Gordon B. Myers

III. Correlation of electrocardiographic and pathologic findings in anteroposterior infarction

Abstract The findings in the Wilson precordial leads and in the standard and Goldberger limb leads have been analyzed and correlated with the pathologic findings in fifty-two cases of coexistent infarction of the anterior and posterior walls of the left ventricle. Autopsy revealed a recent infarct involving the apical one-third or more of the anterior wall and continuing through the septum and around the tip of the left ventricle into the apical one-third or more of the posterior wall in twenty cases, and an old healed infarct of similar distribution in sixteen cases. The pathologic findings were the result of the confluence of independent anterior and posterior infarcts in at least three of these thirty-six cases, and were attributed to simultaneous anteroposterior infarction in the other thirty-three cases because of the anatomical continuity of the lesions and the uniformity in age. Five additional cases were observed with pathologic evidence of simultaneous anteroposterior infarction, complicated by a separate posterobasal lesion. The eleven remaining cases had anatomically separate anterior and posterior lesions. The cases were classified according to the extent of the involvement of the posterior wall into two groups: (a) twenty-two cases of infarction confined to the apical one-third and (b) thirty cases of infarction of more than the apical one-third of the posterior wall. Electrocardiograms were obtained during the acute phase of the posterior infarct in fifteen cases of each group. Lead aV F proved very disappointing for the detection of extensions of a large anterior infarct into the apical one-third of the posterior wall. The pattern in this lead was considered diagnostic of posterior infarction in only two cases, intermittently diagnostic in another, suggestive in three, and negative in sixteen. The negative findings in twelve cases were ascribed to horizontal position, which favored transmission of the potential variations of the right ventricle to the left leg. The negative findings in the other four cases occurred despite intermediate to semivertical position of the heart and were attributable to one or both of the following factors: (1) derivation of the potential variations of the left leg chiefly from those of the intact basal two-thirds of the posterior wall of the left ventricle, and (2) marked reduction in the opposing negative cavity potentials available for transmission through the infarcted apical one-third of the posterior wall, as a result of the extensive lesion of the anterior wall and septum. The influence of cardiac position in one case of infarction of the apical one-third of the posterior wall was exemplified by the registration of an abnormal QR complex in Lead aV F when the heart was in intermediate position and its replacement by a notched R wave when the heart shifted into a vertical position. Lead aV F was a much greater help in the detection of infarcts involving more than the apical one-third of the posterior wall. The findings in this lead were considered diagnostic of the lesion of the posterior wall in eighteen cases, suggestive in five, and negative in the other seven because of the horizontal position of the heart. The continuation of the apical infarct into the middle one-third of the posterior wall increased the incidence of positive findings in Lead aV F . In one case from each group, the findings in Lead aV F were classed as negative despite fulfillment of the requirements for a diagnosis of posterior infarction. A study of the unipolar limb lead in reference to the precordial leads in these cases indicated that the findings in Lead aV F were not due to the posterior lesion, but rather were representative of the potential variations of the infarcted septum, transmitted through the right ventricle to the leg as a result of horizontal position. Typical signs of anteroseptal infarction originally present in one case were obliterated with the development of an extensive posterior infarction. The absence or paucity of diagnostic signs in the precordial leads referable to the anterior infarction in four other cases was regarded as a secondary manifestation of a large posterior infarct and was attributed to reduction in the opposing negative cavity potentials available for transmission through the anterior wall. On the other hand, infarcts limited to the apical one-third of the posterior wall caused no demonstrable alteration in the precordial lead patterns referable to the anterior lesion. Acute RS-T depression in the precordial leads, which is a familiar reciprocal manifestation of recent infarction limited to the posterior wall, was observed in only three of the thirty cases of acute posterior, coupled with recent or old anterior infarction. The downward RS-T displacement in these cases was regarded as a direct manifestation of subendocardial anterior infarction. Further-more, acute RS-T depression was not found in Lead aV F in any of the twenty-eight cases in which acute anterior infarction was accompanied by a recent or old posterior infarction. The standard limb leads were of very limited value in the diagnosis of coexistent anteroposterior infarction. The findings in these leads were not indicative of either lesion in thirteen of the fifty-two cases, and were strongly suggestive of both in only four cases. However, the pattern compatible with anteroposterior infarction was considered a manifestation of posterolateral infarction in one of the latter, and a result of anterolateral plus septal infarction in another.

