Segment Elevation Research Articles

Repetitive Myocardial Ischemia of Prinzmetal Type Without Angina Pectoris

In a patient with a normal electrocardiogram, normal treadmill exercise test, normal coronary arteriogram and no symptoms to suggest angina pectoris, continuous monitoring during several days exhibited repetitive (one to two per hour) S-T segment elevations in the precordial electrocardiographic leads and hemodynamic changes typical of Prinzmetal's angina (reduction in arterial pressure and cardiac index and increase in systemic peripheral resistance and pulmonary wedge pressure). This case demonstrates that electrical and dynamic cardiac alterations of Prinzmetal's angina can occur even in the absence of angina pectoris.

Significance of S-T segment elevations in acute myocardial ischemia: Evaluation with intracoronary electrode technique

A method is described for measuring intracoronary S-T-segment elevations in the closed chest, a technique that appears to provide more reliable measurements of myocardial ischemia. Electrodes were inserted through intracoronary balloon catheters that were placed within a coronary artery and its adjoining vein both proximal and at several points distal to a coronary occlusion. Intracoronary arterial and adjacent venous electrocardiograms produced equivalent tracings. The intracoronary S-T-segment elevations after coronary occlusion resembled those recorded from the epicardial surface but were free of artifacts noted in open chest studies. Study of progressive alterations of the intracoronary S-T segment after proximal occlusion of the left anterior descending coronary artery in 18 closed chest dogs revealed a peak segment elevation of 3.2 ±0.6 mv within 5 minutes, followed within 2 to 3 hours by spontaneous reduction by more than 40 percent of the S-T elevation over the occluded zone. In 44 percent of these animals, the S-T elevation decreased spontaneously to less than 1 mv, and in 22 percent it decreased to the preocclusion control level within 2 hours of occlusion. This spontaneous decrease in S-T elevation was frequently followed by a secondary increase and then S-T segment fluctuations. Reperfusion of the left anterior descending coronary artery after 30 to 60 minutes of occlusion generally led to a prompt reduction in S-T elevation. In some cases S-T elevations persisted up to 14 hours of occlusion, were reduced after reperfusion and exhibited a renewed pronounced increase after subsequent reocclusion of the left anterior descending coronary artery. During the 1st hour after occlusion, the early S-T segment elevation followed by spontaneous reduction generally corresponded temporally with the derangements in myocardial lactate extraction and potassium loss. However, after 1 hour of occlusion no clear-cut correlation could be established between S-T fluctuations and changes in hemodynamic or myocardial metabolic measurements. We conclude that the new closed chest intracoronary electrocardiographic S-T technique might be of use for monitoring the early ischemic myocardial derangements and to assess benefits or drawbacks of treatment in both the experimental animal and man. Correspondence of S-T segment elevation with lactate and potassium alterations in the coronary-occluded region in the 1st hour after occlusion indicates that S-T segment elevation might represent an index of early myocardial ischemia. The spontaneous S-T changes that follow coronary occlusion must be taken into consideration when investigators utilize S-T segment modification as a sign of effectiveness of treatment.

Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition

Myocardial cell pH was measured with 5,5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicatordilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58 percent of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.

Regional and global myocardial effects of intravenous and sublingual nitroglycerin treatment after experimental acute coronary occlusion

The consequences of sublingual and intravenous nitroglycerin treatment after acute coronary occlusion were studied in 18 closed chest dogs. Intravenous (0.1 mg/min) or sublingual (0.4 mg/15 min) nitroglycerin therapy was instituted 1 hour after occlusion and the effects were observed over a period of 2 hours. Hemodynamics and global and regional cardiac function were measured in both the coronary occluded and nonoccluded segments of the left ventricle before and during coronary occlusion, and after administration of nitroglycerin. A similar nine dog control series was used to establish the significance of the measured effects of nitroglycerin. Intravenous nitroglycerin therapy after 1 hour of occlusion resulted in a marked increase in heart rate (37 ± 12 [mean ± standard error of the mean] percent), reduction of systolic blood pressure (9 ± 3 percent), decrease in left ventricular end-diastolic and end-systolic volumes (32 ± 5 percent and 34 ± 5 percent), increase in coronary sinus flow (64 ± 24 percent) and decrease in left ventricular stroke work (29 ± 8 percent). Sublingually administered nitroglycerin produced similar trends but much less pronounced effects. However, intravenous or sublingual administration of nitroglycerin provided no improvement or caused further deterioration in ischemic region lactate extraction and potassium loss. The left ventricular ejection fraction, which was severely depressed after 1 hour of occlusion, changed minimally after administration of nitroglycerin, and there was no evidence of any correction of regional left ventricular akinesia or dyskinesia. Whereas mean systemic vascular resistance changed minimally as a result of nitroglycerin therapy, it increased 19 ± 8 percent during a corresponding period of an untreated coronary occlusion series suggesting that nitroglycerin prevented an anticipated increase. Postocclusion S-T segment elevation in the electrocardiogram persisted after treatment. Our data corroborated that nitroglycerin reduced left ventricular volumes and increased coronary sinus flow; however, these improvements were accompanied by persisting metabolic and mechanical derangements in the ischemic region.

