Epicardial Electrocardiogram Research Articles

Effects of verapamil on infarct size following experimental coronary occlusion.

Open-chest anaesthetized dogs were given verapamil after left anterior descending artery occlusion, and ST-segment alterations and haemodynamic variables were monitored. Verapamil produced a highly significant reduction in ST-segment elevation in the epicardial electrocardiogram and prevented the haemodynamic deterioration seen in the control animals in which ST-segment elevation persisted. The apparent protective effect of verapamil in myocardial ischaemia is discussed in relation to its ability to inhibit selectively the transmembrane fluxes of calcium ions in excitable tissues.

Effect of propranolol and isoprenaline on regional left ventricular blood flow in experimental myocardial ischaemia.

The distribution of left ventricular (LV) blood flow was studied in open chested dogs with acute myocardial ischaemia before and after propranolol and isoprenaline. Regional LV flow was measured with radioactive microspheres and local tissue injury estimated from ST segment elevation in epicardial electrocardiograms. Propranolol reduced blood flow throughout the LV, more so in non-ischaemic than ischaemic regions, but ST segments became less elevated. Isoprenaline increased flow to non-ischaemic regions and the subendocardial portion of ischaemic areas; subepicardial flow in ischaemic regions did not change. Concomitantly, ST segments became more elevated and new ST segment elevations appeared. This disparity between changes in ST segment elevation and blood flow indicates that these beta-adrenergic agents do not alter ischaemia through primary changes in blood flow distribution. Alternative mechanisms are discussed.

Coronary reperfusion in primates. Serial electrocardiographic and histologic assessment.

After acute coronary occlusion in primates, the time period during which reperfusion results in significant salvage of reversibly injured myocardium was investigated. In 23 monkeys, the left anterior descending coronary artery was occluded from 1 to 6 h; and in 5 others, occlusion was maintained for the 1-wk study. Unipolar epicardial electrocardiograms were monitored from mapping points on the anterior and lateral left venticle. S-T segment elevation (S-T upward arrow) and R + S wave amplitude (RS) were measured before occlusion and at regular intervals during occlusion and reperfusion. Summated S-T upward arrow (SigmaS-T upward arrow) and summated RS (SigmaRS), computed for mapping points demonstrating greater than 2 mV S-T upward arrow, were used as serial measures of electrical injury. SigmaS-T upward arrow peaked within 2-h postocclusion and then gradually declined throughout the period of occlusion suggesting the progress of infarction within the area of injury. After reperfusion SigmaS-T upward arrow rapidly declined to near cnotrol values indicating the extent of reversible injury. During the period of occlusion, the magnitude of voltage loss in SigmaS-T upward arrow as a percent of maximum SigmaS-T upward arrow was proportional to the duration of occlusion, though the rate of loss decreased with increasing time of occlusion. Reperfusion after 6 h of occlusion resulted in reversal of only a small remaining component of the maximum current of injury. The voltage decrease in SigmaRS (from control values) was proportional to the duration of occlusion, though the decrease was accelerated during the first 2-h postocclusion. Whereas reperfusion interrupted the decline in SigmaRS, a consistent increase in SigmaRS postreperfusion was observed only after occlusion of 1 h. With respect to reperfusion groups, significance in SigmaS-T upward arrow voltage loss as a percent of maximum SigmaS-T upward arrow was demonstrated between 2-h and 4-h, 4- and 6-h, and 6-h and chronically ligated animals. Significance in SigmaRS voltage loss as a percent of control SigmaRS was demonstrated between 2- and 4-h, and 4- and 6-h reperfusion groups. Hearts were excised at 7 days for histological assessment of infarct size. Planimetric determination of left ventricular areas and areas of necrosis using slides made from 10 serial cross sections were used in estimating the percent of left ventricle infarcted. A significant reduction in infarct size was demonstrated between reperfused animals at 2 h and the 4- and 6-h reperfusion groups. A trend was noted suggesting increasing infarct size up to 6 h after experimental occlusion.

The adequacy of subendocardial oxygen delivery: the interaction of determinants of flow, arterial oxygen content and myocardial oxygen need.

