Temporal changes in body surface peak R isochrone maps and left ventricular function in patients with myocardial infarction

Body surface peak R isochrone mapping and radionuclide ventriculography were performed twice in 22 patients with myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously. For each lead, the time from the onset of QRS to the peak of the R wave was measured. From this data for 87 leads an isochrone map was constructed. The lead points where R waves were not observed were designated the no R-wave area (No-R area), which was postulated to correspond to the unexcited regional myocardium. Other abnormal findings, i.e., delay of peak R time near the No-R area (peri-No-R area delay), crowding of isochrone lines, and an island-like zone of delayed peak R times were postulated to indicate slow conduction in the partially excited regional myocardium. In three patients, abnormal patterns in the peak R isochrone maps during the acute phase (within a month from the onset of myocardial infarction) improved in the chronic phase with a significant increase in left ventricular ejection fraction. In two patients, the No-R area decreased after the left ventricular aneurysmectomy. In other patients, abnormal patterns of the isochrone maps and the ejection fraction remained unchanged during the chronic phase of myocardial infarction. We conclude that the comparison of peak R isochrone map patterns between the acute and chronic phase may be useful in evaluating the balance of reversible and irreversible regional damage in myocardial infarction.     

Clinical significance of body surface isochrone maps for predicting ventricular arrhythmias in patients with previous myocardial infarction

To investigate the utility of body surface isochrone maps for estimating ventricular arrhythmias in patients with previous myocardial infarction, we compared findings of body surface isochrone maps with those of signal-averaged electrocardiograms (SAECGs) and an incidence of ventricular tachycardia (VT). Body surface isochrone mapping was performed in 50 patients with previous myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the patient's anterior chest and back were recorded simultaneously. For each lead, the activation time was measured as the duration from the onset of QRS to the peak of the R wave. SAECGs were recorded in the same patients to detect late potential (LP) which was considered to last more than 30 msec. Activation delay on isochrone maps (D) was found in 31 of 50 patients. The group D+ had a lower ejection fraction and higher incidence of VT (8/31 (25.8%) vs. 1/19 (5.3%)) and LP (13/31 (41.9%) vs. 2/19 (10.5%)) than the group D-. There were four patients with sustained VT who had both D and LP. For predicting VT, D has a sensitivity of 88.9% and a specificity of 43.8%. It was decided that abnormal delay on body surface isochrone maps indicates slow conduction of the surviving myocardium and is related to the occurrence of ventricular arrhythmias. We concluded that body surface isochrone maps can be useful in predicting life-threatening arrhythmias in patients with previous myocardial infarction.     

The body surface distribution of the QT interval in patients with previous myocardial infarction and normal subjects

In spite of the clinical importance of the QT interval, its body surface distribution is still unclear. To determine the spatial distribution of the QT interval, we studied 20 normal subjects and 45 patients with previous myocardial infarction (25, anterior; 20, infero-posterior). Unipolar electrocardiograms were recorded from 87 torso sites. The QT interval in each lead was determined semi-automatically. In normal subjects, the longer QT intervals were located on the left anterior chest and the right shoulder portion. And, the relatively shorter QT intervals were shown on the right inferior chest. In the anterior MI group, the remarkably longer QT intervals were located on the left anterior chest. In the infero-posterior MI group, the longer QT intervals were found on the left lateral and back. In both MI groups, the sites of longer QT intervals corresponded to the sites of infarcted area. In the aneurysm (+) subgroup of the anterior MI group, the remarkably longer QT intervals could be found on the left anterior chest, while in the aneurysm (-) subgroup, these characteristic patterns could not be recognized. Our data suggest that QT intervals are not equal on a torso. In patients with myocardial infarction, the sites of prolonged QT intervals corresponded to the sites of infarcted area. The QT interval was thought to have some bearing on the abnormal repolarization of the residual myocardium in the infarcted area.     