Functional abnormalities in nonoccluded regions of myocardium after experimental coronary occlusion

The performance characterstics of both ischemic and “adjacent” and “remote” nonischemic myocardium were studied in open chest dogs by three mercury-in-Silastic length gauges sutured to the anterior surface of the left ventricle before and after occlusion of the distal left anterior descending coronary artery. The adjacent gauge was separated from the ischemic segment by one large nonoccluded diagonal branch of the left anterior descending artery. Remote myocardium was separated from the ischemic area by two such branches. At the time of occlusion epicardial S-T segment elevation appeared in the ischemic region but not in the adjacent or remote regions. Immediately after occlusion, typical changes of ischemic dysfunction appeared. Late systolic lengthening, depression of systolic shortening and increased diastolic compliance occurred consistently and simultaneously in ischemic and adjacent regions and inconsistently in the remote region. Five minutes after occlusion, fiber shortening was depressed to 21, 58 and 67 percent of control values in ischemic, adjacent and remote regions, respectively. Heart rate did not change, and mean arterial pressure decreased slightly. These changes persisted over time. In 11 of these dogs, end-diastolic pressure was maintained constant 20 minutes after occlusion. Systolic shortening was depressed to 40 and 74 percent of control values in the ischemic and adjacent regions, respectively. In six dogs, end-diastolic pressure was varied from 5 to 20 mm Hg by rapid volume loading during the control state and 30 minutes after occlusion. Systolic shortening in ischemic, adjacent and remote regions was depressed to 20, 40 and 65 percent of control values, respectively. The severity of all functional alterations after coronary occlusion was directly related to proximity to the ischemic region. These results indicate that depression of left ventricular function after coronary occlusion may be partially related to previously unrecognized depression of function in apparently “nonischemic” myocardium.

Methylprednisolone treatment in acute myocardial infarction: Effect on regional and global myocardial function

The effects of methylprednisolone treatment on acute myocardial ischemia were studied in nine closed chest dogs. After 1 hour of proximal occlusion of the left anterior descending coronary artery, an intravenous bolus injection (50 mg/kg body weight) of methylprednisolone was administered and its effects studied during an additional 2 hours of occlusion. After 2 hours of treatment the following significant mean alterations from levels after 1 hour of occlusion were noted: an increase of 16.7 percent in heart rate and decreases of 23 percent in left ventricular end-diastolic pressure, 32 percent in stroke volume, 14 percent in cardiac output and 37 percent in stroke work. Peak systolic pressure, maximal rate of rise of left ventricular pressure (dP/dt), left ventricular end-diastolic volume, systemic vascular resistance and coronary sinus blood flow changed less than 10 percent. Ejection fraction and regional cardiac wall motion were not improved. Metabolic dysfunction of the coronary-occluded myocardium, revealed by regional lactate as well as potassium derangements, persisted throughout the 2 hour treatment period. Comparison of these results with equivalent data from an untreated series of nine dogs with 3 hours of occlusion demonstrated no improvement in the treated series. Methylprednisolone failed to restore regional cardiac metabolic and mechanical function, and treatment was associated with a further rise in S-T segment elevations. Administration of methylprednisolone after 1 hour of proximal left anterior descending coronary occlusion apparently does not reverse cardiac dysfunction in the first 2 hours of treatment.