The interactions of determinants of subendocardial oxygen delivery (flow and oxygen content) and oxygen demand were studied. In open chest dogs, oxygen requirements were increased with aortic stenosis and oxygen delivery reduced with normovolemic anemia. We estimated potential subendocardial flow from a Diastolic Pressure Time Index (DPTI) and oxygen demands from the Tension Time Index (TTI), and detected ischemia with endocardial (Endo) and epicardial (Epi) electrocardiograms (ECG). Subendocardial oxygen delivery per unit of TTI was significantly lowered and Endo ECGs showed ischemia (ST elevation) when Endo/Epi flow ratios (microsphere method) fell below 1.0 ( P < 0.001). Ischemia occurred without anemia (Hgb > 10 g %) in severe aortic stenosis; with mild anemia (Hgb 5-10 g %) and mild aortic stenosis; and with severe anemia (Hgb < 5 g %) without aortic stenosis. Ischemic Endo ECGs occurred with mild supravalvar aortic stenosis and mild anemia despite a 63% (92 to 150 cc/100g/min) average increase in subendocardial flow while Epi ECGs remained normal. Altered flow distributions and abnormal ECGs were always predictable from the ratio: DPTI x O 2 content (Supply)/TTI (Demand). These determinants of Supply and Demand are readily obtained from measurements of hemoglobin, saturation, and blood pressure.

Effect of dopamine and calcium on lipolysis and myocardial ischemic injury following acute coronary occlusion in the dog.

Ischemic myocardial injury was quantified as the sum of S-T segment elevations in epicardial electrocardiogram recordings (ΣS-T) following acute coronary artery occlusions in 17 dogs. ΣS-T rose from 3 ± 1 mv to 26 ± 4 mv ( P < 0.001) following occlusion. Myocardial contractility was similarly stimulated by intravenous infusions of dopamine or calcium. At reocclusions of the coronary artery, ΣS-T increased to 73 ± 12 mv ( P < 0.001) with dopamine and to 41 ± 7 mv ( P < 0.001) with calcium; the difference was statistically significant ( P < 0.005). Arterial concentrations of free fattv acids (FFA a ) were raised from 248 ± 33 µEq/liter to 888 ± 161 µEq/liter ( P < 0.005) with dopamine, but administration of calcium did not influence FFA a . After inhibition of lipolysis with β-pyridyl carbinol, no difference in ΣS-T or FFA a was observed; the mean values were 31 ± 4 mv for ΣS-T and 144 ± 13 µEq/liter for FFA a . Myocardial lipolysis was suggested in three experiments in which β-pyridyl carbinol reduced ΣS-T with dopamine, although FFA a remained unchanged. These measurements suggest that dopamine-induced lipolysis contributes significantly to the enlargement of ischemic injury in the myocardium following acute coronary artery occlusion, probably due to the metabolic stimulation of myocardial oxygen requirements. Test doses of dopamine given to seven patients raised FFA a by 225 ± 87 µEq/liter ( P < 0.03).

Closed chest model of intracoronary occlusion for study of regional cardiac function

A new closed chest animal technique permits selective intracoronary balloon occlusion and measurement of hemodynamic and regional metabolic function before and during occlusion and reperfusion. The distal end of the double lumen balloon catheter provides information about the nature and extent of flow distal to the occlusion and permits blood sampling or administration of pharmacologic agents directly into the ischemic zone. Independent blood sampling from the great cardiac vein by means of a specially designed balloon catheter and from the coronary sinus by cannula allows simultaneous biochemical and regional blood flow measurements from the occluded and nonoccluded segments of the heart. Simultaneous intracoronary epicardial electrocardiograms permit electrophysiologic correlation with regional hemodynamic and metabolic events. The administration of oxygen by tracheal airway can increase partial oxygen tension in the circulation distal to coronary occlusion. When intracoronary pressures distal to occlusion are markedly reduced, the frequency of ventricular fibrillation is much greater.

Relationship between epicardial S-T segment changes and myocardial metabolism during acute coronary insufficiency.

