To simply identify "up or down" displacement of the ST segment in the electrocardiogram can lead to serious errors

The purpose of this brief communication is to emphasize that serious errors can occur when the interpreter of electrocardiograms simply identifies, but does not understand, the mechanism responsible for ST-segment elevated myocardial infarction or non-ST-segment elevated myocardial infarction. Such interpretive errors may, in turn, lead to the incorrect treatment of myocardial infarction. In addition, errors of omission are made when the interpreter states what is not present (non-ST-segment elevated myocardial infarction) rather than stating what is present in the electrocardiogram. Finally, the real question is, why does properly used thrombolytic therapy or angioplasty rejuvenate injured myocytes that are located in the epicardium but do not rejuvenate injured myocytes located in the subendocardial area?     

Transmural gradients of experimental myocardial ischemia: limited correlation of ultrastructure with epicardial S-T segment elevation.

A standardized preparation was developed to investigate the precise relationship between epicardial S-T segment elevation and myocardial ultrastructure. The distal left anterior descending coronary artery was occluded for 20 minutes and epicardial S-T segments were recorded at five-minute intervals. Immediate perfusion-fixation with glutaraldehyde preserved premortem anatomic relationships and allowed precise sampling of the myocardium immediately underlying sites of S-T segment recording. Ischemic and non-ischemic zones were defined both anatomically and by S-T segment mapping. Transmural samples at 0.2 cm. intervals were compared at sites in ischemic and non-ischemic zones. In non-ischemic zones, S-T segment elevations ranged from 0 to 2 mm., and myocardial ultrastructure was normal. In ischemic zones, S-T segment elevations ranged from 0 to 14 mm., and samples showed a gradient of ischemic injury with greatest change in subendocardial blocks. The extent of ultrastructural change at any point was not consistently proportional to the height of S-T segment elevation. S-T segment elevations greater than 2 mm. were always associated with a marked transmural gradient of change, but S-T segment elevations less than 2 mm. in ischemic zones could also be associated with severe subendocardial and mid-myocardial change. In a second group of dogs the coronary artery snare was released after 20 minutes of occlusion and recovery was allowed for 60 minutes before killing and subjecting to perfusion-fixation. These hearts exhibited no abnormality in myocardial ultrastructure when sampled in the same fashion as the first group.In this model a reproducible gradient of transmural, myocardial ultrastructural change was demonstrated under conditions of reversible injury. Prominent S-T segment elevation in ischemic zones always indicated the presence of underlying ultrastructural change, but marked changes were also present when S-T segment elevations were minimal, indicating that the S-T segment maps tended to underestimate the extent of early ischemic change. We were unable to establish a quantitative relationship between the extent of S-T segment elevation and the extent of transmural ultrastructural change.     

Precordial S-T segment elevation mapping: an atraumatic method for assessing alterations in the extent of myocardial ischemic injury. The effects of pharmacologic and hemodynamic interventions

A noninvasive technique for evaluating the extent of myocardial ischemic injury after experimental coronary artery occlusion was devised and applied to study alterations in the extent of injury produced by hemodynamic and pharmacologic interventions. The technique was then extended to the assessment of myocardial ischemic injury in patients with acute myocardial infarction. In 7 closed chest dogs, electrocardiograms were recorded from 15 sites on the chest wall before and after intermittent occlusions of the left anterior descending coronary artery. There was no S-T segment elevation before the occlusion; 15 minutes after occlusion the sum of S-T segment elevations (ΣS-T) averaged 15.0 ± 3.0 mm (SEM, 1 mm deflection = 0.1 mv), and an average of 4.2 ± 0.6 sites exhibited elevations exceeding 0.1 mv (NS-T). Occlusions occurring during administration of isoproterenol (0.25 μg/kg per min) increased ΣS-T to 51.0 ± 9.0 mm and NS-T to 10.6 ± 0.9, whereas occlusions occurring after administration of propranolol (1 mg/kg) decreased ΣS-T to 3.0 ± 1.5 mm and NS-T to 0.2 ± 0.2. In 8 dogs the extent of ischemic injury, manifested by S-T segment changes, was decreased by propranolol and norepinephrine and increased by hemorrhagic hypotension and isoproterenol, applied up to 6 hours after occlusion. Reproducible S-T segment maps, using 35 surface electrodes, were obtained in 19 patients with acute myocardial infarction. In 15 patients studied serially, ΣS-T decreased from 54.25 ± 7.00 to 38.50 ± 6.30 mm and NS-T from 18.7 ± 2.5 to 12.3 ± 2.8, respectively, during a 24 hour period. However, in 3 patients in whom ventricular fibrillation, arterial hypotension and further ischemic pain occurred, ΣS-T and NS-T increased whereas in another patient propranolol decreased ΣS-T and NS-T. Thus, precordial mapping, both in dogs and patients, shows changes parallel to those measured by the epicardial technique and should provide a useful clinical tool for determining acute changes in the extent of ischemic injury.     

