The ECG demonstrated ST segment depression in leads V2 and V3. These findings when considered in conjunction with the physical examination were felt to represent an acute coronary event, either anterior wall ischemia or posterior wall ST segment elevation AMI.
The additional findings of upright T waves and prominent R waves in the same leads suggested posterior wall ST segment elevation AMI. A 15-lead ECG (Figure 2) was performed which revealed ST segment elevation in leads V8 and V9, consistent with an acute posterior wall ST segment elevation myocardial infarction. Unfractionated heparin was added to the patient's medical regimen while cardiology was consulted.
The patient was taken to the cardiac catheterization laboratory where a distal right coronary artery lesion (thrombus with near total occlusion) was noted. This lesion was successfully opened and subsequently stented. Ventriculography demonstrated posterior wall akinesis. Elevated troponin I values confirmed the diagnosis of AMI. The patient had an uneventful hospital course, and was discharged after five days.
Isolated Posterior Wall ST Segment Elevation AMI
Posterior wall myocardial infarction refers to infarction of the dorsal area of the left ventricle and, in most cases, pathophysiologically involves either the left circumflex or the right coronary artery with its posterior descending branches. As predicted from the coronary anatomy, posterior wall myocardial infarction most often occurs along with acute inferior or lateral myocardial infarction.
Acute posterior wall myocardial infarction has been reported to represent 15 to 21 percent of acute myocardial infarctions, the vast majority occurring with acute infarction of the inferior or lateral wall of the left ventricle.1–4 Isolated posterior wall myocardial infarction, however, does occur; the rate of isolated occurrence of posterior wall myocardial infarction is felt to be low.1,2,5 The additional-lead ECG using left posterior thorax leads has increased the reported rate of isolated posterior wall myocardial infarction occurrence from “very low” to a three to seven percent range among all patients with AMI.3,4
From the perspective of the standard 12-lead ECG, the “typical” electrocardiographic findings indicative of acute ST segment elevation myocardial infarction will be reversed. This reversal results from the fact that the endocardial surface of the posterior wall faces the anterior precordial leads (V1 through V3) in the standard 12-lead ECG. In other words, ST segment depression, prominent R waves, and upright T waves in leads V1 through V3 “when reversed” may represent ST segment elevation, Q waves, and T wave inversions, respectively, of acute posterior wall myocardial infarction (Figure 3). If one considers the “reverse nature” of these electrocardiographic abnormalities when applied to the posterior wall, the findings assume a more recognizable, ominous meaning.
Numerous electrocardiographic abnormalities (Figure 4) using the standard 12-lead ECG suggestive of acute posterior wall myocardial infarction have been reported, including various characteristics of the QRS complex (R and S waves), ST segment, and T wave.5,6–9 ST segment depression greater than 1 mm in leads V1 through V3 may indicate AMI of the posterior wall as noted above.
The presence of ST segment depression in the precordial leads, however, does not always indicate acute posterior wall myocardial infarction but rather reciprocal change. Mukharji et al8 explored this issue in acute inferior wall myocardial infarction. Of all patients with inferior AMI, 80 percent of cases demonstrated anterior ST segment depression in leads V1, V2, or V3.
By employing standard electrocardiographic criteria for the diagnosis of PMI, they noted that only one-third of these cases actually experienced acute posterior wall myocardial infarction. Using scintigraphic methods, the investigators noted that posterior infarction had occurred more frequently than they had expected using the standard 12-lead ECG. They demonstrated that approximately two-thirds of these patients actually had suffered a PMI.
Boden et al5 also noted that approximately 50 percent of patients presenting with chest pain or a chest pain equivalent complaint and demonstrating precordial ST segment depression on the 12-lead ECG were found to have had a PMI. In addition to the presence of ST segment depression in the right precordial leads, the actual morphology of the ST segment depression is an important feature to consider.
Boden et al6 noted that horizontal ST segment depression in the right precordial leads was encountered in 100 percent of patients experiencing posterior wall myocardial infarction as compared with patients with non-ST segment elevation AMI who presented with precordial ST segment depression described as down-sloping.