Canine left ventricular wall metabolites (ATP, creatine phosphate, glycogen, glucose, glucose-6-phosphate, and lactate) were assessed in the ischemic region of the wall after 17 minutes of ligation of the left anterior descending coronary artery at its midlevel. Variations in the degree of lactate accumulation were found between different sites in the same ischemic region and between the outer and the inner left ventricular wall at the same site. High levels of lactate were associated with S-T segment elevation in the epicardial electrocardiogram, but no lactate accumulation or only mild lactate accumulation was found at isoelectric sites. Lactate accumulation at isoelectric sites was higher in the outer wall than it was in the inner wall; the opposite tendency was observed at sites of S-T segment elevation. In addition to high lactate levels, sites of S-T segment elevation demonstrated a more pronounced depletion of ATP and creatine phosphate, indicating not only a marked anaerobic glycolysis but also a more pronounced overall anaerobic stress. No relationship was found, however, between the absolute magnitude of S-T segment elevation and the degree of lactate accumulation or ATP depletion at sites of S-T segment elevation within the ischemic region. The data obtained in this study demonstrate that during myocardial ischemia epicardial sites of S-T segment elevation are sites of pronounced subendocardial and epicardial ischemia and of anaerobic metabolism.

Reduction of experimental myocardial infarct size by corticosteroid administration.

The influence of the administration of pharmacologic doses of hydrocortisone on the extent and severity of acute myocardial ischemic injury and on subsequent necrosis after acute coronary occlusion was investigated in 28 dogs. In order to study acute myocardial injury, repeated epicardial electrocardiograms were recorded from 10 to 15 sites on the anterior surface of the left ventricle. Average ST segment elevation (ST) and the number of sites in which ST segment elevation exceeded 2 mV (NST), indices of the magnitude and extent of myocardial injury, respectively, were analyzed at 30 and 60 min after coronary occlusion. In the control group ST and NST did not change significantly in this time interval while in the treated group, which received 50 mg/kg hydrocortisone just after the 30 min recording, ST fell from 3.5+/-0.8 to 1.1+/-0.4 mV (P<0.01) and NST was reduced from 6.7+/-1.1 to 1.4+/-0.8 (P<0.01). In order to study the influence of hydrocortisone on necrosis, epicardial ST segment elevation 15 min after coronary occlusion was compared to myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 h later in each site. In a control group (14 dogs) a relationship was established between ST segment elevation at 15 min (in millivolts) and CPK activity (in international units per milligram of protein) 24 h later: log CPK = -0.0611ST + 1.26 (N = 102 specimens, r = -0.79). In the treated groups, hydrocortisone (50 mg/kg i.v.) was given either at 30 min after occlusion (seven dogs) or at 6 h after occlusion (six dogs). Both groups received supplementary doses of hydrocortisone (25 mg/kg) 12 h after occlusion. The two treated groups exhibited less CPK depression than that expected from ST segment elevation at each site, with slopes of the regression lines which were significantly less steep: log CPK = -0.0288ST + 1.26 (N = 48, r = -0.71) and log CPK = -0.0321ST + 1.31 (N = 48, r = -0.76) in the (1/2) h and 6 h groups, respectively. Histologically, sites with ST segment elevations of less than 2 mV at 15 min after occlusion exhibited normal appearance 24 h later. Sites with ST segment elevations (> 2 mV) in the control group showed histologic changes compatible with early myocardial infarction in 96% of specimens, while this occurred only in 61% and 63% of specimens, respectively, in the treated groups, showing that over one third of the sites were protected from undergoing necrosis due to the intervening hydrocortisone treatment. Thus pharmacological doses of hydrocortisone prevent myocardial cells from progressing to ischemic necrosis even when administration is initiated 6 h after coronary occlusion.

Improvement in Myocardial Function and Coronary Blood Flow in Ischemic Myocardium after Mannitol

The purpose of this study was to evaluate the effect of hyperosmolality on the performance of, and the collateral blood flow to, ischemic myocardium. The myocardial response to mannitol, a hyperosmolar agent which remains extracellular, was evaluated in anesthetized dogs. Mannitol was infused into the aortic roots of 31 isovolumic hearts and of 15 dogs on right heart bypass, before and during ischemia. Myocardial ischemia was produced by temporary ligation of either the proximal or mid-left anterior descending coronary artery. Mannitol significantly improved the depressed ventricular function curves which occurred with left anterior descending coronary artery occlusion. Mannitol also significantly lessened the S-T segment elevation (epicardial electrocardiogram) occurring during myocardial ischemia in the isovolumic hearts and this reduction was associated with significant increases in total coronary blood flow (P < 0.005) and with increased collateral coronary blood flow to the ischemia area (P < 0.005).THUS, INCREASES IN SERUM OSMOLALITY PRODUCED BY MANNITOL RESULT IN THE FOLLOWING BENEFICIAL CHANGES DURING MYOCARDIAL ISCHEMIA: (a) improved myocardial function, (b) reduced S-T segment elevation, (c) increased total coronary blood flow, and (d) increased collateral coronary blood flow.

Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis.

The effects of coronary artery reperfusion 3 hr after coronary occlusion on contractile function and the development of myocardial damage at 24 hr was studied experimentally. In 14 control and 6 reperfused dogs, relationships between epicardial ST segment elevation 15 min after coronary occlusion and myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 hr later were examined. The electrocardiograms were recorded from 10 to 15 sites on the left ventricular epicardium and transmural samples for CPK and histology were obtained from the same sites where epicardial electrocardiograms had been recorded. An inverse relation existed between ST segment elevation (mv) 15 min after occlusion and log CPK activity (IU/ mg of protein) 24 hr later, log CPK = - 0.06ST + 1.26. In dogs subjected to coronary artery reperfusion, there was significantly less CPK depression (log CPK = - 0.01ST + 1.31, [P < 0.01]) than that expected from the control group. In the control group 97% of specimens showing ST segment elevations over 2 mv at 15 min showed abnormal histology 24 hr later. In contrast, in the reperfused group 43% of sites exhibiting elevated ST segment at 15 min showed abnormal histology 24 hr later. In six additional dogs it was shown that the paradoxical movement of the left ventricular wall could be reversed within 1 hr of perfusion. Therefore, by enzymatic and histologic criteria, as well as by functional assessment, coronary artery reperfusion 3 hr after occlusion resulted in salvage of myocardial tissue.

Reduction by hyaluronidase of myocardial necrosis following coronary artery occlusion.

Electrocardiographic, enzymatic, and morphologic signs of myocardial ischemic injury following coronary occlusion have previously been shown to be ameliorated by reducing myocardial oxygen requirements, and/or by increasing the availability of oxygen as well as of substrates for anaerobic ATP production. Since hyaluronidase increases diffusion through the extracellular space and may facilitate delivery of substrates to ischemic cells, the influence of its administration on the size of experimentally produced infarcts was studied. In 14 control dogs epicardial electrocardiograms were taken in 10-15 sites on the anterior surface of the left ventricle before and after occlusion of the left anterior descending coronary artery. Twenty-four hours later, transmural specimens were obtained from the same sites from which electrocardiograms had been recorded, and were analyzed for creatine phophokinase (CPK) activity, for histologic changes, and glycogen content. In control dogs, sites exhibiting S-T-segment elevation 15 min after occlusion showed early structural signs of necrosis and glycogen depletion in 97% of specimens taken after 24 hours. The relationship between S-T-segment elevation at 15 min (mv) and CPK activity 24 hours later (IU/mg protein) was log CPK = –0.061 S-T + 1.26. Hyaluronidase (225 u/kg) was given to 15 dogs; no hemodynamic changes occurred but the depression of CPK activity was reduced following occlusion; log CPK = –0.024 S-T + 1.28. Similarly, only 55% of sites that showed S-T-segment elevation prior to hyaluronidase administration exhibited histologic signs of early infarcts and glycogen depletion 24 hours later. It is concluded that hyaluronidase diminished myocardial necrosis following acute coronary occlusion.

Effects of intraaortic balloon counterpulsation on the severity of myocardial ischemic injury following acute coronary occlusion. Counterpulsation and myocardial injury.

