Segment Elevation Research Articles

Prolonged angina pectoris and persistent negative T waves in the precordial leads: Response to atrial pacing and to methoxamine-induced hypertension

In 18 consecutive patients without a history of myocardial infarction (MI), prolonged angina pectoris with persistent negative T waves in the precordial leads was associated with a high frequency of in-hospital spontaneous angina (14 of 18, 78%), usually accompanied by S-T segment elevation, and occasionally in-hospital MI (4 of 18, 22%). Angina and MI always involved the electrocardiographic leads with negative T waves. Coronary arteriography, performed in 16 patients, revealed ≥ 90% proximal diameter reduction of the left anterior descending (LAD) coronary artery in 14 patients. No patient had severe narrowing of all 3 major coronary arteries, but the 3 who had 100% LAD occlusion lacked collateral circulation. The ejection fraction was ≥ 50% in 13 patients. Atrial pacing performed in 11 patients at an average rate of 142 beats/min produced a 1.0 mm S-T segment change in only 5 patients (45%), 3 of whom had an associated lactate production. Arterial systemic hypertension induced by methoxamine in 14 patients caused reversal of negative T waves without significant S-T segment shifts or chest pain and failed to elicit lactate extraction abnormalities in each of the 5 patients in whom it was determined. Thus, prolonged angina with persistent negative T waves in the precordial leads is almost invariably associated with a critical and proximal LAD obstruction, severe narrowing of 1 or 2 coronary arteries, and poor or absent collateral vessels. The relatively preserved coronary reserve in 55 % of our patients suggests that negative T waves do not represent active myocardial ischemia. The study also suggests that transient “positivization” of the negative T waves may not necessarily relate to myocardial ischemia when associated with acute systemic hypertension.

Role of myocardial ischemia in the genesis of stress-induced S-T segment elevation in previous anterior myocardial infarction

This study tests the hypothesis that myocardial ischemia is responsible for exercise-induced S-T segment elevation in patients with previous anterior myocardial infarction (MI). Exercise stress testing in conjunction with thallium imaging of the myocardium was performed in 28 patients with previously documented anterior MI. Thallium images were analyzed by computer for the presence of initial uptake defects and evidence of abnormal clearance of the isotope from the myocardium (that is, imaging evidence of ischemia). Total S-T segment elevation (∑ST) in precordial leads V1 to V6 at rest was subtracted from ∑ST at peak stress in order to quantitate the extent of S-T elevation induced by stress (ΔST). Two groups of patients were identified; 1 with stress-induced S-T elevation (Group I, ΔST ≥ 4.0 mm) and 1 without this abnormality (Group II, ΔST < 4.0 mm). Evidence of abnormal thallium washout from myocardial scan segments occurred in 12 of 15 Group I patients versus 9 of 13 Group II patients (difference not significant). In addition, abnormal tracer washout from anterolateral or septal scan segments occurred in 5 patients in each group. Likewise, abnormal thallium clearance from inferior or posterior scan segments occurred in 8 of 15 Group I patients versus 7 of 13 Group II patients (difference not significant). The patient with the greatest amount of stress-induced S-T elevation (S-T 11.5 mm) had no evidence of ischemia during the stress test. However, Group I patients did have larger anterolateral plus septal initial thallium uptake defect scores than did those of Group II (10 of 15 with defect score ≥ 350 in Group I versus 1 of 13 in Group II, p <0.002). Similarly, resting left ventricular ejection fraction ≥ 30% was present in only 4 of 15 Group I patients versus 13 of 13 in Group II (p <0.001). Finally, multiple stepwise linear regression analysis demonstrated that ΔST correlated best with the extent of initial anterolateral plus septal thallium uptake defect score (F = 17.3, p < 0.001) and to a lesser extent with resting ejection fraction (F = 5.2, p < 0.05) and change in heart rate from rest to peak stress (F = 8.1, p < 0.01; corrected multiple correlation coefficient = 0.76, p < 0.001). Thus, in patients with previous anterior MI (1) exercise-induced myocardial ischemia occurs as often with as without S-T segment elevation, (2) myocardial ischemia is not required for the production of stress-induced S-T segment elevation, and (3) stress-induced S-T elevation primarily reflects the extent of previous anterior wall damage and to a lesser extent an increase in heart rate between rest and peak stress.

