Apical Infarction Research Articles

The Predictive Accuracy of the Electrocardiogram in Identifying the Presence and Location of Myocardial Infarction and Coronary Artery Disease

In summary, the electrocardiogram is limited in its ability to detect a myocardial infarction. Its sensitivity is compromised seriously by a substantial number of patients (table; see text) with non-Q wave infarction or regression of Q waves. Once a Q wave occurs, the predictive accuracy of those changes, in delineating the location of the infarction, is quite high. The ability of Q waves or ST segment elevation to predict or identify the "culprit artery" is less strong, primarily due to the variation in coronary anatomy commonly found. The relationship between anterior or inferior lead changes and anterior or inferior myocardial damage is close. However, lateral lead changes may more accurately represent anterolateral (I, AVL) or apical (V5-V6) infarction. Tall R waves in anterior precordial leads is most often associated with posterolateral infarction.

Noninvasive evaluation of mid-left ventricular obstruction by two-dimensional and Doppler echocardiography and color flow Doppler echocardiography

Three patients with midventricular obstruction resulting from three different pathophysiologic mechanisms and differing anatomic bases for the development of obstruction are presented. In the first patient, a membrane-like structure appeared to cause some fixed obstruction, but a superimposed dynamic component to the obstruction was also evident. Papillary muscle hypertrophy with approximation of the papillary muscles during systole was the mechanism in the second patient. In the third patient, apical infarction with hyperdynamic contraction of the midand basal portions of the myocardium appeared to be the pathophysiologic mechanism. Color flow Doppler echocardiography was particularly useful in localizing the site of obstruction and allowed further evaluations by pulsed and continuous-wave Doppler techniques to precisely determine pressure gradients.

Indium-111 platelet scintigraphy and two-dimensional echocardiography for detection of left ventricular thrombus: Influence of clot size and age

Two-dimensional echocardiography and indium-111 platelet scintigraphy were performed on 50 dogs to determine the influence of clot age and size on the detection of experimentally induced left ventricular mural thrombus. Thrombus was induced by apical infarction and injection of a sclerosing agent and thrombin. The animals were classified into four groups according to the time of indium-111 platelet injection after thrombus induction: Group I (17 dogs, 1/2 hour after induction; 3 dogs, before induction), Group II (12 dogs, 24 hours after induction) and Group III (12 dogs, 1 week after induction). In Group IV (six control dogs) apical infarction was produced, but thrombin was not injected; indium-111 platelets were injected 1/2 to 1 hour after infarction. The dogs were studied by indium-111 platelet scintigraphy and by two-dimensional echocardiography 1/2 to 5 hours (Group I) and 1 to 5 and up to 72 hours (Groups II to IV) after platelet administration and before death was induced. Two-dimensional echocardiography showed the best overall sensitivity for detection of acute thrombus (97%; 29 of 30). The sensitivity of indium-111 platelet scintigraphy was 86% (18 of 21) for clots greater than or equal to 0.08 ml in size, and 67% (20 of 30) for detection of all clots. Thrombus did not form in 14 dogs of Groups I to III and in 6 of 6 control dogs. The specificity of scintigraphy was 100% (20 of 20) compared with 80% (16 of 20) for echocardiography. Echocardiography was more sensitive than scintigraphy for detecting very small clots in this experimental model.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnostic significance for coronary artery disease of abnormal Q waves in the “lateral” electrocardiographic leads