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.     

Idiopathic hypertrophic subaortic stenosis: evaluation of anginal symptoms with thallium-201 myocardial imaging.

The evaluation of angina pectoris in patients with idiopathic hypertrophic subaortic stenosis is difficult in those in the age group prone to coronary artery disease. Ten patients with angina pectoris, normal coronary angiograms and idiopathic hypertrophic subaortic stenosis were studied with thallium-201 myocardial imaging performed in conjunction with submaximal treadmill exercise testing. The resting electrocardiogram demonstrated left ventricular hypertrophy with S-T segment abnormalities in seven patients, thereby vitiating the further increase in S-T segment abnormalities that developed in these patients during exercise or in the postexercise period. Of the three patients with a normal resting electrocardiogram, one had significant exercise-induced S-T segment depression. Thallium-201 myocardial imaging revealed no significant perfusion defects in 9 of the 10 patients (90 percent). In one patient with severe left ventricular hypertrophy significant perfusion defects developed after exercise that were not present at rest. Stress thallium-201 myocardial perfusion imaging is a useful noninvasive technique that assists in ruling out the presence of significant coronary artery disease in patients with idiopathic hypertrophic subaortic stenosis.     

Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction

To assess various factors associated with anterior S-T segment depression during acute inferior myocardial infarction, 47 consecutive patients with electrocardiographic evidence of a first transmural inferior infarction were studied prospectively with radionuclide ventriculography an average of 7.3 hours (range 2.9 to 15.3) after the onset of symptoms. Thirty-nine patients (Group I) had anterior S-T depression in the initial electrocardiogram and 8 (Group II) did not have such “reciprocal” changes. There was no difference between the two groups in left ventricular end-diastolic or end-systolic volume index or left ventricular ejection fraction. Stroke volume index was greater in Group I than in Group II. There were no group differences in left ventricular total or regional wall motion scores. A weak correlation existed between the quantities (mV) of inferior S-T segment elevation and reciprocal S-T depression. No relation between anterior S-T segment depression and the left ventricular end-diastolic volume index could be demonstrated; the extent of left ventricular apical and right ventricular wall motion abnormalities, both frequently associated with inferior infarction, did not correlate with the quantity of anterior S-T depression.These data show that anterior S-T segment depression occurs commonly during the early evolution of transmural inferior infarction, is not generally a marker of functionally significant anterior ischemia and cannot be used to predict left ventricular function in individual patients. Anterior S-T segment depression may be determined by reciprocal mechanisms.     

ECG Diagnosis and Classification of Acute Coronary Syndromes

In acute coronary syndromes, the electrocardiogram (ECG) provides important information about the presence, extent, and severity of myocardial ischemia. At times, the changes are typical and clear. In other instances, changes are subtle and might be recognized only when ECG recording is repeated after changes in the severity of symptoms. ECG interpretation is an essential part of the initial evaluation of patients with symptoms suspected to be related to myocardial ischemia, along with focused history and physical examination. Patients with ST‐segment elevation on their electrocardiogram and symptoms compatible with acute myocardial ischemia/infarction should be referred for emergent reperfusion therapy. However, it should be emphasized that a large number of patients may have ST‐elevation without having acute ST‐elevation acute coronary syndrome, while acute ongoing transmural ischemia due to an abrupt occlusion of an epicardial coronary artery may occur in patients with ST‐elevation less than the thresholds defined by the guidelines. Up‐sloping ST‐segment depression with positive T waves is increasingly recognized as a sign of regional subendocardial ischemia associated with severe obstruction of the left anterior descending coronary artery. Widespread ST‐segment depression, often associated with inverted T waves and ST‐segment elevation in lead aVR during episodes of chest pain, may represent diffuse subendocardial ischemia caused by severe coronary artery disease. In case of hemodynamic compromise, urgent coronary angiography has been increasingly recommended for these patients.     