The T wave, the association of the T wave and the ST segment, the R wave, and co-existing infarctions are other electrocardiographic features indicative of acute posterior wall myocardial infarction. A tall, upright T wave in leads V1 or V2 is suggestive of acute posterior wall myocardial infarction.9
A combination of horizontal ST segment depression with tall, upright T waves in the right precordial leads is highly suggestive of acute posterior wall myocardial infarction.5 Various abnormalities of the R wave in leads V1 or V2 are reported to be other major electrocardiographic features associated with posterior wall myocardial infarction. A tall, wide R wave in leads V1 or V2 as well as an R/S wave ratio greater than 1.0 in lead V2 are suggestive findings.7
Certain authorities suggest that a prominent R wave in the right precordial leads when associated with posterior wall myocardial infarction may not represent simple, “reverse” change. Rather, they state that such QRS complex morphology may reflect intraventricular conduction disturbance resulting from the ischemic myocardial insult.10
Finally, coexistent acute infarction of either the inferior or lateral walls is another electrocardiographic feature that should raise the clinical suspicion for acute posterior wall myocardial infarction, particularly if ST segment depression and/or prominent R waves are observed in the right precordial leads. Acute inferior myocardial infarction with ST segment depression in the anterior leads V1, V2, and V3 represents coexisting acute posterior wall myocardial infarction in approximately half the cases encountered.5,8
Rapid recognition of acute posterior wall myocardial infarction is of clinical importance for several reasons. Patients with acute inferior or lateral wall myocardial infarction who also have posterior involvement are experiencing a larger-sized infarct. With increasing infarct size, the risk of arrhythmia, left ventricular dysfunction, and death are proportionally increased.
Secondly, the use of acute therapies including treatments aimed at urgent revascularization may benefit patients with acute inferoposterior myocardial infarction more than patients with an isolated infarct of a single wall of the left ventricle. And finally, isolated posterior wall myocardial infarction if not clinically recognized as an ST segment elevation AMI likely will not receive appropriate therapy including thrombolytic agent or urgent angioplasty.
The physician may employ additional-lead ECGs in select cases looking for involvement of the posterior wall in patients with co-existing inferior or lateral acute infarct. Alternatively, in a chest pain patient with a high clinical suspicion for AMI with only ST segment depression noted in the right precordial leads, the additional-lead ECG may reveal acute posterior wall myocardial infarction. The use of additional-lead ECGs among all adult chest pain patients encountered in the ED has not yielded therapeutic or diagnostic benefit.2
Unsuspected acute posterior wall myocardial infarction was not noted in this population, and therapeutic and disposition decisions were not altered. When considering a higher risk population, additional lead ECGs did affect the rate of diagnosis of posterior wall myocardial infarction.1 Greater than 1 mm ST segment elevation in the posterior leads, V8 and V9, confirms the presence of acute posterior wall myocardial infarction and are felt to be superior to the findings noted in leads V1 through V3.1,4,7 The National Heart Attack Alert Program Working Group suggests that the use of posterior thorax leads may assist the clinician in certain circumstances.11
1. Zalenski RJ, Cooke D, Rydman R, Sloan EP, Murphy DG: Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: The 15-lead ECG. Ann Emerg Med 1993;22:786–93.
2. Brady WJ, Hwang V, Sullivan R, et al: A Comparison of the 12-lead ECG to the 15-lead ECG in Emergency Department Chest Pain Patients: Impact on Diagnosis, Therapy, and Disposition. Am J Emerg Med 2000;18:239–43.
3. Pollack M, Thomason G, Williams M, et al: Emergency department diagnosis of acute posterior-wall myocardial infarction using left posterior chest leads. Acad Emerg Med 1997;34:399.
4. Melendez LJ, Jones DT, Salcedo JR: Usefulnesss of three additional electrocardiographic chest leads (V7, V8, and V9) in the diagnosis of acute myocardial infarction. Can Med Assoc J 1978;119:745–8.
5. Boden WE, Kleiger RE, Gibson RS, et al: Electrocardiographic evolution of posterior acute myocardial infarction: Importance of early precordial ST-segment depression. Am J Cardiol 1987;59:782.
6. Rich MW, Imburgia M, King TR, et al: Electrocardiographic diagnosis of remote posterior wall myocardial infarction using unipolar posterior lead V9. Chest 1989;96:489–93.