The effects of intraaortic balloon counterpulsation (IABC) on the magnitude and severity of myocardial ischemic injury were studied in 19 dogs following acute coronary occlusion and in two patients with cardiogenic shock. In the experimental group, epicardial electrocardiograms were taken from 10-14 sites on the anterior surface of the left ventricle following occlusion of the left anterior descending coronary artery or its apical branch. The average S-T-segment elevation ([see Equation in PDF File]) was used as an index of the magnitude of myocardial ischemic injury. In six dogs, two successive 20-min occlusions were performed, and IABC was started prior to the second occlusion. [see Equation in PDF File] 15 min following occlusion decreased from 3.3 ± 0.9 mv after the control occlusion to 1.4 ± 0.4 mv ( P &lt; 0.01) after the occlusion with IABC. In three dogs in which the occlusion was maintained and IABC initiated 30 min later, [see Equation in PDF File] decreased from 1.2 to 0.6 mv. In six dogs in which IABC was started 3 hours after occlusion, it induced a reduction of [see Equation in PDF File] from 4.2 ± 1.1 to 2.8 ± 1.0 mv ( P &lt; 0.01). In four dogs, ischemic injury was augmented by isoproterenol infusion (0.25 µg/kg/min), and while continuing the infusion IABC was initiated. It reduced [see Equation in PDF File] from 8.0 ± 1.9 to 5.7 ± 1.8 mv ( P &lt; 0.05). Thus, IABC reduced the magnitude and extent of myocardial ischemic injury after experimental coronary occlusion, both when IABC was employed prior to, and 3 hours following, coronary occlusion. IABC was also effective in reducing myocardial ischemic injury which had been increased by isoproterenol infusion. Employing a noninvasive technic, which utilizes 35 electrodes on the thorax, the effects of IABC were examined in two patients with cardiogenic shock associated with acute myocardial infarction. Preliminary observations in these patients confirmed the experimental results indicating that IABC reduced myocardial ischemic injury.

Effect of glucose-insulin-potassium infusion on myocardial infarction following experimental coronary artery occlusion.

The effects of glucose-insulin-potassium (GIK) infusion and glucose (G) infusion started 30 min after experimental coronary occlusion and the combination of GIK and propranolol (P) started 3 hours after coronary occlusion on the development of myocardial infarction were studied in 37 dogs. Fifteen minutes after the coronary occlusion, epicardial electrocardiograms were recorded at 10-15 sites; 24 hours later transmural specimens were obtained from the same sites for determination of myocardial creatine phosphokinase (CPK) activity and the evaluation of morphologic changes. In the control group (normal saline infusion) the relationship between S-T-segment elevation (mv) 15 min after occlusion and CPK activity (IU/mg of protein) 24 hours later was: log CPK = –0.064 S-T + 1.24; r = 0.81. In the GIK group, the infusion was begun 15 min following epicardial mapping, and sites with the same S-T-segment elevations showed less CPK depression than did the control group: log CPK = –0.022 S-T + 1.25. The G group also showed less CPK depletion than the control group but to a somewhat lesser extent than the GIK group (log CPK = –0.030 S-T + 1.20). The group receiving GIK and P 3 hours after occlusion also showed less CPK depression than did the control group (log CPK = –0.034 S-T + 1.26). Histologic analysis in 24-hour specimens showed that sites which exhibited S-T-segment elevation 15 min after occlusion showed normal histology in 3% of specimens obtained from control dogs, while the other 97% showed early signs of myocardial infarction. However, in the GIK group, 36% of the specimens with S-T-segment elevation prior to the infusion were histologically normal 24 hours later, while in the G group 30% were normal, and in the GIK and P group 17% were normal. Electron microscopy confirmed the morphologic changes observed by light microscopy. Thus, in the presence of experimental coronary occlusion, GIK exerts a protective effect against myocardial ischemia and reduces the extent of myocardial necrosis. G alone acts similarly but to a lesser degree, while a beneficial effect can also be demonstrated when GIK and P are started 3 hours after the onset of coronary occlusion.

Factors influencing infarct size following experimental coronary artery occlusions.