The electrocardiographic diagnosis of right ventricular hypertrophy

Abstract 1. 1. The electrocardiographic criteria for the diagnosis of right ventricular hypertrophy have been evaluated and elaborated upon through a critical review of the literature and a study of our clinical and autopsy material. A detailed description is given of the findings in the standard limb leads, the Wilson precordial leads, and the Goldberger unipolar extremity leads. 2. 2. An analysis is presented of all of our cases of patients in whom Leads V 1 through V 6 , inclusive, and the standard limb leads were obtained during life and a diagnosis of preponderant hypertrophy of the right ventricle was established at autopsy. The series comprised a total of forty cases. The augmented unipolar limb leads were available in thirty-five of the cases and Lead V 3R in eight. The amplitude of each deflection of the QRS in V 3R , V 1 , V 2 , V 5 , V 6 and aV R was measured and the time interval from the onset of QRS to (1) the nadir of Q, (2) peak of R, (3) nadir of S, (4) peak of R′, and (5) end of QRS was determined in each of these leads with the aid of a Cambridge measuring device. In thirtysix of the patients post-mortem study included injection of the heart with a radiopaque mass, subsequent roentgenogram, and careful dissection. 3. 3. The forty cases of patients proven to have preponderant right ventricular hypertrophy at autopsy were classified according to electrocardiographic pattern into the following six groups: 3.1. (A) Pattern in Leads V 1 through V 6 , inclusive, was considered diagnostic of right ventricular hypertrophy in thirteen cases on the basis of the following criteria: (1) reversal in the ratio of the amplitudes of the R and S waves in V 1 and V 6 characterized by an abnormally large R in proportion to S in V 1 , a diminution in ratio in leads further to the left, and a prominent S in V 6 ; (2) time interval from beginning of QRS to onset of intrinsicoid deflection that was abnormally long in V 1 (generally between 0.03 and 0.05 second) and greater than in V 5 or V 6 ; (3) tendency to a small Q wave in V 1 ; (4) tendency to inversion of the T wave in V 1 and to upright T wave in V 6 ; (5) total duration of QRS less than 0.12 second and generally within the normal range; (6) absence of notching or double peaking of the R wave of V 1 , except in one case where bundle branch block could be excluded and a conduction defect in the outer wall of the right ventricle postulated from the presence of a Q wave followed by a notched R in all leads from the right side of the precordium. The electrocardiographic findings were similar, irrespective of the cause of the right ventricular hypertrophy. 3.2. (B) Pattern typical of right ventricular hypertrophy was present in Lead V 3R , but not in V 1 or V 2 in one patient, and signs of incomplete right bundle branch block were distinctive in V 3R , but not in V 1 or V 2 of another patient. 3.3