Effects of hyaluronidase and hydrocortisone on myocardial necrosis after coronary occlusion

In anesthetized open chest dogs, hydrocortisone (50 mg/kg body weight administered 30 minutes after occlusion and 25 mg/kg 12 hours later) substantially reduced the size of myocardial infarcts, as reflected by both myocardial creatine phosphokinase activity and histologic appearance 24 hours later. Similarly, hyaluronidase, which increases diffusion through the extracellular space and presumably facilitates delivery of substrate to ischemic cells, also reduced the extent of myocardial necrosis after coronary occlusion in the dog. In view of the salutary effects of hyaluronidase and the absence of serious side effects, this agent was administered clinically to two groups of patients, who were compared with two groups of untreated control subjects. Hyaluronidase (500 National Formulary units/kg × 8) was shown to result in a significantly more rapid reduction in the magnitude and the extent of precordial S-T segment elevations, and in patients treated within 4 hours a tendency to a lower incidence rate of Q waves and a smaller reduction of R waves.

Measurement of S-T segment elevation in acute myocardial infarction in man: Comparison of a precordial mapping technique and the frank vector system

Precordial S-T segment mapping has been used to evaluate the extent of ischemie injury in patients with acute myocardial infarction. Because precordial S-T segment mapping is time-consuming and is limited to patients with anterior wall myocardial infarction, we evaluated the possibility of using the magnitude (ST-VM) and direction (ST-VD) of the S-T vector, derived from X, Y and Z leads of the Frank vector system, as a substitute for the precordial S-T segment mapping technique. Precordial S-T segment mapping and Frank system vectorcardiograms were simultaneously obtained in three groups: (1) nine normal subjects; (2) nine patients with persistent S-T segment elevation 2 to 15 months after acute anterior myocardial infarction; and (3) nine patients with acute anterior myocardial infarction studied on 41 occasions. For both systems the S-T segments were analyzed 20 and 60 msec after completion of inscription of the QRS complex. The sum of the S-T segment elevations for the 35 sites (∑ST) and the number of sites (NST) in which S-T segment elevations exceeded 0.1 mv were computed for the precordial S-T maps. The ST-VM and ST-VD were calculated by standard formulas from X, Y and Z lead tracings of the Frank vector system. Good correlations were observed between: ST-VM and ∑ST ( r = + 0.818 and + 0.791 at 20 and 60 msec, respectively, P < 0.001); and ST-VM and NST ( r = + 0.773 and + 0.705 at 20 and 60 msec, respectively, P < 0.001). Furthermore, changes in the location of S-T segment elevations in serial precordial S-T segment maps were reflected by changes in ST-VD. Observations in patients with inferior wall myocardial infarction suggest that ST-VM and ST-VD can be serially followed in such patients. Thus, estimation of the magnitude and direction of the S-T vector is a simple alternative to standard precordial S-T segment mapping that allows for continuous monitoring of S-T segment elevations in all patients with acute myocardial infarction.

Subendocardial S-T Segment Changes During Acute Coronary Occlusion

Subendocardial ischemia during coronary occlusion in dogs was studied using S-T segment elevations in unipolar subendocardial electrodes. Alterations in heart rate or cardiac output caused quantitatively similar changes in subendocardial and epicardial S-T elevation. Increasing blood pressure from 75 to 100 or 75 to 125 mm Hg caused a smaller reduction in subendocardial than in epicardial S-T elevation ( p < 0.01). In this situation, therefore, subendocardial ischemia tends to be maintained while epicardial ischemia is reduced by higher arterial pressures. Hemodynamic manipulations can cause quantitatively different changes in subendocardial and epicardial S-T segment elevation.

Changes in myocardial blood flow and S-T segment elevation following coronary artery occlusion in dogs.

The relationship between regional blood flow and epicardial S-T segment elevation was studied in 26 open-chest anesthetized dogs with left anterior coronary artery ligations. Changes in myocardial blood flow, measured with 15 plus or minus 5mu (diameter) microspheres labeled with 141-Ce, 85-Sr, and 169-Yb, were correlated with summated S-T segment elevations 15 minutes, 1 hour, and 2 hours after coronary artery occlusion. In normal areas, myocardial blood flow was 113 plus or minus 5 ml/min 100 g- minus 1 and summated S-T segment elevation was 0.3 plus or minus 0.2 mv. Fifteen minutes after coronary artery occlusion in 26 dogs, S-T segment elevation was 5.7 plus or minus 0.7 mv over the center of the infarct and myocardial blood flow was 10 plus or minus 1 ml/min 100 g- minus 1; over the border zone, myocardial blood flow was 63 plus or minus 4 ml/min 100 g- minus 1 and S-T segment elevation was 3.1 plus or minus 0.1 mv. One third of the areas with a myocardial blood flow of 10 ml/min 100 g- minus 1 or less had no S-T segment elevation. In the center and border zones of the infarct in 9 dogs, myocardial blood flow increased from 11 plus or minus 2 and 67 plus or minus 8 ml/min 100 g- minus 1 15 minutes after occlusion to 20 plus or minus 4 and 84 plus or minus 12 ml/min 100 g- minus 1, respectively, 2 hours after coronary artery occlusion. These increases were not associated with a significant reduction in summated S-T segment elevation. The results do not suggest a simple quantitative relationship between epicardial S-T segment elevation and myocardial blood flow following acute coronary artery occlusion.