Clinical significance of S-T segment elevation during exercise

Clinical significance of S-T segment elevation during exercise

Detection of acute right ventricular infarction by right precordial electrocardiography

The value of 0.1 mV or greater of S-T segment elevation in at least one right precordial lead (V 4R to V 6R) in defining right ventricular myocardial infarction was assessed prospectively in 43 subjects (33 consecutive patients with enzymatically confirmed infarction of varying type and location, 4 patients with unstable angina and 6 healthy volunteers). Patients with acute myocardial infarction were studied with radionuclide ventriculography and technetium-99m stannous pyrophosphate myocardial scintigraphy 18.2 ± 14.3 (mean ± standard deviation) and 85.1 ± 18.0 hours after the onset of symptoms, respectively. Eleven patients (Group A: 9 patients with transmural inferior infarction, 1 with transmural inferolateral infarction and 1 with transmural anteroseptal infarction) demonstrated right precordial S-T segment elevation and 22 patients (Group B: 6 patients with transmural inferior infarction, 2 with transmural posterior infarction, 3 with transmural inferolateral infarction, 3 with transmural anteroseptal infarction, 3 with transmural extensive anterior infarction, 4 with subendocardial anterior infarction and 1 with unclassified infarction) did not. Right ventricular ejection fraction was significantly lower in Group A (0.47 ± 0.11) than in Group B (0.60 ± 0.12) (p < 0.01). Right ventricular total wall motion score was 63.8 ± 15.6 percent of normal in Group A versus 94.3 ± 8.5 percent in Group B (p < 0.001). Technetium-99m pyrophosphate uptake (2+ or greater) over the right ventricle occurred in nine patients (81.8 percent) in Group A and in one patient (4.5 percent) in Group B (p < 0.001). No patient with unstable angina and no healthy volunteer had S-T segment elevation in a right precordial lead. S-T segment elevation of 0.1 mV or greater in one or more of leads V 4R to V 6R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.

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.

Evaluation of normal variations in S-T segment patterns by body surface isopotential mapping: S-T segment elevation in absence of heart disease

S-T segment elevation is commonly observed in the electrocardiogram of normal persons. To study the possible origins of such patterns, 45 normal volunteers were examined. Electrocardiographic potentials were registered from 150 torso electrodes and processed to construct iso-potential maps at 2 ms intervals throughout the QRS-T interval. The maximal potentials recorded from any of the 150 electrodes were 198 ± 76.4 and 272.1 ± 84.2 μV at instants 40 and 80 ms into the S-T segment, respectively. Maximal voltages recorded by the six standard precordial V leads at these respective time points were 109.7 ± 57.0 and 163.6 ±66.9 μV. Torso maximal potentials were significantly stronger than were those sensed by V leads; the two were significantly correlated but predictability was limited. The duration of overlap between the onset of ventricular recovery and the end of the excitation was determined from isopotential maps and ranged from 4 to 16 ms. There was no significant correlation (p > 0.05) between these values and either torso or V lead potentials at either 40 or 80 ms into S-T segment. These data suggest that (1) standard precordial leads do not accurately predict maximal torso potentials during the S-T segment, and (2) the degree of overlap between repolarization and depolarization is not a major determinant of precordial voltage. Hence, the rationale for use of the term “early repolarization” to describe this clinical condition is not substantiated.

Sudden death in prinzmetal's angina with coronary spasm documented by angiography: Analysis of three necropsy patients

Clinical and necropsy findings are described in three patients who had angina pectoris at rest, S-T segment elevation on electrocardiography during chest pain, coronary arterial spasm on angiography and sudden death. Although significant “fixed” coronary narrowing (that is, narrowing due to atherosclerotic plaques) was appreciated by angiography in only one of the three patients, necropsy disclosed in all three patients severe fixed coronary narrowings involving particularly the artery in which spasm had been demonstrated during life. Additionally, examination of each 5-mm long segment of the coronary artery that had been spastic during life (two patients) disclosed several focally spastic segments at necropsy, indicating that spasm persisted after death. Although most previously described necropsy patients with Prinzmetal's angina had some fixed coronary narrowing, underlying fixed narrowing may be difficult to identify angiographically as demonstrated by the three patients in this study.