I. Correlation of electrocardiographic and pathologic findings in anteroseptal infarction

Abstract The findings in the Wilson precordial leads and in the standard and Goldberger limb leads have been correlated with the pathologic findings in 161 cases in which myocardial infarction was definitely established and accurately localized at autopsy. The cases have been classified in accordance with the anatomic location of the infarct into the following seven groups: anteroseptal, large anterolateral, anteroposterior, septal, posterior, posterolateral, and lateral, When classification into more than one category was possible, because of the large size or multiplicity of the infarct found at autopsy, the lesion of principal electrocardiographic interest became the determining factor. This communication comprises a study of the electrocardiographic and pathologic findings in twenty cases of anteroseptal infarction. In the majority, the infarct was confined to a relatively narrow strip of the free anterior wall and the contiguous anterior portion of the interventricular septum. Serial electrocardiograms taken during the acute phase are presented in six cases and include a control tracing antedating the infarct in four cases, and one or more records after healing in four cases. Single electrocardiograms obtained during the stage of injury are presented in eight additional cases. The remaining six cases came under study after the infarct was completely healed. In fourteen cases, the infarct involved the apical one-third to two-thirds of the anteroseptal wall of the left ventricle. The electrocardiogram in eight of these cases was characterized by a normal initial R wave in Lead V 1 and an abnormal QR or QS complex in one or more of the next three leads (V 2 , V 3 , and V 4 ). The Q wave of a QR complex was considered abnormal when the time interval from its onset to nadir exceeded .02 second and when its amplitude was more than 25 per cent of the voltage of the succeeding R. The electrocardiogram in five of the fourteen cases displayed a QS complex in Leads V 1 and V 2 , as well as an abnormal initial downward deflection in Lead V 3 or V 3 and V 4 . In four of these five cases, the QS complexes in Leads V 1 and V 2 were accompanied by abnormal elevation of the RS-T segment and could be correlated with extension of the infarct into the septum. The electrocardiogram of the last case in the group displayed marked RS-T displacement in Leads V 2 , V 3 , and V 4 without significant abnormalities in the initial phase of the QRS complex. The registration of an R wave in place of a Q wave in these leads could be correlated with the patchy distribution of the infarct through the anteroseptal wall. In two cases, the infarct was centered in the middle one-third of the anteroseptal wall and did not reach either the apex or base. The tracing of one of these displayed a normal initial R wave in Lead V 1 and an abnormal QR or QS complex in the next three leads. Serial changes in the T waves of Leads V 2 and V 3 without significant QRS abnormalities were observed in the other case during the acute stage of an anteroseptal infarct, which subsequently proved to be small in size and intramural in location. The infarct was located in the basal one-third of the anteroseptal wall in the four remaining cases and was manifested by an abnormal QR or QS pattern together with abnormal RS-T displacement confined to the first two or three precordial leads. Extension of the infarct into the basal one-third of the interventricular septum was demonstrated in three of these cases and may have been partly or wholly responsible for the QRS-T abnormalities in Leads V 1 and V 2 . Definitely abnormal Q waves were not found in Leads V 5 or V 6 in any case where the infarct was confined to the anteroseptal wall, but borderline QR complexes were recorded in these leads in two cases and were attributed to reference of the potential variations of the anteroseptal infarct toward the axilla as a result of clockwise rotation of the heart on its longitudinal and anteroposterior axes. Diagnostic signs of anterior infarction were found in the standard limb leads in only two of the twenty cases. These three leads, together with a single precordial lead, would have been inadequate for diagnostic purposes in the majority of the cases in this series and would have been insufficient for localizing purposes in all cases. On the other hand, multiple precordial leads furnished adequate evidence in all cases for a positive or presumptive diagnosis of myocardial infarction and for a clinically satisfactory prediction of the position of the lesion.