To determine the diagnostic significance for coronary artery disease of abnormally large Q waves in leads I, aVL, V 5 and V 6—the “lateral” electrocardiographic leads—the electrocardiograms of 240 patients who had undergone cardiac catheterization were studied. First, the electrocardiograms of 99 subjects proved normal by cardiac catheterization (group 1) were studied to determine the values of the durations of Q waves in leads I, aVL, V 5 and V 6 that should be exceeded to be considered abnormal. These values were 30, 30, 20 and 25 ms, respectively. Then, 67 patients were identified who had abnormal Q waves in at least 1 of these leads (group 2) and 74 patients with at least 1 angiographic abnormality but without abnormal Q waves in any of these leads (group 3). Group 2 had generally more extensive left ventricular disease and a higher prevalence of anterior, inferior and apical healed myocardial infarction (MI) than group 3. However, compared with group 3, group 2 had lower prevalences of significant narrowing of the coronary arteries that supply the left ventricular lateral wall. Within group 2, abnormal Q waves in leads I and aVL (traditionally designated high lateral MI) were associated with anterior as well as apical MI, and abnormal Q waves in leads V 5 and V 6 (traditionally designated anterolateral MI) were associated with inferior as well as apical MI. Thus, abnormal Q waves in leads I, aVL, V 5 and V 6 tend to reflect apical rather than lateral MI and the term anterolateral MI is especially misleading.

Detection of local abnormalities in ventricular activation sequence by body surface isochrone mapping in patients with previous myocardial infarction.

Body surface isochrone mapping was performed in 36 normal subjects and in 85 patients with previous myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously. For each lead, activation time was measured as the time from the onset of QRS to the peak of the R wave. The lead points where R waves were not observed were designated the "no R wave area" (NR area). Isochrone maps of normal subjects had a consistent pattern, with isochrone lines extending from the right upper anterior chest to the left anterior chest and then to the back. NR area was small and was located only on the right upper chest or the upper back. On the isochrone maps of patients with myocardial infarction, abnormal findings were observed; NR area was found in 26 of 28 patients with anterior infarction on the upper to middle anterior chest, in 13 of 22 patients with inferior infarction on the lower chest, and in 24 of 25 patients with anterior and inferior infarction on the upper to lower anterior chest. Activation time was delayed near the NR area (peri-NR area delay) in 37 patients. In patients with apical infarction, an islandlike zone of delayed activation was typically found on the left precordium. These abnormal patterns are considered to indicate local abnormalities in the activation of infarcted myocardium; the NR area indicates dead unexcitable scar, and the peri-NR area delay and islandlike zone of delayed activation indicate partially infarcted myocardium of slow activation. Patients with NR area had greater degree of left ventricular asynergy and lower ejection fraction than those without.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial infarction and stroke.

We used a computer data bank to evaluate 740 consecutive patients admitted to a cardiac care unit with myocardial infarction. Stroke occurred in 18 (2.4%) patients in the hospital; the anterior circulation was involved in 76% of strokes. Hospital mortality was 61% in patients with stroke and 13% in patients without stroke. Atrial arrhythmia was a significant (p less than or equal to 0.03) risk factor for stroke, but peak creatine kinase and ventricular arrhythmia were not. Cardiac pump failure, apical or anterior-lateral myocardial infarction, and history of previous stroke were associated with an increased risk of stroke. Clinical and pathologic data suggested an embolic etiology for most strokes that complicate acute myocardial infarction.

Insensitivity of the electrocardiogram in apical myocardial infarction

The ability of the standard ECG to identify myocardial infarction (MI) involving primarily the left ventricular (LV) apex is controversial. Therefore, the ECGs of 62 consecutive patients with acute infarction and isolated akinesia or dyskinesia of the LV apex on gated blood pool scintigraphy performed at rest 9 ± 4 days after MI, were reviewed. The following distribution of Q waves was found: none, 26%; inferior leads only, 23%; anterior leads only, 32%; inferior + 1 or more V leads, 13%; lead I and/or aVL + 1 or more V leads, 6%. Only 12 patients (19%) demonstrated one of the “combination” Q-wave patterns thought to indicate apical infarction. Although the 20 patients with a history of MI did not differ in age or ejection fraction from those with a first MI, the combination of inferior and anterior Q waves was present in 6 of them (30% ), vs only 2 of the remaining 42 patients (5%) (p < 0.02). The 24 patients with apical dyskinesia had a lower ejection fraction (36 ± 14 vs 48 ± 12, p < 0.001), a lower prevalence of isolated inferior Q waves (8 vs 32%, p < 0.05) and a greater prevalence of isolated anterior Q waves (46 vs 24%, p = 0.09) than those with akinesia. Thus, in patients with recent MI localized to the LV apex on radionuclide ventriculography, pathologic Q waves are commonly confined to the anterior or inferior leads or absent altogether. The insensitivity of the various proposed criteria for the electrocardiographic diagnosis of apical MI emphasizes the value of imaging techniques in detecting this common clinical entity.