Body surface isopotential maps in old inferior myocardial infarction undetectable by 12 lead electrocardiogram

The purpose of this study is to examine the value of body surface isopotential maps in the diagnosis of old inferior myocardial infarction that can not be diagnosed by 12 lead ECG. Forty-three patients with a Q wave of at least 0.02 sec but less than 0.04 sec in width and also less than 25% of the R wave in depth in lead a VF of the 12 lead ECG were selected for this study. The patients were divided into infarction and noninfarction groups based on their clinical histories and cardiac catheterization data. The infarction group showed characteristic surface maps with a minimum which moved from the left posterior chest to the lower back or from the lower back to the right anterior lower chest in the early phase of QRS. The noninfarction group exhibited a minimum which shifted from the back to the right upper chest or from the left anterior chest to the lower back in the same phase. Thus, both groups were clearly distinguishable from each other by the positional change of the minimum in the early phase of QRS. This study suggested that body surface maps contain diagnostic information concerning the presence or absence of inferior myocardial infarction which is not easily available from the 12 lead ECG.     

Relation between localization of coronary artery disease and local abnormalities in ventricular activation during exercise tests

To examine whether or not the location of local abnormalities on body surface isochrone maps reflects the site of myocardial ischemia, 48 coronary artery disease patients without myocardial infarction were studied. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously before and after the submaximal treadmill exercise. For each lead, the duration from the QRS onset to the time of the most rapid decrease in QRS voltage was measured (index of ventricular activation [IVA]). Based o the data provided by these 87 leads, IVA isochrone maps (IVA map) in preexercise and in postexercise, as well as IVA maps showing the difference between preexercise and postexercise, were constructed. The IVA was defined as abnormal when it exceeded (mean + 2 SD) the normal range. We called the area with the abnormal IVA, the "+2SD area." In patients having a stenosis in the left anterior descending artery, the +2SD area in each map was located mainly on the left anterior chest, whereas in patients having a stenosis in the right coronary artery, the +2SD area in each map was located mainly on the right lower thoracic surface. Moreover, the +2SD area of patients with both left anterior descending and right coronary artery disease appeared on both the left anterior chest and the right lower thoracic surface. In patients with left circumflex artery disease, however, the location of the +2SD area did not suggest a stenotic site because of its small population. On the other hand, it was difficult to determine the ischemic site from the body surface distribution of ST segment depression.(ABSTRACT TRUNCATED AT 250 WORDS)     

Qualitative and quantitative analysis of characteristic body surface potential map features in anterior and inferior myocardial infarction

Body surface potential maps were recorded from 120 electrode sites in 236 normal subjects and 258 patients with initial evidence of either anterior myocardial infarction (MI) or inferior MI to identify characteristic map patterns in both groups. After time normalization, averaged map distributions were displayed at 18 equal time intervals during both QRS and ST-T waveforms from the normal, anterior MI and inferior MI groups. At each time instant, the 120-point averaged normal map was subtracted in turn from the corresponding anterior and inferior MI maps; the resulting differences at each electrode site were divided by the pooled standard deviation and the obtained values (discriminant indexes), plotted as contour lines with 1 standard deviation increments, producing discriminant maps for each bi-group comparison. The most consistent discriminant patterns in 114 patients with anterior MI were observed in early QRS in the upper left anterior chest where abnormal negative voltages reflected loss of electric potentials while reciprocal changes were noticed in the lower back; by mid-QRS, both distributions had moved jointly and vertically, the former in the lower torso on the midsternal line, the latter in the upper back. In 144 patients with inferior MI, abnormal positive distributions were observed in early QRS in the upper back, followed later by excessive negative voltages in the inferior right anterior chest; at mid-QRS, both distributions had migrated horizontally, the former proceeding toward the upper anterior torso, the latter to the lower left dorsal area.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes of ventricular activation time in patients with left anterior fascicle block and bifascicular block

