ECG Criteria for Myocardial Infarction

John E Madias

Mount Sinai School of Medicine/New York University and Cardiology Division, Elmhurst Medical Center,
Elmhurst, NY, USA

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1.  Background and Introduction to MI Session

Criteria for the diagnosis of myocardial infarction (MI) have been devised long time ago, and have been implemented in our practice and for contacting research.¹ The word "criteria" conjures up notions of stability, permanence and stolidity. Although criteria constitute an effort to systematize and classify, are not "written in stone", and often are surpassed as experience accumulates or new scientific insight emerges. Criteria are meant to be kept, if they continue to be useful in the ever changing scientific landscape, modified to accommodate new developments, or abandoned if necessary.² Ours is a discipline, which may on the one hand be considered old, since we recently celebrated its centennial. However on the other hand Electrocardiology is a young science, full of vitality and opportunities and creative energy. After all that's why we are here!

Recently we have witness a concerted effort to redefine "acute coronary syndromes".³ The American Heart Association, the American College of Cardiology, the European Society of Cardiology, and the British Cardiac Society held their meetings and issued guidelines according to which the acute ST-segment or Q-wave MI are now parts of the spectrum of "acute coronary syndromes". Also troponins (I or T) are now "enhanced" as specific biochemical markers, whose rise signifies myocardial necrosis, and consequently the diagnosis of acute MI can occasionally be made in the presence of normal or seemingly normal ECG. Consequently the prevalence of MI will rise "overnight" with implementation of these notions, and this will be a parallel of what happened to the prevalence of diabetes mellitus with the recent change of diagnostic for this condition criteria. The implications for such enhanced sensitivity in diagnosing MI is currently assimilated, implemented and discussed.³

In the spirit of this momentous times, and with the intention of reexamining the beliefs we hold and of proposing new ideas, we have organized this session entitled "ECG criteria for myocardial infarction". A cadre of outstanding thinkers and workers in the field has been assembled to enlighten us about the old, and awaken us about what is coming and what more can be done. Thus, and in the following sequence, Dr. Galen Wagner will be speaking about the ST-elevation/Q-wave anterior and inferior MI; Dr. Rory Childers will elaborate on the diagnosis of right ventricular MI; Dr. Peter Clemmensen will discuss the diagnostics of posterior/lateral/high lateral MI; Dr Ronald Selvester will clarify how we should be going about detecting MI when it is associated with intraventricular conduction delays, including RBBB, LBBB, and pacemaker-triggered ECG; and Dr. Bertil Lindahl, will delve in the characterization of the non ST-elevation/non-Q-wave MI/"acute coronary syndromes"/new guidelines on diagnostic criteria for MI.

In all these expositions an effort will be made to avoid redundancy, while differing viewpoints, new ideas and personal insights are encouraged, and controversy in the speakers' comments and the audience's responses is welcome. We all are going to try to keep redundancy to a minimum. However some overlap is unavoidable and even desirable particularly when material is presented from different points of view. Naturally accepted criteria of MI (hyperacute/acute/subacute/chronic), of the different locations from the old and recent literature will be outlined; also the speakers will offer their personal speculations about diagnosis, even if it is controversial, or it is the object of currently contacted research by others or themselves. The issues pertaining to links between thrombolysis or other pharmacological therapies, or percutaneous coronary interventions and particular types of acute MIs will be touched upon. The diagnostic corroboration of the presence, size and location of an MI offered by the employment of other "non-ECG" correlative modalities like autopsy, and imaging (echocardiographic/CT-scan/MRI/angiography) will be emphasized. Confirmation of an MI by all these modalities is important both in practice and research, for solidifying what we already know, and provide the impetus for new discoveries.

Daily experience in the hospital and office settings disclose the lamentably poor knowledge on "materia electrocardiographica" physicians display, particularly in environments with easy accessibility to so called "high tech" modalities, or without adequate exposure to ECG teaching and application. We, in this Society, should return from this Congress and be strong advocates in our working sites of a revitalization of the diagnostic role of the ECG.       

2.  Problematic MI Issues

For the sake of avoiding redundancy I will not refer here to any "core" material pertaining to the issue of criteria for MI. Instead I will mention some "peripheral" issues, to set the stage of what is going to follow, and even to possibly ignite some controversy or heated discussion about issues which may need revision or where we should be more specific. I should warn you that what follows includes more question marks than answers to the posed questions. Here is an outline of some of the problematic areas:

1) Reduction of the amplitude of ST-segment elevation is exclusively used when response to thrombolysis is being evaluated; there should be rekindling of interest in using early in the clinical course changes in the QRS complexes, drawing on experience derived from the era of "reduction of the MI size".

2) We need to do our best to bring into the "thrombolysis loop" as many patients as possible; some patients with posterior MI are often managed as such with "non ST-elevation" MI. If ST-elevation is thought to be an indispensable requirement for thrombolysis, should we make recording of V₇-V₉ mandatory?