II. Correlation of electrocardiographic and pathologic findings in large anterolateral infarcts

Abstract The findings in the Wilson precordial leads and in the standard and Goldberger limb leads have been analyzed and correlated with the pathologic findings in fifty-seven cases of infarction of the apical one-third or more of the anterior and lateral walls of the left ventricle. The infarct was distributed transmurally through the apical one-third or more of both the anteroseptal and lateral walls in twenty-four cases; it was transmural in the anteroseptal wall and subendocardial in the lateral wall in fourteen cases; and was confined to the subendocardial one-fourth to three-fourths of both the anteroseptal and lateral walls in nineteen cases. A QS deflection was recorded in Leads V 3 and/or V 4 in twenty-nine of the thirty-eight patients with transmural infarction of the apical one-third or more of the anteroseptal wall of the left ventricle and corresponded closely with the findings at autopsy. An abnormal QR complex was present in both leads in three other cases and was explainable by the pathologic findings. Good correlation between a QS deflection in Lead V 5 or in both V 5 and V 6 and transmural infarction of the apical one-third or more of the lateral wall of the left ventricle was obtained in twelve of twenty-four cases and a satisfactory explanation was found for an abnormal QR complex recorded in one or both of these leads in eight other cases. An abnormal QR or very coarsely notched QS complex was present in Leads V 3 and V 4 in eleven of the nineteen patients with infarction of the subendocardial portion of the anteroseptal aspect of the left apex and conformed closely with the pathologic findings. A smooth or slightly notched QS deflection found in these leads in four additional cases was adequately explained. Good correlation between an abnormal QR pattern in Lead V 5 or in both V 5 and V 6 and infarction of the subendocardial portion of the lateral aspect of the left apex was obtained in twenty-seven of thirty-three cases and a satisfactory explanation was found for a smooth or slightly notched QS complex recorded in one or both of these leads in three other cases. An initial upstroke was recorded in Leads V 3 and V 4 in ten cases, despite the presence of subendocardial or transmural infarction of the anteroseptal aspect of the left apex, and a similar finding was obtained in Leads V 5 and V 6 in seven of these cases, in spite of a comparable lesion in the lateral wall of the left apex. The causes for the registration of an initial R, rather than a Q, under these circumstances, were as follows: (1) displacement of the transitional zone leftward to the anterior axillary or mid-axillary line; (2) left bundle branch block; (3) infarction of the left side of the septum, necessitating activation of intact septal remnants from right to left; (4) early recording of the electrocardiogram soon after the onset of symptoms and before the myocardial changes have progressed to the point of obliterating the response to the activating impulse; (5) patchy infarction with preserved islands of muscle in the subendocardial layer or scattered through the wall; and (6) extensive infarction of the posterior wall of the left ventricle with consequent reduction in the opposing negative potentials available for transmission through the anterolateral infarct to the precordium. The QS complexes associated with recent transmural infarction were usually accompanied by abnormal elevation of the RS-T junction and straightening or upward convexity of the segment, followed by progressive covelike inversion of the T wave in serial tracings. This RS-T pattern indicated the presence of subepicardial muscle that was injured, but not dead. In three cases, the QS complexes were accompanied by slight RS-T elevation, upwardly concave RS-T segment, and upright T waves, which exhibited no significant change in a repeat tracing a few days later. These findings were correlated with recent transmural infarction, which had completely destroyed the subjacent myocardium. Recent subendocardial infarcts were generally accompanied by upward displacement of the RS-T segment, less marked in degree, but similar in contour to that customarily found in transmural infarction and attributable to injury to the subepicardial layer. A less common, but more characteristic finding in recent subendocardial infarction consisted in acute RS-T depression, attributable to injury localized to the subendocardial layer. A positive differentiation between recent and healed infarction could not be made from a single electrocardiogram because of the tendency for abnormal RS-T elevation and/or cove inversion of the T wave to remain as a permanent finding in ventricular aneurysm.

Normal variations in multiple precordial leads.

Abstract 1.1. Wilson precordial leads have been correlated with autopsy findings in a group of 1,000 cases. In this communication, an analysis is presented of the precordial electrocardiograms of fifty-two patients whose hearts were considered normal by gross and microscopic examination. 2.2. The P wave was consistently upright in Leads V 4 , V 5 , and V 6 and varied from erect to diphasic in Leads V 1 , V 2 , and V 3 , depending upon the position of the electrode in reference to the right atrium. 3.3. The total QRS interval and the duration of each component phase were determined in Leads V 1 , V 2 , V 5 , and V 6 with aid of a Cambridge measuring device. The average QRS interval was 0.078 second and the upper limit in this series was 0.098 second. There was a trend toward slight lengthening of QRS duration with increasing cardiac weight. 4.4. A QRS complex was found in both Leads V 1 and V 2 in two cases, but was not present in leads further to the left. An initial Q with succeeding R was not found in leads over the right ventricle, but was present in at least one lead over the left ventricle in approximately two-thirds of the cases. This Q wave was brief in duration, reaching its nadir within 0.02 second, and was small in magnitude, amounting to less than 25 per cent of the amplitude of the succeeding R wave. 5.5. The interval elapsing from the onset of the R wave to its peak was taken as an index of the time required for the impulse to pass through the segment of ventricular wall beneath the exploring electrode. The time interval from onset to peak of R was invariably minimal in Lead V 1 and increased progressively in leads further to the left to reach a maximum in Leads V 5 or V 6 . The significantly longer duration of the R wave in leads over the left than in leads over the right ventricle was in keeping with the normal difference in thickness of their respective walls. There was a trend toward a slightly greater duration of the R wave in Lead V 6 with increasing ventricular weight. As the electrode was moved from positions over the right to positions over the left ventricle, a progressive increase in the amplitude of the R wave and a reciprocal decrease in the S wave was found in every case. Low voltage R waves that were less than 7 mm. in height in all six precordial leads were found in four normal subjects in this series. Normal variations in the position of the transitional zone and form of QRS complexes recorded in this zone are illustrated and discussed. 6.6. An elevation of the RS-T take-off of 0.5 to 2.0 mm. may be considered as a normal variant, provided that the tracing immediately begins to rise above the RS-T junction in an arc with upward concavity to end in a tall upright T wave. Depression of the RS-T junction is very rare in the precordial leads of subjects with normal hearts and should be regarded as abnormal if it amounts to 0.5 mm. or more, provided that pseudodepression from tachycardia or a prominent auricular T wave are excluded. 7.7. An inverted T wave was a frequent finding in Lead V 1 and was present in Lead V 2 in three normal women, 19, 31, and 45 years of age, respectively. The T wave was upright in Leads V 3 , V 4 , V 5 , and V 6 except in two subjects, one of whom had an isoelectric T in V 3 associated with an inverted T wave in Leads V 1 and V 2 . The other had an isoelectric T in Lead V 6 associated with low voltage of the QRS.