Nondiagnostic electrocardiogram in patients with acute myocardial infarction. Clinical and anatomic correlations

The electrocardiograms of 78 of 230 patients with acute myocardial infarction showed only nondiagnostic changes in the S-T segment and T waves. On the basis of serum enzyme curves, two groups were defined: group A, 45 patients with definite myocardial infarction and group B, 33 patients with probable myocardial infarction. Three subgroups emerged in each group: group I, 38 patients with significant S-T segment depression with or without T wave changes; group II, 34 patients with significant T waves changes only; and group III, 6 patients with significant S-T segment elevation with or without T wave changes. The incidence of sinus tachycardia was significantly greater in group AI (13 patients or 48 per cent) (p <0.05) than in groups AII, AIII, BI, BII and BIII, but that of other arrhythmias was similar in all. The incidence of shock in group AI (eight patients or 30 per cent) was significantly greater than in groups AII, AIII, BI, BII and BIII (p <0.1). Mortality was also greater in group AI (13 patients or 47 per cent) (p <0.05) than in groups AII, AIII, BI, BII and BIII. There was no significant difference in the incidence of arrhythmias, shock or mortality among groups BI, BII and BIII. Postmortem examination of 8 of 18 patients (44 per cent) revealed recent transmural myocardial infarction with associated prior infarction in all.We have identified a subgroup of patients (group AI) with acute myocardial infarction and nondiagnostic electrocardiograms who appear to be at a greater risk of dying. The electrocardiographic changes correlated poorly with major clinical manifestations, as well as the magnitude or geographic location of the myocardial infarction. For all patients with acute myocardial infarction and nondiagnostic electrocardiograms, the ultimate prognosis appears to be determined by the extent of recent infarction, as reflected in the enzyme rise, as well as the magnitude of prior myocardial necrosis.     

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.     

Exercise testing for detection of myocardial ischemia in patients with abnormal electrocardiograms at rest.

This review consists of two parts: (1) discussion of the electrophysiologic mechanisms that are believed to produce ventricular repolarization changes during the electrocardiographic stress test, and (2) clinical assessment of the electrocardiographic changes with stress in patients with an abnormal electrocardiogram at rest. In the first part, the mechanisms of S-T segment elevation, S-T segment depression, T wave changes and linked S-T and T wave changes are reviewed. In the second part, all electrocardiographic abnormalities at rest are grouped into four categories: (1) changes that mask the manifestations of ischemia, (2) changes that stimulate or exaggerate the manifestations of ischemia, (3) changes that have no important effect on the manifestations of ischemia, and (4) changes that reproduce the patterns of acute myocardial infarction after an apparent healing. The reported studies of electrocardiographic stress testing in patients who have abnormal electrocardiogram at rest are summarized.     

Effect of heparin in anticoagulant doses on the electrocardiogram and cardiac enzymes in patients with acute myocardial infarction. A clinical pilot study.

The effect of heparin in clinical anticoagulant doses on S-T segment and cardiac enzymes was studied in 18 patients with acute myocardial infarction by electrocardiogram and enzyme evaluation 1 hour and 24 hours after initial heparin infusion. Intestinal mucosa heparin was given by infusion, 10,000 units after the admission electrocardiogram, and 5,000 units every 6 hours. Data in the nine control and nine treated patients were statistically similar on admission. The electrocardiograph findings were improved, but not significantly, 1 hour after administration of heparin. At 24 hours of heparin therapy, the S-T deviations were reduced 64% (from 139 +/- 2.1 [standard error of the mean] to 50.5 +/- 1.2 mm); in control patients S-T deviations were reduced 21% (from 109 +/- 1.8 to 86 +/- 0.9 mm (t=2.9, P less than 0.019). At 24% hours electrocardiographic leads with 2 mm or more deviation were reduced 86% in heparin-treated patients and 28% in control subjects. Cardiac enzymes were comparably elevated at 24 and 48 hours in both groups, with no clear trend. It is concluded that heparin in anticoagulant doses reduces the 12 lead electrocardiographic pattern of injury without discernibly modifying cardiac enzymes. The question of heparin efficacy in acute myocardial ischemic injury, reopened by findings with large dose heparin in therapy in dogs and anticoagulant dose in this study, awaits further expanded investigation.     

