A new, precise definition of acute myocardial infarction

Cleveland Clinic Journal of Medicine. 2009 March;76(3):159-166 | 10.3949/ccjm.75a.08092

March 1, 2009|Cleveland Clinic Journal of Medicine

Shaun Senter, MD, MS;Gary S. Francis, MD

ABSTRACTSeveral international cardiovascular societies have revised their diagnostic criteria for acute myocardial infarction (MI) (J Am Coll Cardiol 2007; 50:2173–2188). The cornerstone of diagnosis remains a high level of clinical suspicion, serial electrocardiograms, and troponin levels. This article reviews the new definition and the appropriate clinical tools necessary to diagnose acute MI accurately.

KEY POINTS

The clinical presentation of acute MI varies considerably from patient to patient. Therefore, one must consider the symptoms, serial electrocardiographic findings, and serial biomarker results in concert.
Troponin I or T is now the preferred biomarker of myocardial necrosis. Still, troponin can be elevated in many conditions other than ischemic heart disease.
Electrocardiographic signs of acute ischemia have been precisely defined, but electrocardiography can give false-positive or false-negative results in a number of conditions.
MI is now categorized into five types depending on cause.

CLINICAL FEATURES VARY WIDELY

Sir William Osler said, “Variability is the law of life, and as no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions which we know as disease.”⁸

Just so, patients with acute MI display a wide variety of presentations, from no symptoms (about 25%) to severe, crushing chest pain. Discomfort may occur in the upper back, neck, jaw, teeth, arms, wrist, and epigastrium. Shortness of breath, diaphoresis, nausea, vomiting, and even syncope may occur. Unlike in acute aortic dissection, the discomfort is not usually maximal at its onset: it builds up in a crescendo manner. It is not usually changed by position, but can lessen in intensity upon standing. The discomfort in the chest is deep and visceral, and typically not well localized. A pressure sensation, air hunger, or “gas buildup” can be described. The only symptom may be shortness of breath or severe diaphoresis. The symptoms can last from minutes to hours and can be relieved by sublingual nitroglycerin. Atypical or less-prominent symptoms may make the diagnosis more difficult in the elderly, patients with diabetes mellitus, and women.

The physical examination during acute MI usually finds no clear-cut distinguishing features. The patient may appear pale and diaphoretic, and the skin cool to the touch. Heart sounds are generally soft. A fourth heart sound may be audible. Blood pressure may be low, but it can vary widely. Tachycardia, particularly sinus tachycardia, and pulmonary edema are poor prognostic signs.

In view of the wide variation in presentations, the history and physical findings can raise the suspicion of acute MI, but sequential electrocardiograms and measurements of biomarkers (troponin) are always necessary.

ELECTROCARDIOGRAPHY: NECESSARY BUT NOT SUFFICIENT

Figure 1. Acute pericarditis with elevation of the ST segment in all leads, often up-sloping (red arrows), and PR depression in all leads (blue arrows), except for PR elevation in aVR (black arrow).

Electrocardiography is a key part of the diagnostic evaluation of suspected acute MI. As in the 2000 paper, the 2007 update reiterates the same classic changes that may be seen on an electrocardiogram. It should be ordered and reviewed promptly as soon as the diagnosis is suspected, and repeated frequently if the initial tracing is normal.

Although electrocardiography is necessary, it cannot distinguish myocardial ischemia from MI. In addition, electrocardiography alone cannot reliably be used to diagnose acute MI, as many conditions result in deviation of ST segments and may be misinterpreted as acute MI. Common examples include acute pericarditis (Figure 1), early repolarization, hyperkalemia, left ventricular hypertrophy, and bundle branch block.⁹

ST-elevation MI vs non-ST-elevation MI

Figure 2. Anterolateral ST-elevation MI with ST elevation in V1 through V3 indicating infarction of the anteroseptal myocardium (red arrows), and in V4 through V6 and I and aVL indicating lateral wall involvement (blue arrows). Note the reciprocal ST depression in inferior leads, ie, III and aVF (black arrows).

Cases of acute myocardial ischemia and acute MI are traditionally divided by electrocardiography (Table 2) into those in which the ST segment is elevated (Figure 2) and those in which it is not (Figure 3). This dichotomy is useful clinically, as patients with ST-elevation MI are usually taken directly to the catheterization laboratory or given fibrinolytic therapy if they have no contraindications to it, whereas those with non-ST-elevation MI are brought to the catheterization laboratory less urgently, depending on various associated risk scores.

Changes in the ST segment can be very dynamic, making sequential tracings very useful. Rhythm disturbances and heart block are also more likely to be recorded when using sequential readings.

Pitfalls to electrocardiographic diagnosis

Figure 3A. Poor R wave progression (red arrows) with terminally symmetric T waves in leads V1 through V6 (blue arrows), which suggests possible myocardial injury; this patient had positive troponin consistent with non-ST-elevation MI.

Figure 3B. ST depression across the precordium (V1–V6) suggestive of subendocardial injury (black arrows). An electrocardiogram 12 minutes later showed normalization of these changes; however, cardiac troponin was positive and consistent with non-ST-elevation MI.

The electrocardiographic diagnosis of acute MI can be very straightforward or quite subtle, and many pitfalls can confound the correct diagnosis (Table 3). When the diagnosis is in doubt, frequent sequential readings are very useful.

Prior MI. Q waves or QS complexes, when the Q wave is sufficiently wide (≥ 0.03 msec) or deep (≥ 1 mV), usually indicate a previous MI. However, many nuances that further raise or lower the suspicion for previous MI need to be considered. These are beyond the scope of this brief review but are available in the 2007 update.

Posterior MI (or inferobasal MI) is more difficult to identify than anterior MI and is frequently missed on electrocardiography due to the absence of ST elevation on 12-lead readings. Changes on electrocardiography that raise the suspicion of posterior MI are prominent R waves in V₂ with accompanying ST-T depression. Patients with posterior MI are less likely to be taken directly to the catheterization laboratory unless ST elevations are seen due to concomitant infarction involving the inferior (Figure 4) or lateral (Figure 5) wall, or unless there is high suspicion for myocardial injury based on cardiac enzymes and information from the history and physical examination.

Right ventricular infarction often requires the use of right-sided leads, which may reveal ST elevation in V₄R.

ECHOCARDIOGRAPHY IF THE DIAGNOSIS IS IN DOUBT

Figure 4. Inferoposterior ST-elevation MI with ST elevation in II, III, and aVF (red arrows) indicating injury in the inferior wall in addition to possible involvement of the posterior wall, as suggested by tall R waves (black arrows) with ST depression and T wave inversions (blue arrows) in V1 and V2.

Figure 5. Inferolateral ST-elevation MI with ST elevation in II, III, and aVF (red arrows) indicating injury in the inferior wall in addition to ST elevation in V4 through V6 (blue arrows).

In many cases, acute MI is suspected on clinical grounds but electrocardiography does not verify an acute process. Troponin levels may not have had time to rise very much, if at all, or the results may not yet be known. Decisions to go to the catheterization laboratory or to do a computed tomographic scan of the chest to exclude aortic dissection must be made quickly.

Echocardiography is an excellent way to assess wall-motion abnormalities. In the absence of any wall-motion abnormality, a large ST-elevation MI is unlikely. A large wall-motion abnormality would verify the probability of ongoing acute MI and thus would help with rapid decision-making.

Furthermore, echocardiography can help determine the likelihood that the patient has aortic dissection or pulmonary embolism, either of which can mimic acute MI but requires very different treatment.

References

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