Recognition of left anterior fascicle block is usually a diagnostic problem. Isochrone maps, displaying results of the body surface potential mapping are helpful in solving this problem. The isochrone maps present changes of heart electric field, especially those concerning a pathway of the depolarization front propagation within the heart conduction system. Body surface potential mapping registrations were performed using a Fukuda Denshi cylindrical system, which enables simultaneous recordings of electrocardiographic signals from the 87 leads. The examined group consisted of 29 patients with left anterior fascicle block (LAFB) and complete right bundle branch block (RBBB) complicated by LAFB. The first group consisted of 7 females and 8 males with the mean age of 62 +/- 11.3 yr., and the second group comprised 8 females and 6 males (the mean age: 64 +/- 5.01 yr.). The control group comprised 30 healthy subjects--the mean age of 50.3 +/- 5.63 yr. In all of examined patients, elementary biochemical tests, echocardiography and X-ray chest examinations were performed. In order to obtain a pattern reflecting a depolarization trajectory in the patients' heart, the ventricular activation time maps (VAT) were constructed, using the own software. This kind of maps is more precise than standard electrocardiograms and makes possible monitoring an activity propagation, as well as its velocity within the heart conduction system. In the patients demonstrating left anterior fascicle block, a subendocardial layer of the bottom left surface of the interventricular septum is the earliest stimulated area of heart (similarly, as in normal subjects). Afterwards, the front of stimulation wave crosses the septum from left to right side. In the next phase, the activation comprises right surface of the septum, as well as subendocardial surfaces of right ventricle free walls, however in the free wall of left ventricle, as a result of left anterior fascicle block, the activation spreads through back part of bundle branch. At this moment, isochrone lines arrange in bottom-right-forward direction. Subsequently, the delayed stimulation wave penetrates the anterior and lateral walls. Isochrones on the right torso are directed rightward and upward. In the final phase, the activation spreads over remaining part of the free wall of left ventricle, moving leftward, upward and backward. On isochrone maps, the final stage of activation propagation is seen on whole upper back part of the torso. In patients demonstrating RBBB with LAFB, the stimulation time is notably delayed. As a result of blocking the right ventricle and left anterior fascicle, the stimulation wave goes to the free wall of left ventricle through the back bundle. Isochrones distribution is similar like in left anterior fascicle block. However, different time of stimulation dispersal in downward direction is observed. Next, the wave propagation moves downward and leftward, coming to the anterior and lateral walls. Later on, a stimulation of the remaining part of the left ventricle free wall is observed, and isochrones wander to the heart bottom. Finally, after about 80 ms from the beginning, a delayed stimulation wave reaches the right ventricle, passing around the blocked area and spreading through terminal fibres within right ventricle. In the both examined groups no significant differences in relation to isochrones distribution were observed, therefore the averaged VAT maps were assumed as a reference pattern for the given groups. A pattern of VAT maps distribution and values of ventricular activation time can be useful in the further investigations concerning an analysis of wave propagation in bundle branch blocks.     

ST segment changes in exercise body surface mapping after myocardial infarction in patients with isolated left anterior descending coronary artery disease

To investigate the clinical significance of exercise-induced ST segment elevation and ST segment depression after myocardial infarction (MI), we performed 87-lead ECG mapping after previous anterior infarction in 24 patients with isolated left anterior descending coronary artery disease before and 1.5 minutes after treadmill exercise. Thirteen patients showed ST segment elevation only, seven patients showed both ST segment elevation and depression, and four patients showed ST segment depression only. ST segment elevation most frequently occurred in the left anterior chest leads corresponding to the QS area, and ST segment depression developed in the left lower chest and left lower back leads. There was good correlation between the number of lead points showing ST segment elevation (nSTe) after exercise and the number of lead points showing QS waves (nQS) before exercise (r = 0.65). nSTe was also correlated with the asynergy index (r = 0.43). These findings suggest that ST segment elevation is mainly the result of aggravation of wall motion abnormalities of the infarcted myocardium. Body surface distribution of ST segment depression was similar to that in effort angina pectoris without MI. We conclude that exercise-induced ST segment depression in MI mainly reflects the ischemia of the surviving myocardium of small infarcts or the peripheral area of large infarcts.     