Cardiovascular effects of tiapamil (Ro 11-1781), a new calcium-entry blocker.

We studied the hemodynamic effects of the new calcium antagonist tiapamil (Ro 11-1781) in anesthetized open-chest dogs and compared them with those of verapamil. Increasing doses of tiapamil injected intravenously caused the following hemodynamic effects: increase in coronary flow and decrease in coronary vascular resistance, followed by decreases in heart rate, blood pressure, and total peripheral resistance. Tiapamil did not depress myocardial contractility over a rather wide dose range, while verapamil did. Tiapamil was more effective in increasing coronary flow than verapamil. Cardiac autonomic denervation did not modify the tiapamil-induced decrease in coronary vascular resistance and did not cause tiapamil to display negative inotropism. Both tiapamil and verapamil reduced the extent of S-T segment elevation in the epicardial electrocardiogram produced by transient occlusion of the left anterior descending coronary artery. Neither drug had this effect when heart rate was kept constant by atrial pacing. In contrast to nitroglycerin, tiapamil dilated small but not large coronary arteries. Tiapamil raised PO2 relatively more in the subendocardial than in the subepicardial layers of the myocardium. The hemodynamic and electrocardiographic effects of tiapamil were not changed by diphenylhydantoin and disopyramide or by pindolol, a beta-adrenoceptor blocking agent with intrinsic sympathomimetic activity. However, the decreases in heart rate and blood pressure in response to propranolol were enhanced by tiapamil.

Surgical Therapy for Prinzmetal's Variant Angina

Fifty-two patients underwent coronary artery bypass grafting between 1973 and 1979 for variant angina, defined as pain, usually at rest, associated with S-T segment elevation. Only patients with fixed occlusive coronary artery disease, defined as greater than 70% narrowing in diameter, were included. When fixed coronary artery stenosis is present, variant angina—whether presenting as stable, unstable, or postinfarction angina, and regardless of the number of vessels diseased—is effectively treated by myocardial revascularization. Preoperative intraaortic balloon pumping is a useful therapeutic adjunct in the unstable subset refractory to medical therapy. The results of revascularization in patients with Prinzmetal's variant angina and fixed coronary disease were no different from those in patients with classic angina pectoris of comparable clinical categories.

Large dose sublingual nitroglycerin in acute myocardial infarction: Relief of chest pain and reduction of Q wave evolution

Thirty patients with acute myocardial infarction admitted 2.1 ± 1.1 (mean ± standard deviation) hours after the onset of pain and with S-T segment elevation in multiple leads in the standard electrocardiogram were given either intravenous morphine (15 patients) or sublingual nitroglycerin (15 patients), and the effect on pain and QRS changes was observed. Nitroglycerin was administered repetitively in large doses while systolic blood pressure was maintained above 100 mm Hg. Chest pain failed to respond within 30 minutes In two patients who received nitroglycerin. In the remaining 13 patients nitroglycerin produced partial relief of pain in 17 ± 5 minutes and complete relief in 127 ± 65 minutes, requiring a cumulative dosage of 23.7 ± 38.7 mg in 16 ± 7 divided doses. An average of 14.9 ± 7.1 mg of morphine in 3.3 ±1.5 divided doses produced complete relief of pain in a similar period (134 ± 77 minutes [difference not significant]). In patients receiving morphine, Q waves developed at 24 and 48 hours, respectively, in 62 (72 percent) and 66 (77 percent) of a total of 86 sites with initial S-T segment elevation in the standard 12 lead electrocardiogram. In nitroglycerin responders, Q waves developed at 24 and 48 hours, respectively, in only 21 (28 percent, p < 0.001) and 22 (29 percent, p < 0.001) of the 76 sites with initial S-T segment elevation. Other electrocardiographic estimates of the extent of myocardial necrosis, including the percent reduction in R wave amplitude and the relative changes in R and Q wave amplitude, also were significantly less in those receiving nitroglycerin. There was no in-hospital mortality. Thus, large and frequent doses of nitroglycerin when used in the hyperacute phase of acute myocardial infarction can effectively abolish chest pain and limit later electrocardiographic signs of myocardial necrosis.