The purpose of this study was the determination of whether hemodynamic and pharmacologic factors influence the extent and severity of myocardial necrosis produced by coronary occlusion. In 48 dogs, 10 to 14 epicardial leads were recorded on the anterior surface of the left ventricle in the distribution and vicinity of the site of occlusion of a branch of the left anterior descending coronary artery. The average S-T segment elevation for each animal was determined at 5-min intervals after occlusion. This elevation was used as an index of the presence and severity of myocardial ischemic injury. The number of sites showing this elevation provided an additional measure of the size of the injured area. Occlusion alone raised the average S-T segment elevation from 0.22 ± 0.04 to 3.32 ± 0.37 mv (SEM). Isoproterenol, ouabain, glucagon, bretylium, and tachycardia given prior to a repeated occlusion increased the severity and extent of ischemic injury, while propranolol decreased it. Elevation of arterial pressure with methoxamine reduced the occlusion-induced S-T segment elevation, and lowering of the mean arterial pressure by hemorrhage had the opposite effect. In 19 additional experiments, propranolol, isoproterenol, and alterations in arterial pressure produced similar alterations in S-T segment elevation when these interventions were applied as long as 3 hr after ligation. In a third group of dogs, myocardial creatine phosphokinase (CPK) activity was determined 24 hr after occlusion at the same sites at which epicardial electrocardiograms were taken. Depression of myocardial CPK activity in injured portions of the left ventricle 24 hr after coronary artery ligation correlated well with S-T segment elevation in the same sites 15 min after ligation. Moreover, isoproterenol increased and propranolol decreased the area of depression of myocardial CPK activity. We conclude that the hemodynamic status and neurohumoral background at the time of occlusion and for up to 3 hr thereafter can alter the extent and severity of myocardial ischemic injury and myocardial necrosis.

Effects of catecholamines on hemodynamics and myocardial contractility in dog--especially the effects of norepinephrine, epinephrine and isoproterenol

Catecholamines play an important role in main-trance of circulatory function and are widely employed in treatment of shock states. There have been many experimental studies on cardiovascular effects of catecholamines. However, few has been reported on comprehensive observations of their hemodynamic effects in animals maintaining normal circulation. The purpose of the present study is to investigate the effects of catecholamines on hemodynamics and myocardial contractility in special reference to influence of different dosage and manners of administration. Methods Adult mongrel dogs anesthetized with intraperitoneal pentobarbital sodium (30 mg/kg) were subjected to thoracotomy under artificial respiration. The following six tracings were simultaneously recorded on an electromagnetic oscillograph; (1) aortic blood flow curves with the probe of an electromagnetic flowmeter fixed around the aortic root, (2) aortic blood pressure curves with a catheter tip lodged in the left common carotid artery, (3) left atrial pressure curves with a catheter inserted in the left atrial appendage, (4) left ventricular cavity through the apex, (5) the first derivatives of the left ventricular pressure using an R-C differentiating circuit whose time constant was 0.5 msec, and (6) unipolar left ventricular epicardial electrocardiogram. These simultaneous tracings were analyzed for the following parameters; the heart rate, aortic blood pressure and flow, stroke volume, mean left atrial pressure, left ventricular external power, stroke work, Isometric Time-Tension Index [(dp/dt)/IIT], and total peripheral vascular resistance. A catheter lodged in the femoral vein was used for intravenous administration of catecholamines. For evaluation of the effects of a single bolus dose of the drugs, each of eight dogs was subjected, at an interval of 5 to 8 minutes, to rapid intravenous injections of six different drug-dose combinations (0.1 and 0.8 μg/kg of ISP, EP and NE). The effects of sustained intravenous infusion of NE was also investigated. A constant flow pump was employed for intravenous infusion of 5% dextrose solution for 3 hours throughout the experiment. Control data was obtained during the first one hour when only the dextrose solution was infused. NE was given at a rate of 0.8 μg/kg/min for the next one hour. For the last one hour continuous observation was also made with the dextrose solution alone infused. A similar experiment was also performed in spinal dogs who had undergone ligation of the bilateral vertebral arteries and disconnection of the bilateral cervical vagus nerves and the spinal cord at the level of the second cervical vertebra.

Comparison between metabolic changes in local venous and coronary sinus blood after acute experimental coronary arterial occlusion

A technique for the study of local metabolic changes in coronary venous blood draining from a small area of ischemic myocardium is described. Overt left ventricular failure, ventricular arrhythmias and possible secondary effects on local metabolic changes were avoided. Metabolic changes in local coronary venous blood and in coronary sinus blood were compared. Gross changes detected by local coronary venous sampling were not observed in coronary sinus blood samples. The possible relevance of this observation to clinical studies was noted. The small ischemic lesion usually involved less than 10 percent of the heart volume and was characterized by acute S-T segment elevation in the epicardial electrocardiogram and by positive changes in values for local coronary venous blood lactate, pyruvate, lactate/ pyruvate ratio, glucose, potassium and phosphate. Free fatty acids and beta hydroxybutyrate and acetoacetate levels were also studied. The technique and its results are compared with other methods of study of the metabolism of ischemic heart tissue.

