areas with normal QRS width had no epicardial ST-segment elevation 15 min after coronary occlusion. About 44% of the areas which An abstract embodying the results was presented at the 48th Annual Scientific Meeting of the American Heart Association, Anaheim, Calif., November 1975 and has been published as an abstract in Circulation. 51, 52: II-6, (1975 developed pathological Q-waves in the electrocardiogram at 24 h had no ST elevation 15 min after coronary ligation. Late evolution of abnormal Qwaves occurred almost invariably in areas in which the early MBF was reduced to less than 50% of normal and in areas which subsequently had myocardial creatine phosphokinase levels reduced to less than 60%o of normal. After coronary occlusion, the severity of the ultimate myocardial damage, which was directly proportional to the degree of reduction in MBF, was therefore not reliably predicted by the early epicardial ST-segment elevation. The data obtained in these studies suggest the need for caution in the use of acute ST-segment elevation as a predictive index of the extent or severity of myocardial ischemic damage.

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The Polarizing Treatment in Cardiovascular Conditions Experimental Basis and Clinical Applications

Cited by 15 publications

References 0 publications

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

Ineffectiveness of Glucose, Potassium, and Insulin Infusion During Pacing Stress in Chronic Ischemic Heart Disease

Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs.

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