V. Correlation of electrocardiographic and pathologic findings in posterior infarction

Abstract The findings in Lead aV F have been analyzed and correlated with cardiac position and with the pathologic findings in 110 patients with infarction of the posterior wall of the left ventricle. The infarct was recent in forty-three cases and healed in the other sixty-seven. Determination of the electrical position of the heart was essential to the interpretation of the findings in Lead aV F , since the direction of the initial phase of the QRS complex was dependent upon the surface of the septum that faced downward, whereas the potential variations of the left leg throughout the remainder of the cycle were governed principally by those of the epicardial surface that rested upon the diaphragm. Findings in Lead aV F in Thirty-Five Cases of Posterior Infarction With Electrocardiographic Evidence of Horizontal to Semihorizontal position of the Heart .—In twenty-two of the group, Lead aV F displayed a small R and deep S wave, representative of the customary findings due to transmission of the potential variations of the right side of the septum and epicardial surface of the posterior wall of the right ventricle to the left leg and in no way suggestive of the posterior infarct found at autopsy. In nine others, a continuation of the infarct into the septum was manifested by one of the following three diagnostic patterns in Lead aV F : a small Q, small R, and deep S wave; a small Q and tall late R wave similar to the pattern in Lead V 1 and referable to septal infarction with right bundle branch block; and a QS comple: attributable to septal infarction after establishment of the presence of transverse position and exclusion of the QS complex that occurs as a normal variant under these circumstances. The latter was present in two of the thirty-five cases. Lead aV F in the two remaining cases displayed a broad, slurred QS and QR complex, regarded as a manifestation of left bundle branch block in a horizontal and semihorizontal heart, respectively, and considered independent of the posterior and and septal infarcts found at autopsy. Criteria for the Diagnosis of Posterior Infarction in the Presence of Intermediate, Semivertical, or Vertical Position of the Heart .—Under these conditions, the potential variations of the epicardial surface of the posterior wall of the left ventricle had the predominant effect upon the QRS-T pattern in Lead aV F . The abnormal QR pattern due to posterior infarction was differentiated from the normal QR complex in Lead aV F by the time interval from onset to nadir of the Q wave, the ratio of the amplitude of the Q to that of the R wave, and the duration and contour of the ascending limb of the R wave. QR complexes of 0.5 millivolt or more, with a Q wave measuring 0.03 second or more from onset to nadir and a Q R ratio over 25 per cent were considered diagnostic of posterior infarction. QR complexes that met part, but not all, of the foregoing requirements were generally classed as borderline to strongly suggestive, but were also considered diagnostic, provided that (a) the time interval from onset to nadir of the Q wave was 0.04 second or more; (b) the Q wave was followed by an abnormally prolonged, notched, or coarsely slurred upstroke; (c) the tracing was obtained within twenty-four hours of the onset of symptoms and showed classical displacement of the RS-T segment; or (d) previous tracings were available, showing perfectly normal patterns prior to the development of the borderline QR complex. QS deflections of 0.5 millivolt or more, which consumed 0.03 second or more from onset to nadir, were considered diagnostic of extensive transmural posterior infarction, provided it could be established that the heart was in intermediate to vertical position and not in horizontal or semihorizontal position. Findings in Lead aV F in Seventy-Five Cases of Posterior Infarction With Electrocardiographic Evidence of Intermediate to Vertical Position of the Heart .—On the basis of the criteria described, the findings in Lead aV F were classed as diagnostic of posterior infarction in forty-two cases, borderline to strongly suggestive in seventeen cases, and negative in sixteen cases. The findings in Lead aV F , as classified into the foregoing three categories, were correlated with the size and position of the infarct in reference to the long axis of the left ventricle. Of thirty-one patients with infarction extending two-thirds or more of the length of the posterior wall, Lead aV F was negative in only one. The normal QRS pattern in this case was probably due to the fact that the lesion was posterolateral in position and spared the septal half of the posterior wall. The incidence of diagnostic failures in patients with smaller posterior infarcts varied with the size and location of the lesion and was lowest when the infarct involved the middle third of the posterior wall, as shown by the following observations. Lead aV F was negative in only one of five patients with infarction confined to the middle third of the posterior wall. On the other hand, the findings in Lead aV F were negative in eight of fourteen patients with infarction confined to the apical third, but in only two of fourteen other patients in whom the posteroapical infarct continued into the middle third. Both of these failures were explained by the presence of left bundle branch block. The findings in Lead aV F were negative in all three patients with infarction confined to the basal third of the posterior wall, but in only one of eight patients in whom the posterobasal lesion continued into the middle third. The latter failure occurred despite the fact that serial tracings were available before and after the development of the infarct. A QRS-T pattern that was considered diagnostic of posterior infarction was found terminally in Lead aV F of one patient with hemopericardium due to dissecting aneurysm. Esophageal leads were obtained in five patients and were considered diagnostic of the posterior infarct found at autopsy. Recent posterior infarction was generally manifested by reciprocal changes in the RS-T segment of precordial leads when the anterior wall was intact, but not when the anterior wall was infarcted. Standard Leads II and III failed to provide diagnostic evidence of posterior infarction in cases where Lead aV F was negative. Furthermore, the application of the Pardee criteria to the interpretation of the findings in the standard leads led to errors in a number of cases where correct diagnoses could be made from the findings in Lead aV F .