Identification of best electrocardiographic leads for diagnosing anterior and inferior myocardial infarction by statistical analysis of body surface potential maps

In view of the increasing interest in quantifying and modifying the size of myocardial infarction (MI), it is important to look for clinically practical subsets of electrocardiographic leads that allow the earliest and most accurate diagnosis of the presence and electrocardiographic type of MI. A practical approach is described, taking advantage of the increased information content of body surface potential maps over standard electrocardiographic techniques for facilitating clinical use of body surface potential maps for such a purpose. Multivariate analysis was performed on 120-lead electrocardiographic data, simultaneously recorded in 236 normal subjects, 114 patients with anterior MI and 144 patients with inferior MI, using as features instantaneous voltages on time-normalized QRS and ST-T waveforms. Leads and features for optimal separation of normal subjects from, respectively, anterior MI and inferior MI patients were selected. Features measured on leads originating from the upper left precordial area, lower midthoracic region and the back correctly identified 97% of anterior MI patients, with a specificity of 95%; in patients with inferior MI, features obtained from leads located in the lower left back, left leg, right subclavicular area, upper dorsal region and lower right chest correctly classified 94% of the group, with specificity kept at 95%. Most features were measured in early and mid-QRS, although very potent discriminators were found in the late portion of the T wave.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determination of the site of myocardial infarction by QRST isointegral mapping in patients with abnormal ventricular activation sequence

QRST isointegral maps were constructed from 87-lead ECGs in 37 patients with abnormal ventricular activation, such as ventricular premature beats, WPW syndrome, left bundle branch block and right bundle branch block. Patients were divided into 2 groups, the old myocardial infarction (OMI) group (n = 18) and the non-infarction group (n = 19). In the latter group, QRST isointegral maps showed smooth bipolar surface distributions, with positive values located over the precordium and negative values over the right upper anterior chest and the back, independent of the ventricular activation sequence. In the OMI group, for individual patients, the distribution patterns of QRST isointegral maps were similar between normal sinus rhythm and VPB or WPW conduction. Including the patients with BBB, a decrease of the time-integral value was consistently found in leads which corresponded to an asynergic site indicated by left ventriculography. To evaluate the abnormalities of QRST isointegral maps, particular attention was given to the area where the QRST time-integral value was less than the lower limit determined by 40 normal subjects; this area was designated as the negative departure area. Characteristic distribution patterns of the negative departure area seem to indicate the asynergic site, independent of the activation sequence. Thus, the QRST isointegral map may be useful for identifying the asynergic site in patients with abnormal ventricular activation sequence, that is hardly detected with conventional electrocardiograms.     

Use of body surface electrocardiographic mapping to localize the asynergic site in previous myocardial infarction

Body surface electrocardiographic (ECG) maps of myocardial infarction were analyzed using the departure mapping technique, which represents the abnormal potential distribution out of normal ranges. Body surface ECG mapping using 87 leads was performed on 65 patients with previous myocardial infarction and on 40 normal volunteers. Potential departure maps at 10, 20, 30, 40, and 50 msec after the onset of QRS were constructed; each map indicated, if present, the area of abnormal decreased potential that is more than 2 standard deviations from the normal range (-2 SD area). In patients with myocardial infarction, the appearance time and the location of the -2 SD area were specific for the sites of left ventricular asynergy; the sensitivity and specificity were 86% and 100% for the asynergy of segment 2 (20 msec, on the upper left anterior chest), 87% and 97% for segment 3 (30 msec, on the middle anterior chest), 86% and 80% for segment 4 (20 or 30 msec, on the lower right anterior chest), and 88% and 90% for segment 5 (30, 40, or 50 msec, on the middle back), respectively. The sensitivity of these criteria was better than that of 12-lead ECG, while the specificity was comparable. In the analysis of body surface ECG mapping data, departure maps aid in depicting abnormalities and in making an accurate assessment. Body surface ECG mapping can be used to improve the diagnostic ability of ECG to detect myocardial infarction.     