7. Aufderheide TP, Brady WJ: Electrocardiography in the patient with myocardial ischemia or infarction. In Gibler WB, Aufderheide TP (eds) Emergency Cardiac Care, Mosby-Year Book, Inc., St. Louis, MO, 1994.
8. Mukharji J, Murray S, Lewis SE, et al: Is anterior ST depression with acute transmural inferior infarction due to posterior infarction? A vectorcardiographic and scintigraphic study. J Am Col Cardiol 1984;4:28–34.
9. Eisenstein I, Sammarco ME, Madrid WL, Selvester RH: Electrocardiographic and vectorcardiographic diagnosis of posterior wall myocardial infarction. Significance of the T wave. Chest 1985;88:409–16.
10. Brembilla-Perrot B, De La Chaise AT, Issaz K, Pernot C: The tall R wave in lead V1 in posterior myocardial infarction: A reciprocal sign of a His-Purkinje conduction disturbance? Pacing Clin Electrophys 1989;10:1650–9.
11. Selker HP, Zalenski RJ, Antman EM, et al: An evaluation of the technologies for identifying acute cardiac ischemia in the emergency department: A report from the National Heart Attack Alert Program Working Group. Nonstandard ECG leads and body surface mapping. Ann Emerg Med 1997;29:28–33.
Children with Diabetes at Risk for Severe Complications
Some children remain at high risk for developing life-threatening complications from type 1 diabetes that researchers say can potentially be prevented, according to a study in the May 15 issue of the Journal of the American Medical Association.
Arleta Rewers, MD, PhD, of the University of Colorado School of Medicine and the Children's Hospital in Denver, and colleagues from the Barbara Davis Center for Childhood Diabetes, examined the incidence of acute complications of ketoacidosis levels leading to increased blood acidity, coma, and death) and severe hypoglycemia in children with diabetes to determine the risk factors that may predict those complications.
Both diabetic ketoacidosis (DKA) and severe hypoglycemia are theoretically preventable, the authors reported. “Diabetic ketoacidosis often leads to an emergency department visit and hospital admission, and contributes to the high costs of care for children with type 1 diabetes. Cerebral edema, a devastating complication of DKA, is one of the leading causes of mortality among children with type 1 diabetes,” the authors wrote.
For this study, a cohort of 1,243 patients (583 girls, 660 boys) with type 1 diabetes, treated at the Barbara Davis Center for Childhood Diabetes in Denver, were followed from Jan. 1, 1996 through Dec. 31, 2000 to measure acute complication events. All patients were younger than 20 years of age and resided in the Denver metropolitan area. The researchers defined acute events as DKA and/or severe hypoglycemia episodes leading to an emergency department visit or a hospital admission.
The researchers report there were 320 hospital admissions and/or emergency department visits due to DKA and 768 incidences of severe hypoglycemia events among this group of children. The overall incidence of DKA was eight per 100 patient-years (eight cases per 100 patients in one year). The annual incidence of severe hypoglycemia was 19 per 100 patient-years (19 cases per 100 patients in one year).
Adolescent girls were at the highest risk for DKA while severe hypoglycemia especially affected the youngest patients and boys of all ages. The authors state that 80 percent of complications occurred among 20 percent of children who had recurrent events.
“In this study, children with type 1 diabetes, while managed by a state-of-the-art multidisciplinary team, still experienced significant numbers of severe, potentially preventable complications,” the authors stated. Lack of insurance and the presence of psychiatric disorders (such as major depression, bipolar, anxiety or panic disorders) were significant predictors of severe diabetes complications. The authors wrote that major psychiatric disorders may result in missed insulin injections, missed meals, infrequent blood glucose testing, suicidal attempts, chaotic lifestyle, and lack of compliance.
“Acute complications in children with type 1 diabetes increase directly and indirectly the costs of care,” the authors reported. An estimated 150,000 type 1 diabetes patients are 20 years old or younger in the U.S., according to the authors.” The combined direct medical care charges for DKA and severe hypoglycemia in U.S. children with diabetes probably exceeded $100 million per year during the late 1990s,” the authors stated. That figure does not include indirect costs such as lost productivity and a diminished quality of life for those patients, the authors note. The authors suggested those costs could be reduced by providing interventions for the identified risk factors that can be modified.