Water and electrolyte content of cardiac and skeletal muscle in heart failure and myocardial infarction.

Abstract The water and electrolyte content of cardiac and skeletal muscle from patients dying of congestive failure or recent myocardial infarction was compared with the composition of specimens from patients dying of noncardiac causes. Myocardial blocks from four standard sites in the left ventricle were analyzed for water, sodium, potassium, chloride, magnesium, and phosphorus in twenty-nine cases and for water, sodium, and potassium in eighteen additional cases; blocks from the pectoralis major were analyzed for all six substances in twenty-five cases and for water, sodium, and potassium in four additional cases. The control group comprised sixteen patients with normal hearts at autopsy and no evidence of a metabolic disorder. Myocardial analyses yielded averages of 78.8 Gm. of water, 4.96 meq. of sodium, 8.32 meq. of potassium, 4.04 meq. of chloride, 0.445 meq. of magnesium, and 3.88 meq. of phosphorus per 100 Gm. of wet tissue. Estimates of the partition of water between the extracellular and intracellular compartments and of the concentrations of base within the cells were made according to the method of Newburgh. Skeletal muscle from the same patients was comparable to myocardium in total water content, but showed a relatively smaller extracellular and larger intracellular volume. The concentration of total base in the cells was essentially the same as that in myocardium, but sodium level was slightly higher and potassium and magnesium levels were slightly lower. Uncomplicated left ventricular hypertrophy was found in fourteen patients who showed no evidence of congestive failure during hospitalization and died of noncardiac causes. The average content of water and each electrolyte in the myocardium was almost identical with that in the normal control group. Congestive failure, complicating left ventricular hypertrophy, was present during hospitalization and at autopsy in eight patients. Analyses of cardiac and skeletal muscle showed significant reduction in potassium below the control values, but no significant change in content of water, sodium, chloride, magnesium, or phosphorus. The estimated partition of water in both cardiac and skeletal muscle was similar to that in the controls. The estimated intracellular concentration of total base was reduced to a similar level in cardiac and skeletal muscle, largely from potassium loss. The significance of these observations is discussed. Recent myocardial infarction was responsible for the death of seven patients. Separate analyses were made of blocks from infarcted areas and of blocks from distant areas that appeared uninfarcted to gross examination. Infarcted myocardium showed a marked but proportionate increase in sodium and chloride, reflecting a severe interstitial edema, and an even more marked reduction in potassium, magnesium, and phosphorus, reflecting primarily losses from dead and dying cells. The analyses of distant blocks that were not grossly infarcted gave results for all five electrolytes that were intermediate between the values obtained from infarcted segments and those from normal controls. The abnormalities in chemical composition of myocardium well beyond the boundaries of a recent infarct were attributed to ischemia. Analysis of skeletal muscle from these patients did not deviate significantly from the normal.