Natural history of S-T segment elevation after acute myocardial infarction

Clinical, electrocardiographic and cineventriculographic data in two patient groups were analyzed to define the natural history of S-T segment elevation after myocardial infarction. In sixteen of 22 patients (73 percent) with acute inferior myocardial infarction, S-T segment elevation was present on hospital admission, persisting in 1 (5 percent) by the 2nd week. S-T segment elevation was present on admission in 18 of 23 patients (78 percent) with acute anterior myocardial infarction and persisted in 13 after 1 week and in 9 of 14 (64 percent) during a follow-up period of 1 to 6 months. S-T segment elevation lasting more than 2 weeks after myocardial infarction did not resolve. Compared with patients with inferior myocardial infarction or anterior infarction without persistent S-T segment elevation, patients with anterior infarction and persistent S-T segment elevation had a higher level of mean maximal serum creatine phosphokinase (CPK), more severe left ventricular decompensation and a greater frequency of death in the early follow-up period. In a separate series of 95 patients with cineangiographically documented coronary artery disease, 40 of 65 patients (62 percent) with advanced anterior and apical asynergy had persistent S-T segment elevation. By contrast, only 1 of 30 (3 percent) with coronary disease and normal ventriculograms had persistent S-T segment elevation. We concluded that (1) the natural history of S-T segment elevation after myocardial infarction is resolution within 2 weeks in 95 percent of inferior but in only 40 percent of anterior infarctions; (2) S-T segment elevation persisting more than 2 weeks after myocardial infarction does not resolve; (3) persistent S-T segment elevation is associated with clinically more severe myocardial infarction; and (4) in patients with coronary artery disease, persistent S-T segment elevation after myocardial infarction is a specific but insensitive index of advanced asynergy.

Prinzmetal's variant angina: Hemodynamic and angiographic observations during pain

Hemodynamic and angiographic data obtained during pain from four patients with Prinzmetal's variant angina are reported. The left ventricular pressure-time index did not increase before or during attacks of angina in three of the four patients; left ventricular systolic performance was impaired during pain in all three. In one of these three patients left ventricular pressure-volume data obtained during angina suggested a reduction in diastolic compliance; in another, pain and S-T segment elevation were present during coronary arterial spasm. The fourth patient had an increase in both arterial blood pressure and heart rate before an attack; in this patient coronary arterial spasm could not be demonstrated during the period of pain and S-T elevation. The data presented suggest that hemodynamic factors that increase the myocardial Oxygen requirements are absent and that coronary arterial spasm is present in some, but not all, patients with variant angina.

Circulatory effects of tazolol in experimental myocardial infarction

The hemodynamic effects of tazolol, a new long-acting beta-stimulating drug, were studied in dogs with acute pump failure caused by experimental myocardial infarction and the results were compared with the actions of isoproterenol given in small and large doses. Tazolol produced a significant and sustained increase in cardiac output and stroke volume, while causing a decrease in peripheral resistance and mean aortic pressure. Heart rate was only modestly increased. Compared with isoproterenol at equivalent doses, tazolol appeared to cause less S-T segment elevation at the margin of infarction. The increase in double product (systolic pressure X heart rate) produced by tazolol was also considerably less than that of isoproterenol. Tazolol may prove to be a useful addition to the drugs available for the treatment of myocardial failure of various causes. It Is now being studied in patients with heart failure due to coronary artery disease.

Remote electrocardiography. Clinical experience with telephone transmission of electrocardiograms.