The pathologic correlates of the electrocardiogram: complete left bundle branch block.

To assess whether gross pathologic differences exist between hearts with left bundle branch block (LBBB) and left-axis deviation (LAXD) and those with LBBB and a normal frontal plane axis, we examined 70 hearts with LBBB in a series of 1410 sequential dissections (5%). Thirty-two hearts had LAXD and 34 had normal axes on the correlative ECG. Left ventricular enlargement occurred frequently (93%). No significant differences were found in age distribution, left ventricular weight, coronary anatomy or infarct location. Quantitative analysis revealed larger inferoposterolateral and apical infarcts in hearts with LBBB and LAXD (p less than 0.01). The accuracy of various electrocardiographic signs of left ventricular enlargement and myocardial infarction in the presence of LBBB was assessed. Voltage criteria and QRS duration poorly define anatomic chamber enlargement. Anterior infarction is suggested by a q or pathological Q wave in lead I, a q wave in leads I, V5 and V6, or notched S waves in V3 or V4. Pathologic q waves or ST shifts in the inferior leads have high diagnostic specificity but low sensitivity for inferior infarction.

Regional assessment of myocardial metabolic integrity in vivo by positron-emission tomography with 11C-labeled palmitate.

To determine whether positron emission tomography (PET) after the combined administration of /sup 11/C-palmitate intravenously to image myocardium and /sup 11/CO by inhalation to image the cardiac blood pool with /sup 11/CO-hemoglobin provides quantitative delineation of the locus and extent of myocardial infarction, 28 patients with suspected myocardial infarction were studied. Twenty-one patients had electrocardiographically documented transmural infarction and in seven, the diagnosis of infarction was ultimately excluded based on enzymatic and electrocardiographic criteria. To assess reproducibility, four patients were studied on two occasions 1 month apart. Inferior and apical infarcts were readily localized with sagittal and coronal as opposed to transaxial reconstructions. Complete electrocardiographic and tomographic concordance was observed for the locus of all transmural infarcts. Reproducibility of tomographic estimates was within 10%. Tomographic estimation of the extent of infarction with /sup 11/C-palmitate in a subset of patients in whom right ventricular contributions to overall enzyme release could be excluded was facilitated by delineation of the endocardial border with the /sup 11/CO-hemoglobin cardiac blood pool image in the same plane. The correlaion between enzymatic (serial plasma MB-CK method) and tomographic estimates of infarct size was close (r = 0.92). Thus, as has been shown in experimental animals, PET withmore » /sup 11/C-palmitate permits quantification and localization of myocardial infarcts in patients.« less

The electrocardiographic diagnosis of apical infarction.

Summary Dyskinetic areas of the left ventriculograms of 151 patients were related to electrocardiographic signs of infarction. Apical dyskinesia alone or in combination with anterior or inferior dyskinesia could be associated with inferior and/or anterior infarction patterns. Appreciation of this fact prevents over-estimation of the severity of coronary artery disease from a resting electrocardiogram, showing both ‘anterior and inferior infarction’.

Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction: retrospective study of patients with typical anterior and posterior infarcts.