Dynamic intercoronary collateral flow in a patient with variant angina and coronary artery spasm

Intermittent intercoronary collateral flow was observed in a patient with coronary vasospasm associated with variant angina. Collateral flow began almost immediately after total occlusion of the right coronary artery, but did not prevent pain or S-T segment elevation. Some collateral vessels may pre-exist ischemic conditions and flow across these channels may be immediately dependent on the pressure gradient across them.

Myocardial blood flow and metabolism in the diving seal.

The adaptations of myocardial metabolism to diving asphyxia have been studied in 12 harbor seals (Phoca vitulina). Unanesthetized animals were submerged for periods of 10-16 min. Heart rate decreased from 135 to 12 beats/min. Myocardial blood flow decreased to an average of 10% of predive values and remained constant during the dive. The progressive reduction in arterial O2 content was associated with an increase in myocardial lactate and hydrogen ion production, but no change in glucose or free fatty acid extraction occurred. After restoration of breathing a reactive myocardial hyperemia and an immediate return to myocardial uptake of lactate were observed. Despite increased glycogenolytic activity throughout the dive, coronary flow distribution was fully controlled, and no evidence of ischemic dilatation of the left ventricle or S-T segment elevation in the electrocardiogram was observed. These adaptations to diving asphyxia in the seal myocardium permit a reduction of coronary blood flow comparable to that observed in the infarcted dog myocardium and therefore have relevance for therapeutic approaches to reduction of myocardial ischemic injury in humans.

Infarct size restriction in cats by the β-adrenergic blocker timolol

The β-adrenergic antagonist, timolol, was previously shown to exert a protective effect in cats subjected to 5 h of myocardinal ischemia. The present study was designed to determine the effect of timolol on infarct size in cats 24 h after coronary occlusion. Timolol (25 μg/kg) or vehicle (0.9% NaCl) was administered 0.5, 5, 10, 15 and 20 h after acute ligation of the left anterior descending coronary artery. There was no significant difference in arterial blood pressure or heart rate in MI cats receiving timolol or vehicle. Timolol markedly decreased S-T segment elevation at 2–12 h (P<0.05). Left ventricular weights in MI+ vehicle cats (8.5±0.7g, n=6) were similar to timolol-treated MI cats (8.9±0.4 g, n=7). However, the percent of the left ventricular myocardium infarcted, determined by nitroblue tetrazolium staining, was significantly less (P<0.001) in timolol MI cats compared to saline-treated cats, 9.8±1.2% (n=7) vs 18.9±1.8% (n=6), respectively. Hemodynamic or cytoprotective actions of timolol do not appear to explain these results. Rather, the mechanism of infarct size reduction by timolol is probably explained by antagonism of β-receptor-mediated metabolic effects.

Reduction in infarct size by synchronized selective coronary venous retroperfusion of arterialized blood

The effectiveness of selective synchronized pulsatile coronary venous retroperfusion for the temporary metabolic support of a region of acutely ischemic myocardium has previously been demonstrated. This study was designed to determine the degree of reduction in ultimate infarct size that may be achieved when coronary venous retroperfusion initiated early after coronary occlusion is combined with later anterograde reperfusion. In 10 baboons, the proximal left anterior descending coronary artery was occluded for 4 hours at which time anterograde reperfusion was restored. In five baboons (Group A), coronary venous retroperfusion was initiated 15 minutes after occlusion. Five baboons (Group B) underwent an identical procedure without coronary venous retroperfusion. Epicardial electrograms were recorded from 24 sites overlying the ischemic region. At 24 hours, hearts were excised and serial transverse sections of the left ventricle were stained with nitroblue tetrazolium for stereometric determination of infarct size. In Group A 12 ± 5.4 percent (mean ± standard error of the mean) of epicardial sites with S-T segment elevation at 15 minutes after occlusion showed subsequent Q waves, compared with 96 ± 2.3 percent in Group B (p < 0.01). In Group A 4.8 ± 1.7 percent of the left ventricular mass was infarcted, compared with 30.6 ± 4.2 percent in Group B (p < 0.01). The results demonstrated the effectiveness of coronary venous retroperfusion in preserving ischemic myocardium such that anterograde reperfusion resulted in a mean reduction of 84 percent in ultimate infarct size.