Two hundred three electrocardiograms were sent by 27 patients without assistance over standard telephone lines by means of a small device capable of multiple electrocardiographic lead transmission and automatic switching. Five patients with infrequently occurring symptoms were shown not to have paroxysmal arrhythmia. One with atypical chest pain had S-T segment elevation in a single electrocardiographic lead with pain, thus confirming the diagnosis of "variant angina." Drug dosage and other therapy of non-life-threatening arrhythmia were facilitated in eight patients. There were neither clinical nor electrocardiographic events of note in 11 patients who had been hospitalized with acute myocardial infarction and ventricular arrhythmia, in whom frequent remote ECGs were obtained during the month following hospital discharge. The value of remote electrocardiography during convalescence from acute myocardial infarction remains speculative. (JAMA230:1293-1294, 1974)

Remote Electrocardiography

Two hundred three electrocardiograms were sent by 27 patients without assistance over standard telephone lines by means of a small device capable of multiple electrocardiographic lead transmission and automatic switching. Five patients with infrequently occurring symptoms were shown not to have paroxysmal arrhythmia. One with atypical chest pain had S-T segment elevation in a single electrocardiographic lead with pain, thus confirming the diagnosis of variant angina. Drug dosage and other therapy of non-life-threatening arrhythmia were facilitated in eight patients. There were neither clinical nor electrocardiographic events of note in 11 patients who had been hospitalized with acute myocardial infarction and ventricular arrhythmia, in whom frequent remote ECGs were obtained during the month following hospital discharge. The value of remote electrocardiography during convalescence from acute myocardial infarction remains speculative. (JAMA230:1293-1294, 1974)

Prinzmetal's variant angina pectoris.

PRINZMETAL’S VARIANT ANGINA PECTORISDAVID C. LEVIN, M.D., MICHAEL WOLK, M.D. and DONALD N. SUMMERS, M.D.Audio Available | Share

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.

Prinzmetal Angina With Transient Complete Heart Block

In 1959, Prinzmetal and his associates^1,2described a form of angina quite different from classic Heberden angina pectoris. Arrhythmia occurred in about 50% of cases during the peak of S-T segment elevation. This paper describes a patient with this variant of angina pectoris, associated with transient, complete atrioventricular (AV) block. Recurrent episodes of syncope would not be controlled in this patient by isosorbide dinitrate and required insertion of a transvenous demand pacemaker. Advanced degree of AV block is a rare complication and only few cases have been reported.^1-4Because of this rarity and the subsequent management of our patient, we believe this report may be of general interest. <h3>Patient Summary</h3> A 76-year-old black man was admitted to the Veterans Administration Hospital in Cleveland because of loss of vision in the left eye. He had been treated for glaucoma for many years, losing vision in his right eye in

Cardiac abnormalities in subarachnoid hemorrhage: a resumé.

There have been numerous reports demonstrating electrocardiographical changes secondary to subarachnoid hemorrhage, consisting of atrial and ventricular arrhythmias, alterations in QRS configuration, Q-T interval prolongation, T-wave abnormalities, and S-T segment elevation or depression. Abnormalities of cardiac muscle and subendocardial hemorrhage have been seen in patients dying of subarachnoid hemorrhage. Experimental work has shown that electrical impulses in the sympathetic nervous system and hypothalamus produce most of these changes, and the implication is that these changes can be prevented by sympathetic blockade. Pulmonary edema also has been shown to occur frequently after subarachnoid hemorrhage, and again the sympathetic nervous system is implicated in the pathophysiology. Studies done illustrating these points are discussed and conclusions drawn with reference to therapy.

Effects of various agents on regional ischemic myocardial injury: Electrocardiographic analysis

Myocardial unipolar electrical potentials were recorded in 52 open-chest dogs from multiple epicardial and subendocardial sites in an area judged to be perfused by a small branch of the anterior descending coronary artery. The degree of individual electrode S-T segment shift was utilized as a measurement of the degree of localized myocardial ischemia. Individual electrode voltage shifts were summed (Σ) from the respective recording areas and expressed in millivolts as total epicardial and subendocardial Σ S-T segment elevation. Repeated five-minute occlusion challenges at 30 minute intervals resulted in reproducible degrees of Σ S-T segment shifts at both sites after the second occlusion challenge. Isoproterenol (0.25 and 1.0 μg per kilogram per minute) and norepinephrine (1.0 μg per kilogram per minute) infused intravenously increased the degree of the Σ S-T segment response during the ischemic chanllenge, as did increasing the heart rate an average of 42 beats per minute. Conversely, norepinephrine (0.1 μg per kilogram per minute) and propranolol (1 mg. per kilogram) reduced the degree of ischemic Σ S-T segment response. Consistent regional differences in either the direction or magnitude of the ischemic Σ S-T segment shifts were not observed during any of the above interventions. It is concluded that changes in the epicardial electrograms largely reflect the degree of subendocardial ischemia as determined electrocardiographically under the above experimental conditions.