This retrospective study correlates electrocardiographic and histopathologic findings in 24 patients with single well-circumscribed infarcts to determine 1) whether ECG terms commonly used to describe the location of myocardial infarcts are significant, and 2) whether the extent of infarct can be determined using QRS characteristics. Transverse sections of the hearts were photographed. Based on histologic sections, the infarct was outlined on the photograph and each section was planimetered via a sonic digitizer into a computer that was programmed to divide the left ventricle into 8 radial sectors and also into basal, mesial, and apical thirds. The percentage of infarct in each of these areas was then calculated. Of the 24 hearts evaluated 12 had posterior infarcts and 12 had anterior infarcts. Posterior infarcts principally involved the basal and mesial levels, whereas the anterior infarcts were more extensive in the apical and mesial thirds, with relative or total sparing of the base. Posterior infarcts were associated with Q waves in leads II, III and aVF in 11 instances. The other posterior infarct was associated with markedly diminished R waves in leads II, III and aVf in the presence of a horizontal axis. All anterior infarcts were associated with Q waves or markedly diminished R waves in the right precordial leads. Eight of the anterior infarcts exhibited circumferential apical involvement and all eight were associated with Q waves or markedly diminished R waves in the left precordial leads. This study documents the electrocardiographic identification of anterior, posterior, and apical infarcts by correlation with pathologic anatomy.

Electrocardiogram in the normal rat and its alteration with experimental coronary occlusion.

A reliable and reprodueible method of recording rat electrocardiograms is described, including the use of precordial electrodes This system was utilized in studying 44 nor mal animals and in recording the electrical abnormalities associated with the ligation of the left coronary artery in 10 rats. The char acteristics of the normal electrocardiogram of the rat arc described. Following apical and anterior infarction, Q waves in associatioii with transitory R-wavc augmentation ap peared, with prolongation of the Q-T interval, electrical axis deviation, and inversion of the T wave. No abnormal conduction patterns were noted. The pathological lesions are described, and attention is called to the absence of mural intraventrienlar thrombosis despite transmnral infarction.

Anterior and posterior wall infarction of the heart: A statistical comparison based on autopsy findings

Statistical analysis of 514 cases of anterior and posterior wall infarcts of the heart reveals that the chief pathologic features of both types are similar. Anterior apical infarcts often extend to the adjacent endocardium and epicardium, and thus give rise to mural thrombus formation and pericarditis more frequently than do posterior basal ones. The differences in incidence of these complications in the two types of infarcts are great enough to be reasonably conclusive ones. Differences in incidence of other characteristics are also noted but these are not of sufficient magnitude to exclude the possibility of chance variation. Some of these unproved differences would be of clinical importance if they could be confirmed by other analyses. They will, therefore, be summarized briefly: (1) The ratio of anterior wall to posterior wall infarction may increase progressively with advancing age. (2) Acute posterior wall infarction may have a slightly higher mortality rate than acute anterior wall infarction despite the lower incidence of mural thrombosis and pericarditis in the former. (3) Superimposed new infarcts in areas of old infarction may be found more frequently in the anterior wall. (4) Anterior wall infarcts in men tend to be larger than posterior wall lesions; the reverse may be true in women. (5) Healed posterior wall infarcts in women may be more often clinically manifest than other healed infarcts. (6) Thrombi in the right ventricle and both auricular appendages, as well as in the left ventricle, may less frequently complicate posterior than anterior wall infarction. (7) Pre-existing hypertension may persist more frequently in acute posterior wall than in acute anterior wall infarction and may be a poor prognostic sign. (8) The coincidence of diabetes may be particularly high in fatal acute posterior wall infarction.