VII. Correlation of electrocardiographic and pathologic findings in lateral infarction

Abstract Infarction of the lateral wall of the left ventricle was demonstrated pathologically in 105 cases, which represents an incidence of 65 per cent in a series of 161 cases. The cases of anterolateral infarction and those of posterolateral infarction have been analyzed in previous reports and the present study was concerned with a correlation of electrocardiographic and pathologic findings in twenty-seven cases of primary lateral infarction. These cases were classified into three groups, according to the distribution of the lesion at autopsy: (A) high, (B) low, and (C) midlateral infarction. 1. A. High lateral infarction, involving chiefly the basal one-half of the lateral wall, but continuing for a variable distance into the apical one-half, was found in fourteen cases. The infarct was limited to the subepicardial layer in one case and was manifested by normal QRS complexes and deeply inverted T waves typical of the findings in pericarditis. Despite the fact that the high lateral infarct was transmural in five cases and subendocardial in the other eight, it was manifested by a diagnostic QR pattern in Lead V 5 or V 6 in only one case. The rarity of abnormal Q waves in Leads V 5 and V 6 of this group contrasted sharply with their frequency in association with infarction of the apical one-third of the anterolateral wall and was ascribed to the fact that high lateral infarcts generally spared most or all of the apical one-third of the anterolateral wall. On the other hand, Lead aV L yielded a QR pattern which was considered diagnostic of lateral infarction in two cases, strongly suggestive in five cases, and suspicious in four cases. Standard Lead I was not an adequate substitute for Lead aV L because it failed to show an initial downstroke in five of the eleven patients with Q waves in aV L , because of greater initial negativity of the right than the left arm. Signs suggestive of infarction in the customary precordial or left arm leads constitute an indication for exploration of the upper precordium and axilla. Leads at the intersection of a horizontal line through the sternal terminus of the third intercostal space with vertical lines in the plane of precordial Positions 3, 4, 5, and 6 were obtained on four patients who were followed to autopsy. In one case, the findings in the customary precordial leads were equivocal, those in Lead aV L were strongly suggestive, but those in the high precordial leads were pathognomonic of the high lateral infarct found at autopsy. The findings in the high precordial leads taken in conjunction with those in the customary leads in the other three cases aided in establishing the diagnosis and in localizing the position of the infarct. 2. B. Low lateral infarction was found in eleven cases and was largely or entirely confined to the apical one-third of the lateral wall in eight of these. Abnormal Q waves diagnostic of infarction were present in Lead V 5 , V 6 , and/or aV L in five cases, and strongly suggestive QR patterns were found in three others. The electrocardiogram was negative in one case and conformed to the pattern of Wood, Wolferth, and Bellet in the other two cases. The RS-T depression in V 4 , V 5 , and V 6 could be correlated with acute infarction which involved the subendocardial and mid-zones, but spared the subepicardial layer, and the absence of Q waves was explained by the patchy character of the subendocardial lesion. A similar pattern was recorded in an electrocardiogram taken four and one-half hours after the onset of the pain in one other case, but was subsequently replaced by a QR complex diagnostic of the subendocardial infarct found at autopsy. 3. C. Small mid-lateral infarcts, involving the subendocardial layer of the middle one-third of the lateral wall, were found in two cases. A pattern resembling that of Wood, Wolferth, and Bellet was found in both cases, but could have been produced by a combination of left ventricular hypertrophy and digitalis action in one of these. The absence of Q waves may have been due to the small size of the lesion and the failure to take high axillary leads. QRS-T abnormalities in one or more of the first four precordial leads, which were suggestive of anteroseptal infarction, but were actually a manifestation of the lateral infarction, were found in five cases. Transmission of the potential variations of the infarcted lateral wall to the precordium was facilitated by marked counterclockwise rotation in three of these cases. This situation was the opposite of that in previously reported cases where abnormal Q waves were recorded in Leads V 5 and V 6 as a result of clockwise rotation sufficient to cause reference of the potential variations of an infarcted anteroseptal wall to the axilla.