Localization of coronary artery disease with exercise electrocardiography: correlation with thallium-201 myocardial perfusion scanning

In 61 patients with single vessel coronary artery disease (70 percent or greater obstruction of luminal diameter in only one vessel) and no previous myocardial infarction, the sites of ischemic changes on 12 lead exercise electrocardiography and on thallium-201 myocardial perfusion scanning were related to the obstructed coronary artery. The site of exercise-induced S-T segment depression did not identify which coronary artery was obstructed. In the 37 patients with left anterior descending coronary artery disease S-T depression was most often seen in the inferior leads and leads V 4 to V 6, and in the 18 patients with right coronary artery disease and in the 6 patients with left circumflex artery disease S-T depression was most often seen in leads V 5 and V 6. Although S-T segment elevation was uncommon in most leads, it occurred in lead V 1 or aVL, or both, in 51 percent of the patients with left anterior descending coronary artery disease. A reversible anterior defect on exercise thallium scanning correlated with left anterior descending coronary artery disease (probability [p] < 0.0001) and a reversible inferior thallium defect correlated with right coronary or left circumflex artery disease (p < 0.0001). In patients with single vessel disease, the site of S-T segment depression does not identify the obstructed coronary artery; S-T segment elevation in lead V 1 or aVL, or both, identifies left anterior descending coronary artery disease; and the site of reversible perfusion defect on thallium scanning identifies the site of myocardial ischemia and the obstructed coronary artery.

Comparative study of myocardial ischemia during angina at rest and on exertion using thallium-201 scintigraphy

To compare the results of thallium-201 myocardial scintigraphy during angina at rest with those observed during effort angina, 81 patients were selected in whom the existence of acute myocardial ischemia was indicated both by typical transient S-T segment or T wave changes and by typical anginal pain. In these patients, scintigrams were obtained during 58 attacks of angina on effort (group 1) and during 40 attacks of angina at rest (group 2); 16 patients were studied during both types of angina. The attack at rest was spontaneous in 20 patients and induced by ergonovine maleate in 20 patients. In the presence of S-T segment elevation or transient normalization of inverted T waves, scintigrams were positive in all 24 studies at rest and in 19 of 20 studies during exercise. By contrast, in the presence of S-T segment depression scintigrams were positive in 14 (95 percent) of 15 studies during angina at rest, but in only 20 (53 percent) of 38 during angina on effort. Neither the degree of S-T segment changes nor their duration after injection of thallium was significantly different in resting studies relative to exercise studies, but the heart rate and double product were consistently higher during exercise. The marked difference in sensitivity in detecting ischemia in angina at rest with S-T segment depression compared with detection during exertional angina, even in the same patients, suggests that different pathogenetic mechanisms are responsible for the attack. Conversely, a similar mechanism operating in angina at rest and on exertion during S-T segment elevation and normalization of T waves is suggested by the similarity of thallium-201 scintigraphic findings in this situation. The findings are compatible with the hypothesis of a regional reduction in myocardial blood flow in angina at rest, independently of the direction of S-T segment change, and in exertional angina with S-T segment elevation or normalization of inverted T waves; they suggest an inadequate increase in myocardial blood flow in angina on effort with S-T segment depression.

Variable threshold of angina during exercise: A clinical manifestation of some patients with vasospastic angina

Two patients complained of chest pain while at rest and during physical activities. However there seemed to be no direct relation between exertional angina and an increasing level of work performed, indicating that these patients had a variable threshold of angina during exercise. In one patient spontaneous chest pain was associated with transient S-T segment changes in precordial leads, and during coronary arteriography the administration of ergonovine induced spasm of the left anterior descending coronary artery. The other patient showed S-T segment elevation in inferior leads during an ergonovine-induced anginal attack and coronary arteriography revealed a spontaneous spasm of the right coronary artery. In both patients repeated exercise tests yielded different results, because the chest pain and S-T segment depression occurred at different work loads with large differences in heart rate-systolic blood pressure product. It is concluded that a variable threshold of angina during exercise is a clinical manifestation in some patients with vasospastic angina and is probably due to the difference in coronary arterial tone at the onset of exercise.