Significance of subendocardial S-T segment elevation caused by coronary stenosis in the dog: Epicardial S-T segment depression,local ischemia and subsequent necrosis

A model of partial thickness ischemia has been developed using subendocardial S-T elevation without epicardial S-T elevation to detect partial thickness ischemia which is sufficient to cause subsequent necrosis. Subendocardial blood flow in this model (measured with radioactive microsphere techniques) may be reduced to 25 percent of normal (P < 0.001) by coronary stenosis and tachycardia while subepicardial flow remains normal. Epicardial S-T depression seems to indicate reciprocally subendocardial S-T elevation as long as a layer of nonischemic epicardial muscle is present, but when ischemia becomes transmural, epicardial S-T elevation occurs. Regional pressure-flow relations were determined as distal coronary pressure was reduced at a constant aortic pressure, heart rate and cardiac output. These relations revealed remarkably effective autoregulation of epicardial blood flow concomitant with progressive subendocardial ischemia.     

Pathophysiologic significance of S-T and T wave abnormalities in patients with the intermediate coronary syndrome.

The frequent association of new ST-T wave changes without Q waves in the surface electrocardiogram of patients with the intermediate coronary syndrome necessitates a better understanding of the pathophysiologic significance of this finding. A previous study in patients with stable coronary artery disease indicated that the surface electrocardiogram is insensitive in detecting epicardial Q waves. This relation was evaluated in 21 patients with the intermediate syndrome, characterized by recurrent chest pain at rest associated with significant new S-T or T wave abnormalities, or both, and no new Q waves in the surface electrocardiogram at the time of open heart coronary bypass surgery. Unipolar electrograms were recorded from the epicardial surface of the left ventricle before the bypass procedure. In 19 patients, epicardial electrograms revealed initial R waves over areas of the left ventricle in which the acute S-T and T wave abnormalities were evident in the surface electrocardiogram. Two patients had epicardial Q waves (one laterally and one inferiorly). In seven patients, a transmural biopsy specimen was also obtained from the ischemic area. All showed histologically normal myocardium without evidence of early inflammatory or necrotic tissue. Of the 19 patients discharged, only one demonstrated new postoperative Q waves that had been detected by epicardial recordings before bypass. In summary, patients with the intermediate syndrome exhibiting S-T or T wave abnormalities, or both without new Q waves in the surface electrocardiogram generally do not have Q waves either in the intraoperative epicardial or postoperative surface electrocardiogram. In addition, no histopathologic abnormalities are apparent in biopsy specimens taken from the ischemic area.     

Electrocardiographic diagnosis of right ventricular infarction

The electrocardiographic findings in 11 cases of acute right ventricular infarction associated with acute left ventricular inferior wall myocardial infarction are described. The diagnosis of right ventricular infarction was proved by autopsy findings in five cases and supported by hemodynamic data in the other six. Ten of the 11 patients had typical electrocardiographic changes of acute inferior myocardial infarction and one had that of inferior wall injury. Transient S-T segment elevation was present in one (lead V₁) or more of the right precordial leads in eight cases. In the absence of other explanations for the S-T segment elevation, acute right ventricular infarction was most likely the cause. Therefore, when acute inferior myocardial infarction is accompanied by S-T segment elevation in the right precordial leads, the coexistence of right ventricular infarction should be suspected. The sensitivity and specificity of this electrocardiographic sign are yet to be determined.     