Joint and skeletal muscle manifestations in sarcoidosis.

Abstract Four cases of sarcoidosis in which the diagnosis was established by demonstration of noncaseating epithelioid granulomas by muscle or lymph node biopsy are reported. These cases illustrate the following manifestations hitherto regarded as rare or coincidental: (1) migratory febrile polyarthritis, resembling rheumatic fever, which was refractory to salicylates but gradually subsided to leave little or no deformity; (2) asymptomatic granulomatous infiltration of striated muscle. Erythema nodosum was present in three cases. Pronounced hilar lymphadenopathy consistent with either sarcoidosis or erythema nodosum was demonstrable in all patients and was accompanied with finely nodular pulmonary infiltration in two and generalized lymphadenopathy in two. Healed chorioretinitis was found in one patient and acute uveitis and parotitis in another. The results of this study suggest that random muscle biopsy may constitute a valuable adjunct for the establishment of the diagnosis of sarcoidosis, particularly in patients without cutaneous lesions or significant lymphadenopathy.

VI. Correlation of electrocardiographic and pathologic findings in posterolateral infarction

Abstract In thirty-three cases of pathologically established posterolateral infarction, electrocardiograms consisting of precordial Leads V 1 through V 6 and the Goldberger and standard limb leads were studied to evaluate the evidence furnished by these leads for the detection and localization of the infarct. The findings in Lead aV F were employed as an index of the posterior aspect of the lesion and the findings in Leads V 5 , V 6 , and aV L were used as an index of the lateral aspect. The interpretation of Lead aV L has been discussed in detail, whereas the criteria used for the other leads were established in previous reports. In eleven of the sixteen patients observed during the acute stage, precordial Leads V 1 through V 4 revealed reciprocal depression of the RS-T segment or exaggeration in the height of the R and/or T waves, sufficient to arouse the suspicion of posterolateral infarction. On the other hand, the standard limb leads were much less dependable than the unipolar limb leads and supplied no additional information. The findings in Leads aV F , aV L , V 5 , and V 6 were regarded as strongly suggestive to diagnostic of both aspects of the infarct in ten cases; of the posterior, but not the lateral, lesion in nine cases; of the lateral, but not the posterior, lesion in twelve cases; and were negative in the other two cases. The commonest cause for failure to detect the posterior portion of the infarct in Lead aV F was counterclockwise rotation into a semihorizontal to horizontal position. However, lesions that involved the posterolateral, but spared the posteroseptal, wall were sometimes not recognizable from Lead aV F , even though the heart was in a vertical to intermediate position. The commonest cause for failure to detect evidence of posterolateral infarction in Lead aV L was clockwise rotation. In nine patients with extensive infarction of the basal portion of the posterolateral wall, the QRS pattern in Lead aV L resembled that in one of the first four precordial leads, indicating that the potential variations of the left arm were transmitted chiefly from the anteroseptal wall of the right or left ventricle. Leads V 5 and V 6 seldom yielded abnormal Q-wave patterns unless the posterolateral infarct continued into the apical third of the anterolateral wall. The occasional association of abnormal Q-wave patterns in Lead V 6 or both Leads V 6 and V 5 with infarction of the apical third of the posterolateral wall was attributed to counterclockwise rotation of the heart or anterior displacement of the apex. Precordial Leads V 1 through V 6 , together with the Goldberger and standard limb leads, are inadequate for the accurate localization of posterolateral infarction, but generally reveal sufficient evidence to arouse the suspicion of at least one aspect of the lesion. Under these circumstances, Leads V 7 , V 8 , and supplementary high axillary leads are indicated to explore the apical and basal aspects, respectively, of the posterolateral wall.