Regional left ventricular function in acute myocardial infarction: Evaluation with quantitative radionuclide ventriculography

Regional and global left ventricular performance was noninvasively assessed with quantitative gated equilibrium radionuclide ventriculography in 43 patients an average of 40 hours after the onset of a first acute transmural myocardial infarction. In all 16 patients with anterior infarction, regional ejection fraction, a quantitative measure of regional left ventricular performance, was uniformly depressed in the infarcted zone. In patients with inferior infarction the abnormalities of regional performance were less severe. Fourteen of 20 patients (70 percent) with inferior infarction had depressed performance in the infarcted zone. Function in noninfarcted zones was abnormal in only 6 of the 20 patients (30 percent) with inferior infarction, but it was abnormal in 11 of the 16 patients (69 percent) with anterior infarction, particularly in those with severe pump failure. As a consequence, global left ventricular ejection fraction was significantly lower in patients with anterior than in those with inferior infarction (mean ± standard error of the mean 31 ± 3 percent versus 51 ± 3 percent, p < 0.005). Prognosis and clinical functional class were related to performance not only in infarcted zones, but also in noninfarcted zones as assessed with electrocardiography.It is concluded that depressed function in apparently noninfarcted left ventricular zones contributes significantly to left ventricular dysfunction after acute myocardial infarction, particularly in patients with anterior infarction.     

Effects of coronary occlusion on cardiac and body surface PQRST isoarea maps of dogs with abnormal activation simulating left bundle branch block

The possibility of detecting myocardial infarction in the presence of left bundle branch block by analysis of cardiac and body surface PQRST isoarea maps was studied in nine open-chest and six closed-chest dogs. Recordings were taken during supraventricular drive or right atrial plus right ventricular pacing in control periods and at intervals for up to 10 hr after left anterior descending coronary artery occlusion. Right ventricular pacing was used to simulate left bundle branch block. Myocardial infarction was documented with triphenyl tetrazolium staining. The PQRST areas during supraventricular drive and right atrial plus right ventricular pacing were highly correlated to each other both before and after coronary occlusion. The PQRST isoarea maps after coronary occlusion showed a strong pole overlying the ischemic area on the cardiac surface in open-chest animals and over the left anterior thorax in closed-chest animals. The PQRST pole was positive during the first 1 to 2 hr of occlusion and became negative after several hours. The findings demonstrate that localized abnormalities due to ischemia and infarction are manifest in body and cardiac surface PQRST isoarea maps of both supraventricular complexes and right ventricular paced complexes. The findings suggest that PQRST isoarea maps may aid in identification and localization of ischemic or infarcted myocardium in the setting of abnormal activation such as left bundle branch block.     

New diagnostic evidence on the T wave map indicating involved coronary artery in patients with angina pectoris

To define the clinical significance of T wave map changes in patients with angina at rest, body surface isopotential T distributions were obtained in 48 patients with single-vessel disease (left anterior descending artery, 34; right coronary artery, eight; left circumflex artery, six) documented angiographically and were compared with those in 120 healthy subjects and those in 19 patients with left ventricular overload whose electrocardiograms showed negative T waves accompanied by an increase in R wave amplitude in left precordial leads. The T wave map abnormalities were observed in 24 of 48 patients (50%) with angina and were classified into three types: (1) type I (18 patients, 37.5%) was characterized by a segmental negative potential in the positive area located at the left thorax and the minimum at the peak of T wave positioned in the upper portion of the left anterior chest, (2) type II (three patients, 6.3%) was characterized by a negative potential with a minimum in the inferior thorax and an indentation of negative potential at the lower margin of the positive potential located over the upper thorax, and (3) type III (three patients, 6.3%) was characterized by a negative potential with a minimum at the back throughout the period of T wave. All patients showing T wave map abnormalities of type I had a significant stenosis of the left anterior descending artery. Likewise, all patients with type II or III had single-vessel disease of the right coronary or left circumflex artery, respectively. All types of T wave map changes observed in patients with angina were different from those in patients with left ventricular overload, whose maps showed the generalized negative potential at the inferior thorax and the left back and the minima clustered at the precordium. In seven patients with lesions of the left anterior descending artery, T wave map abnormalities of type I recovered to normal after successful percutaneous transluminal coronary angioplasty. The behavior of the negative potential and its extrema on the T wave map, which was not available from routine electrocardiography, was indicative of the involved coronary artery and probably of its associated ischemic area in one-half of our patients with angina pectoris.     