Myocardial infarction in the dog: Effects of intravenous propranolol

The effects of propranolol on myocardial perfusion and metabolism during acute myocardial infarction were studied in 18 mongrel dogs. A reversible snare was placed on the left anterior descending coronary artery; regional myocardial perfusion was continuously measured using the short-lived isotope krypton-81m, and myocardial metabolism was assessed using the epicardial electrocardiogram and measurement of release of creatine kinase activity from the affected segment of myocardium. Six dogs with no arterial occlusion acted as “sham operated” dogs; six others in which the snare was occluded acted as a control group and a third group of six were given propranolol, 0.5 mg/kg, 30 minutes after coronary occlusion. All variables were recorded before and for 5 hours after coronary occlusion. Dogs treated with propranolol showed a significant improvement in regional myocardial perfusion to the affected segment, decreased loss of electrically active myocardium at the end of each experiment for any given degree of early S-T segment elevation and a delay in the local release of creatine kinase activity compared with that in the control dogs. These results suggest that propranolol exerts a beneficial effect on the progress of ischemic myocardial damage when given shortly after the onset of infarction.     

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% of the S-T elevation over the occluded zone. In 44% of these animals, the S-T elevation decreased spontaneously to less than 1 mv, and in 22% 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 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.     

Epicardial ischemia as delineated with epicardial S-T segment mapping andnicotinamide adenine dinucleotide (NADH) fluorescence photography.

In isolated rabbit hearts with an experimental coronary arterial occlusion, epicardial ischemia was identified by reduced nicotinamide adenine dinucleotide (NADH) fluorescence photography, a technique that detects areas of myocardial anoxia. Epicardial S-T segment mapping was performed to evaluate the S-T segment changes across an ischemic border defined by NADH fluorescence. After S-T segment mapping and perfusion with a fluorescein dye, serial selections of the hearts revealed that the ischemic area was transmural and and the border was nearly perpendicular to the epicardial surface. As the epicardial ischemic border was approached, S-T segment elevation was first detected 3.3 mm outside the ischemic border, and increased over a transition zone 7 mm wide. S-T segment negativity was not detected immediately outside the ischemic border. It is concluded from these studies that S-T segment changes give relatively imprecise definition of an ischemic border, and that S-T segment changes across an ischemic border are not consistent with those predicted by solid angle analysis.     

Effects of hypoxemia on the extent of myocardial necrosis after experimental coronary occlusion

Arterial oxygen tension is variable in patients with acute myocardial infarction, and the effect of hypoxemia on the extent of myocardial necrosis after coronary occlusion has not been defined. In 11 anesthetized open chest dogs the left anterior descending coronary artery or one of its major branches was occluded for 20 minutes, and 10 to 15 epicardial electrocardiographic leads were recorded in the distribution and vicinity of the site of occlusion. Average S-T segment elevation and the number of sites showing S-T segment elevation greater than 2 mv, 15 minutes after occlusion were used as indexes of the severity and extent of ischemic injury. After occlusion with an inspired oxygen concentration of 20 percent these indexes were, respectively, 2.0 ± 0.5 mv (mean ± standard error) and 3.6 ± 0.8 sites; the respective values increased to 3.3 ± 0.5 mv (P < 0.01) and 6.7 ± 0.7 sites (P < 0.01) after occlusion with an inspired oxygen concentration of 10 percent, and arterial partial pressure of oxygen decreased from 92 ± 5 to 45 ± 3 mm Hg. In 23 dogs the occlusion was maintained for 24 hours and the S-T segment elevation 15 minutes after occlusion was compared with myocardial creatlne phosphokinase (CPK) activity and histologic appearance 24 hours later. In control dogs (inspired oxygen concentration of 20 percent) sites with no S-T segment elevation 15 minutes after occlusion showed normal myocardial CPK activity 24 hours later, whereas in sites with S-T segment elevation exceeding 2 mv there was an inverse relation between S-T segment elevation in each site and its myocardial CPK activity 24 hours later. Histologic examination revealed early myocardial necrosis in 98 percent (82 of 84) of sites with S-T segment elevation greater than 2 mv. In experimental dogs (inhaling a 10 percent Oxygen concentration for the first 8 of the 24 hours of occlusion) many sites that showed no S-T segment elevation before hypoxemia was induced exhibited S-T segment elevations 30 minutes later and showed abnormally low CPK activity and histologic evidence of early necrosis. We conclude that after experimental coronary occlusion, hypoxemia is deleterious because it substantially increases myocardial damage.