S-T segment elevation and coronary spasm in response to exercise

The prevalence rate of exercise-induced S-T segment elevation of 0.1 mV or greater in symptomatic patients is 3.0 to 6.5 percent in most studies. S-T segment elevation is associated with a more severe degree of myocardial ischemia than depression and frequently implies a high grade coronary stenosis in the vessel that supplies the site of ischemia. Leads V 4 to V 6 and bipolar lead CM 5 have been found to be relatively insensitive in detecting exercise-induced S-T segment elevation. The pathogenesis of S-T segment elevation is different in three clinical patient subsets reviewed. In patients after infarction, the largest of the three subgroups, exercise-induced S-T segment elevation usually appears in leads with Q waves, is more common after anterior myocardial infarction and implies underlying akinetic or dyskinetic wall motion. Of patients with variant angina, 10 to 30 percent have during exercise S-T segment elevation that is most likely provoked by coronary arterial spasm. The natural history of variant angina is cyclic, and clinical observations and laboratory findings are dependent on particular phases in the disease process and treatment. Finally, 0.2 to 1.7 percent of symptomatic patiënts without infarction or variant angina have exercise-induced S-T segment elevation. Although most of the latter have fixed high grade coronary arterial stenoses at angiography, the exact pathogenetic mechanism of S-T segment shift in this patient group is not yet fully understood.

Defining the anatomic perfusion bed of an occluded coronary artery and the region at risk to infarction: A comparative study in the baboon, pig and dog

To assess selectively the effectiveness of therapeutic interventions to reduce infarct size, it is important to assess both ultimate infarct size as well as the size of the region of myocardium at risk to infarction. The anatomically defined perfusion bed of an occluded artery has generally been assumed to be synonymous with the region at risk of infarction. This assumption was tested by delineating the anatomic perfusion bed of an occluded artery with microvascular dyes and by examining the relation of the anatomic perfusion bed to the region of acute ischemic injury. In 8 baboons, 12 pigs and 15 dogs a major branch of the left anterior descending or left circumflex coronary artery was occluded. At 2 and 30 minutes after occlusion the eplcardial area of ischemic injury was determined by epicardial S-T segment mapping. The boundary of epicardial S-T segment elevation was resolved to within 1 mm and marked directly on the ventricular surface. The heart was then excised and the perfusion bed of the occluded artery was delineated by either (1) injecting different colored silicone rubber microvascular dyes into the previously occluded artery as well as the adjacent perfusion beds (direct method), or (2) injecting dye only into the adjacent perfusion beds (defect method). Serial cross-sections of the left ventricle from the direct and defect dye-perfused hearts in all three species showed the perfusion bed of the occluded artery to be readily demarcated. Microscopic examination demonstrated no evidence of capillary anastomoses and minimal inter-digitation of capillaries at the perfusion bed boundaries. In dye-perfused hearts, the baboon and the pig showed no evidence of precapillary anastomoses between perfusion beds; however, the dog demonstrated numerous epicardial collateral channels. The epicardial area of the anatomic perfusion bed correlated closely with the epicardial area of S-T segment elevation at 2 minutes after occlusion in the baboon (r = 0.97), pig (r = 0.99) and dog (r = 0.96). The epicardial area of S-T segment elevation did not change through the 30 minute period of occlusion in the baboon and the pig, but in the dog it showed a progressive and variable reduction reflecting the gradual recruitment of existing collateral channels from adjacent perfusion beds. It is concluded that the techniques of direct and defect dye delineation accurately define the anatomic perfusion bed of an occluded coronary artery. This anatomic perfusion bed corresponds to the region of myocardium undergoing acute ischemic injury and hence the region at risk to infarction immediately after coronary occlusion in the three species studied.

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 V 1) 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.