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ECG in Multiple Myocardial Infarction and the Progression of Ischemic Heart Disease: New Criteria for Diagnosis of Concealed MI

John Boineau


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ECG in Multiple Myocardial Infarction and the Progression of Ischemic Heart Disease: New Criteria for Diagnosis of Concealed MI Retail Price: $90.00
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Product Information:
ISBN-13: 9780976400509
ISBN-10: 0976400502
Publisher: Cardiorhythms
Format: Softcover, 417 pages
Pub Date: 2004
Edition Number: 1




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Synopsis

The Concept (Brief Description)
This book presents a unique view of the ECG in ischemic heart disease. New criteria predict location of single and multiple MIs in ECGs without Q-waves, in IVCDs of ischemic cardiomyopathy, LBBB, V. pacing, in VPDs. Also precise criteria for diagnosis of LVH and to distinguish between left axis and fascicular block. The anatomic and electrophysiologic mechanisms of these complex ECGs and the bases of the novel criteria are illustrated.

The Concept (Full Details)
The ordinary 12-lead electrocardiogram contains a lot more information than is currently being used in clinical diagnosis. Although this is true for the ECG in general, it is especially true for patients with ischemic heart disease and myocardial infarction. It is estimated that more than 60% of infarcts actually present are undetected by the ECG using current criteria. There are several reasons for this disparity. One is that current criteria are poor, relatively insensitive, and based primarily on the presence of "significant" Q-waves. However, infarcts cause changes in the entire QRS complex, early, mid, and late, and also in STT. These less obvious non-Q changes go unnoticed. Another factor is that often patients have more than one Ml and a second opposing Ml alters the criteria (Q-waves) of the first Ml and vice versa. Presently, no criteria exist for these opposing MIs which can obscure the diagnostic Q-waves. A third factor is that LBBB or a nonspecific left ventricular conduction delay alters the sequence of AV conduction and eliminates the initial Q-wave evidence of an Ml. Finally, the basic anatomic and electrophysiologic mechanisms causing the abnormal QRS and STT in Ml have not been clearly identified and used to explain the abnormal ECGs. This is in sharp contrast to arrhythmia diagnosis, where the basic pathophysiologic substrates for each individual arrhythmia have been identified.

This book addresses the problem of how to identify the difficult to diagnose Ml by ECG using criteria not previously presented. It is focused on old healed infarcts (acute Ml will be covered in a later publication). Many new criteria have been developed to diagnose these infarcts. As many as 22 criteria are used to identify and locate single inferoposterior MIs. Many of these are totally new and used for the first time in this book. Criteria have also been developed to diagnose two opposing MIs in the absence of Q-waves. In addition, other criteria are used to identify Ml in the presence of LBBB, VPDs, and ventricular pacing. Finally, new criteria in addition to voltage are used to diagnose left ventricular hypertrophy by ECG more accurately.

All of these criteria evolved from anatomic and electrophysiologic (mapping) studies performed directly on the exposed heart in subjects with Ml, LVH, BBB, etc. In addition, these criteria were "tweaked" by daily correlations between ECG and anatomic data obtained from cardiac catheterization. These criteria have been combined into a scoring system of individual and weighted parameters which are summed to achieve a "diagnostic threshold" for predicting the number and sites of infarction.

Why is this important? Because of advances in the treatment of ischemic heart disease and its complications, patients are living longer and many experience repeated insults over a prolonged period of time. Each of these insults can affect the ECG because of a new and more complex distribution of infarction. Many physicians are aware of these changes, but often the ECG evidence of infarction becomes unrecognizable - the tracing looks abnormal but the basis for the abnormality is unclear. Also, one encounters ECGs in new patients which seem bizarre, QRS may be prolonged, the QRS axis is shifted, there are funny notches in the tracing, etc. The physician suspects or may even know that these patients have ischemic heart disease or a history of prior Ml but cannot recognize it in the tracing.

The purpose of this book is to introduce a new set of criteria, explain the pathophysiologic mechanisms for the complex ECG in ischemic heart disease, and explain how and why the criteria were derived. This information is useful for any physician taking care of patients with ischemic heart disease. It is especially relevant to physicians and cardiologists who follow patients long term or care for patients who have had multiple ischemic episodes or admissions for Ml, left ventricular dysfunction, congestive heart failure, and arrhythmias. The ECG is the least expensive first pass test the patient receives. If interpreted correctly, in many patients the ECG can be more useful than ultrasound in predicting the extent and distribution of infarction.

About the author:

Professor of Surgery, Medicine, and Biomedical Engineering, Washington University in St. Louis, School of Medicine

Dr. Boineau has broad interests in both basic and clinical cardiac electrophysiology. Since 1963, he has been involved in mapping to determine the mechanisms of abnormal and complex electrocardiograms in myocardial infarction, ischemic cardiomyopathy, hypertrophy, congenital heart disease, and various different cardiac arrhythmias.

In the 1960s, he initiated arrhythmia ablation surgery with Dr. Will Sealy and worked out many of the basic substrates for a variety of arrhythmias, including those associated with myocardial infarction, preexcitation syndromes, atrial flutter and fibrillation.

Later, with Drs. James Cox and Richard Schuessler and others, he developed procedures for ablating atrial fibrillation, including the Maze and Radial procedures, and postoperative atrial flutter in patients with congenital heart defects.




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