Body surface mapping of high-frequency components in the terminal portion during QRS complex for the prediction of ventricular tachycardia in patients with previous myocardial infarction

To study the clinical significance of terminal QRS high-frequency components for the prediction of ventricular tachycardia, an 87-lead body surface signal-averaged mapping was performed in 21 healthy subjects (control) and in 41 patients with previous myocardial infarction (anterior, 20; inferior, 21). Mapping data were analyzed and averaged (129.7 +/- 26.5 beats) for 160 seconds, and the signal-averaged beat was filtered with a bidirectional bandwidth (80-250 Hz) digital filter. J-point was determined from the 87-lead RMS voltage of nonfiltered QRS. For each lead, we calculated the sum of the absolute value of filtered QRS from 20 msec ahead of the J-point to the J-point (A-20). The body surface distribution of A-20 was expressed as A-20 map. The maxima in A-20 maps were mainly located on the upper sternal region in healthy subjects, on the left anterior chest in patients with previous anterior myocardial infarction, and on the central anterior chest in patients with previous inferior myocardial infarction. In the patients in both the group with anterior myocardial infarction and the group with inferior myocardial infarction, the value of maximum was significantly greater than in the subjects in the control group (0.181 +/- 0.086 and 0.138 +/- 0.048, respectively, vs. 0.075 +/- 0.031 mV.msec; p less than 0.01). In patients with myocardial infarction (n = 41), the value of maximum was significantly greater with ventricular tachycardia (n = 11) than without ventricular tachycardia (n = 30) (0.240 +/- 0.076 vs. 0.130 +/- 0.043 mV.msec; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

The isopotential mapping of the T wave in myocardial infarction

The isopotential mapping of the T wave in myocardial infarction was studied to find the characteristic abnormality. The negative area on the mapping at the deepest point of the negative T wave was located on the left precordial region or on the left precordial and lateral regions in cases with anterior or anterolateral infarction. In some cases with anterolateral or inferior infarction and in cases with high posterior infarction, an extensive negative area was found on the left back region. In cases with inferior infarction, the negative area was situated on the lower area of the precordial region and/or back region.The ischemic area (the area of the abnormal repolarization) was determined by studying the relation of the zero line of the maps in normal subjects and cases with myocardial infarction. Finally, a comparison between the direction of the maximum T vector and the location of the ischemic area was made.     

Interpretation of the body surface isopotential maps of patients with right bundle branch block. Determination of the region of the delayed activation within the right ventricle