Depression of the S-T segment in epicardial electrocardiogram associated with experimental major coronary artery constriction

Electrocardiograms in more than 15 leads were recorded from the left ventricular surface during graded constriction of the major coronary arteries or their branches in anesthetized dogs. With mild to moderate constriction of the left circumflex, the anterior descending artery or their distal branches, a horizontal or flat depression of the S-T segment was recorded from leads over the distribution area of each constricted artery. The depth of S-T depression was of greatest magnitude at the border and decreased as the center was approached. S-T elevation or decreasing magnitude of S-T depression began to develop following severe constriction. These results will provide an experimental basis for interpretation of electrocardiographic changes during angina pectoris. In contrast to the border of the ischemic area, where S-T depression was recorded with any degree of constriction, elevation after severe constriction was not infrequently the only S-T displacement at the center. It is suggested that the direction of S-T displacement following coronary artery constriction depends on the position of the electrode with respect to the ischemic area. The epicardial S-T depression observed in this study is thought to be a reciprocal effect of subendocardial injury, as has been generally accepted.

Observations on D. C. and very low frequency components of the electrocardiogram.

SummaryThe authors described an experimental method of measuring the D. C. and very low frequency components of the electrocardiograms, (relative T-Q and S-T segment shifts) using a commercially available clinical model of electrocardiograph and laboratory type calomel electrodes. Several experimental trials included observation of changes in D. C. and very low frequency components of epicardial electrocardiograms under the influence of electrolytes and local ischemia and served primarily the purpose of testing out the sensitivity of the method. The observations served as a basis for discussion of usefulness of this type of ECG analysis for further theoretical studies on the electrical field of the heart and its applicability for more precise clinical diagnosis of the anatomical state of the heart. The problem of recording equipment and nonpolarizing electrodes was discussed briefly.

Correlation of intramyocardial electrocardiograms with polarographic oxygen and contractility in the nonischemic and regionally ischemic left ventricle.

A new technique for simultaneous amplification and recording of intramyocardial oxygen-reduction currents and electroeardio-graphic voltages from the tips of platinum oxygen electrodes was combined with cinematographic muscle contraction records from exposed dog hearts. The picture of localized ischemia produced by occlusion of medium-sized coronary arterial branches was compared, under stable systemic circulatory conditions, with the changes of myocardial oxygenation, electrical activity, and contractility, separately or together. Myoeardial electro-cardiographic abnormality appeared as early as disturbances of local oxygen and contraction at the centers of ischemic areas; at the borders, only the myocardial electrocardiogram was unequivocally abnormal. The epicardial electrocardiogram could be normal despite severe, acute disturbance of electrical activity in the underlying myocardium, and was not useful for the study of small isehemic areas, the onset of ischemia, or the borders of any isehemic area. No single index of myocardial function was dependable for following the course and estimating the extent of regional ischemic dysfunction, or for distinguishing it from traumatic or nonisehemic myocardial disturbances. The most complete description of the sequence of ischemic events was derived from the analysis of changes in local myocardial electrical activity. For this, however, it was necessary to interpret and compare direct heart-body electrocardiograms from myocardial and epicardial sites inside and outside an ischemic area, with attention to simultaneous records of myocardial oxygen and local contraction. Such a combination of indices is considered essential for adequate description and differentiation of any localized myocardial change in a working, blood-perfused heart.

A study on direct epicardial electrocardiogram concerning QRS patterns.

Direct epicardial electrocardiograms were recorded in 97 cases of normal hearts and various heart diseases, and the patterns of the QRS complex of the chest lead electrocardiograms were analysed with normal heart, left or right ventricular hypertrophy, combined ventricular hypertrophy, and right bundle branch block. In the case of the left ventricular hypertrophy the left chest ECG agreed well with the direct epicardial ECG. In the case of right ventricular hypertrophy the right chest ECG may be a mere reflection of the potential variations at the base of the right ventricle or conus arteriosus. The right bundle branch block of the mitral stenosis appears to be not due to a genuine conduction disturbance but to represent the potential variations in the base of the right ventricle.