The Electrocardiogram in Myocardial Infarction : PART II. ANTERIOR INFARCTION

In the previous report, the author describeda generalisation of findings obtained by comparing the electrocardiographic patterns with the postmortem findings of 35 autopsied cases. In this communication, the findings in the unipolar precordial leads and in the standard and goldberger limb leads have been analyzed and correlated with the postmortem findings of 21 cases with anterior infarction in this series of 35 cases. Of 21 cases of anterior infarction, 2 had recently developed and 19 had healed infarctions at autopsy, nut in 9 of the latter group electrocardiograms were taken also during the acute stage. To avoid the errors derived from the difference of extent and location of infarction, the author divided the ventricular wall into the six portions, as shown in the previous communication, each infarction being precisely described according to the pathologic findings; for example, the infarction involved the anterior free wall and the anteroseptal portion of the left ventricle, and the half of the interventricular septum, or the infarction involved the anterior free wall and the lateral wall of the left ventricle etc. The correlation between the pathologic findings and the electrocardiographic patterns was discussed after analysis of these data was made. 1. In 15 cases, the infarctions involved the apical one-third to full length of the anterior free wall and the anteroseptal portion of the left ventricle, and the interventricular septum. In 14 of them, the electrocardiographic pattern showed an abnormal Q wave in one or more of Leads V_1 to V_4. In 9 of these 14 cases, an abnormal QS or QR(S) pattern accompanied by abnormal elevation of the RS-T segment was present in two or more leads of Lead V_1 through V_4. In addition 7 of these 9 cases showed an inversion of T wave at least in one of these leads in which the RS-T segment was found to be elevated abnormally. Another 2 cases of the 14 cases in which abnormal Q waves were noted, had right bundle branch block, characterized by the presence of an abnormal Q wave in place of the customary initial R wave, and the depression of RS-T segment and/or the inversion of T wave. In another 2 cases of them, the amplitude of the initial R wave in Leads V_1, V_2 and V_3 decreased as the electrode was moved from right to left, and finally an abnormal QS or QR complex was recorded in Lead V_4 or V_3. The electrocardiogram of the last case in this group displayed an abnormal elevation of the RS-T segment in Leads V_1, V_E, V_<3R> and V_<4R>, and occasionally displayed a qrS complex in Lead V_2. 2. In one case in which the infarct involved the subepicardial one-fourth to two-thirds of the anterior free wall and the subendocardial two-thirds of the anteroseptal portion of the left ventricle and the left side of the anterior small portion of the inter-ventricular septem, the amplitude of the initial R wave in Leads V_1, V_2 and V_3 showed abnormal decrease as the electrode was moved from right to left, and its QRS pattern was accompanied by the marked elevation of the RS-T segment and a inverted T wave. 3. Interpretation of the abnormal QS or QR pattern in Leads V_1 and V_2 in regards to the differentiation of myocardial infarction from non-infarction cases, was discussed in detail. In myocardial infarction, the abnormal Q wave in Leads V_1 and V_2 is indivative of the infarction of the interventricular septem, not of the infarction of the anterior wall. 4. In 2 cases of the infarction involving the free anterior wall and the anteroseptal portion of the left ventricle, and the interventricular septem, an abnormal qrS complex was recorded in Leads V_1, V_2 and V_3, or in V_2. 5. In an apical infarction, confined to the one-fifth of the anterior free wall and the anteroseptal portion of the left ventricle, and the interventricular septum, abnormal reduction of the initial R wave in Lead V_3 and a biphasic T wace in Lead V_4 were

III. Correlation of electrocardiographic and pathologic findings in anteroposterior infarction

III. Correlation of electrocardiographic and pathologic findings in anteroposterior infarction

Posterior basal cardiac infarction affecting a young man, followed a year later by anterior apical infarction

According to our search of the literature, 318 cases of coronary thrombosis among patients less than 41 years of age have been reported. If we were able to validate two additional cases reported in foreign journals, the total would be brought to 320. Our patient, whose case is here reported, suffered two attacks of coronary thrombosis. The first attack occurred at the age of 39 years, and resulted in infarction of the posterior basal portion of the left ventricle; the second occurred at the age of 40 years, and caused infarction of the anterior apical portion. The electrocardiograms depiet the accuracy with which this diagnostic aid may reflect the presence and the location of myocardial infarction.