3) In cases of posterior MI shouldn't we emphasize changes in lead V₂ instead of V₁ as per "Perloff's criteria",⁴ since the former is so insensitive? Dr Clemmensen will clarify this for us.

4) Since right chest leads for the diagnosis of right ventricular MI are occasionally inadvertently not done, we should try to popularize among physicians that larger ST-segment elevation in lead III than II points to right ventricular MI.⁵

5) How can one reconcile ideas about cancellation of generated depolarization fronts, with the "Selvester score" which attempts to diagnose MI involving many myocardial territories? What are the implications of recurrent MI with "normalization" of the ECG on the applicability of ECG scores for net MI size? Drs Wagner's and Selvester's view on this will be most appreciated.

6) An effort should be made to employ both in practice and research the concept of "quantitative ECG" (measurements in mm or mV of all parts of ECG curve).

7) There is a real need for corroborating all our statements about ECG diagnostics with information from non-ECG tests.

8) Designations of "inferior" or "posterior" MI are occasionally used interchangeably; also designations like "lateral" and "apical" are employed interchangeably. I hope that Dr. Clemmensen will elaborate on these.

9) Some confusion has arisen about the proper way of diagnosing an MI and/or administering thrombolysis in patients with LBBB: for some the mere presence of LBBB is enough, others try to establish whether LBBB is new (a frequently impossible task), and some look for the specific repolarization changes Dr. Selvester will talk about.⁶ A problem which some have encountered is the non-specificity of ST-elevation in leads V₁-V₃ in patients with LBBB, particularly in subjects with large S-waves in the same leads who may have enormous ST-segment elevation in the absence of an MI.

10) The non-reproducibility of serial ECGs is the norm in most clinical settings. Obtaining ECGs from stable chest landmarks is a prerequisite for making an accurate diagnosis of MI, particularly in the presence of LBBB;⁷ shouldn't marking of chest wall be compulsory?

11) Repeating the ECG at frequent time intervals on admission (every 20-30 min) may contribute to accurate detection of an MI or "acute coronary syndrome".

12) Current notions suggest that acute MI frequently occurs in association with normal ECGs; are these "troponin MIs" associated with really normal or "normal" ECGs. Dr. Lindahl will elaborate on this. Can we do something to enhance the sensitivity of the ECG in such situations?

13) Durations of time intervals are difficult to measure manually; and particularly this pertains to the differentiation between "pathological" and "non-pathological" Q-waves. Should we start relying on the automated ECG measurements for this?

14) There is no doubt that multi-lead recordings are more informative than the 12-lead ECG. Realistically however all we can hope of having is appropriately recorded 12-lead ECG. Thus we should use what we have in an innovative manner to generate new diagnostic insights for detection of MI. A case in point is the recent proposal that ST-segment depression in aVR (a lead often dubbed "useless" or "redundant") in patients with ST-segment elevation MI is seen more frequently in patients with inferior/posterior MI, and "points to a coronary artery with a large area of supply as the culprit vessel.⁸ 

15) Diagnosis of MI often is cumbersome in the presence of intraventricular conduction delays other than LBBB; left ventricular hypertrophy is often associated with impressive ST-segment elevation in V₁-V₃ leads and ST-segment depression in V₅ and V₆ leads. These areas require our scrutiny and our investigative probing.

16) We should work to employ the ECG as a prognostic tool following an acute MI. Also more research is needed on improving the role of ECG in diagnosing an old MI in association with ventricular aneurysm, intraventricular conduction abnormalities, or left ventricular hypertrophy.

These are some of the points, which along with others, will receive the attention of our expert panelists and the response of the audience, as the session on ECG criteria of MI gets under way.

References

1. World Health Organization. Working group on the establishment of ischemic heart disease registers. Report of the fifth working group. Copenhagen. In: Report No: Eur 8201 (5). Geneva: WHO, 1971.

2. Madias JE. Killip and Forrester classifications. Should they be abandoned, Kept, reevaluated or modified? Chest 2000; 117:1223-26.

3. Dargie H. Myocardial infarction: redefined or reinvented? Heart 2002;88:1-3.

4. Perloff JK. The recognition of strictly posterior myocardial infarction by conventional scalar electrocardiography. Circulation 1964; 30: 706-718.

5. Andersen HR, Nielsen D, Falk E. Right ventricular infarction: Diagnostic value of ST elevation in lead III exceeding that of lead II during infeior/posterior infarction with right-chest leads V3R to V7R. Am Heart J 1989;117:82-86.

6. Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, Califf RM, Wagner GS. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med 1996; 334:481-7. 

7. Madias JE. Serial ECG recordings via marked chest wall landmarks: An essential requirement for the diagnosis of myocardial infarction in the presence of left bundle branch block. J Electrocardiol 2002;35:299-302.

8. Senaratne M, Weerasinghe C, Smith G, Mooney D. Clinical utility of ST-segment depression in lead AVR in acute myocardial infarction. J Electrocardiol 2003;36:11-16.