Body surface isopotential maps were produced by computer processing of the 85 electrocardiograms obtained from the entire thorax of 28 patients with complete or incomplete right bundle branch block (RBBB). We divided the map patterns into the following 3 groups. Type I map pattern (10 cases): at the early stage of QRS, the maximum was located in the left chest. It shifted to the left from the normal position; at the instant of 44 msec, on the average, after the onset of QRS breakthrough minimum appeared over the left chest. Its appearance was delayed and its site shifted to the left as compared with the normal; at the late stage, the positive zone covered extensively the right chest and the right back; terminally, the maximum was positioned along the right parasternum. Type II map pattern (13 cases): at the early stage of QRS, the maximum was in the left chest as in Type I; breakthrough minimum appeared at 38 msec on the average, later than in the normal, but the site of breakthrough minimum varied from the left chest as in Type I to the midsternal region as in the normal; at the late stage, the positive zone covered the upper part of the right chest and the right back, less extensively than in Type I; the terminal maximum was in the upper sternal region. Type III map pattern (5 cases): the map pattern passed normally until the late stage, but thereafter a small positive zone survived over the upper sternal region. In Type I the delayed activation was presumed to occur all over the right ventricle, in Type II mainly over the smaller area of the right anterior free wall, and in Type III over the localized area of the outflow tract. Patients with complete RBBB showed Type I pattern. Patients with incomplete RBBB showed Type II or Type III pattern, although electrocardiograms failed to differentiate Type II patients from Type III patients. These findings suggest that the electrocardiographic pattern of incomplete RBBB probably arises from the various mechanisms.     

Residual myocardial jeopardy in patients with Q-wave and non-Q-wave infarctions

The correlation between the presence of areas of jeopardized myocardium and the electrocardiographic patterns of anterior and inferior Q-wave and non-Q-wave infarctions was studied in 486 patients who had had stable symptoms for at least six months after a single myocardial infarction. Myocardial jeopardy was identified on a ventriculogram in the right anterior oblique position if normal or hypokinetic wall motion was seen in all segments distal to a lesion that caused stenosis of greater than 50% and less than 100% in the proximal or mid left anterior descending coronary artery (anterior jeopardy), or in the proximal or mid right coronary artery or proximal circumflex coronary artery in a left dominant circulation (inferior jeopardy). Patients with non-Q-wave anterior infarctions had a significant increase in the frequency of jeopardized myocardium when compared with patients with Q-wave inferior or anterior infarctions. The group with non-Q-wave anterior infarction also had a significantly lower percentage of myocardial segments with absent wall motion in the area of infarction than all other groups. This combination of coronary narrowing with retained wall motion may contribute to the increased frequency of reinfarction seen in some studies of non-Q-wave infarction.     

Residual myocardial jeopardy in patients with Q-wave and non-Q-wave infarctions.

The correlation between the presence of areas of jeopardized myocardium and the electrocardiographic patterns of anterior and inferior Q-wave and non-Q-wave infarctions was studied in 486 patients who had had stable symptoms for at least six months after a single myocardial infarction. Myocardial jeopardy was identified on a ventriculogram in the right anterior oblique position if normal or hypokinetic wall motion was seen in all segments distal to a lesion that caused stenosis of greater than 50% and less than 100% in the proximal or mid left anterior descending coronary artery (anterior jeopardy), or in the proximal or mid right coronary artery or proximal circumflex coronary artery in a left dominant circulation (inferior jeopardy). Patients with non-Q-wave anterior infarctions had a significant increase in the frequency of jeopardized myocardium when compared with patients with Q-wave inferior or anterior infarctions. The group with non-Q-wave anterior infarction also had a significantly lower percentage of myocardial segments with absent wall motion in the area of infarction than all other groups. This combination of coronary narrowing with retained wall motion may contribute to the increased frequency of reinfarction seen in some studies of non-Q-wave infarction.     

Tritiated digoxin. XX. Tissue distribution in experimental myocardial infarction

The role and potential hazards of digitalis glycoside administration in acute myocardial infarction remain controversial. We investigated the concentration of tritiated digoxin in normal, ischemic, and infarcted left ventricular myocardium of the dog after ligation of the anterior interventricular coronary artery. The normal homogeneous distribution of tritiated digoxin in the normal canine left ventricle was altered following acute myocardial infarction. The ischemic and infarcted zones exhibited a marked diminution in digoxin concentration. Oxidative phosphorylation determinations confirmed tissue hypoxia in the infarcted zone. The gradient of digoxin concentration between normal, ischemic, and infarcted zones of myocardium may potentiate the development of an arrhythmia in the electrically unstable infarcted myocardium.