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Myocardial injury, ischemia, and infarction

 
 
Guideline Recommendations:
 
Threshold for ST-segment changes:
1. Men >40 y/o, abnormal J-point elevation is 2mm in leads V2 and V3, and 1mm in all other leads.
2.  Men <40y/o, abnormal J-point elevation is 2.5mm in leads V2 and V3
3.  Women, abnormal J-point elevation is 1.5mm in leads V2 and V3, and >1mm in all other leads
4.  Men and women, abnormal J-point elevation in V3R and V4R is 0.5mm
5.  Men and women, abnormal J point elevation is 0.5mm
6.  Men and women, threshold for abnormal J-point depression is 0.5mm in leads V2 and V3 and 1mm in all other leads.
 
Myocardial injury, ischemia, and infarction - Overview:

ECG definitions used in this guide:

  • Myocardial infarction: Pathologic changes in the QRS complex reflecting ventricular activation away from the area of infarction.
  • Myocardial injury: Injury always points outward from the surface that is injured. Epicardial injury: ST elevation in the distribution of the occluded artery, when viewing the epicardial surface of the ventricle. Endocardial injury: ST elevation in aVR (which views the endocardial surface of the ventricle) and produces reciprocal diffuse ST depression in the remaining leads.
  • Myocardial ischemia: Various definitions are used. The term commonly refers to diffuse ST segment depression, usually withassociated T wave inversion. It usually reflects subendocardial injury, reciprocal to ST elevation in lead aVR. Ischemia may also may refer to only inverted T waves with a symmetric, sharp nadir.
  • Reciprocal changes: Passive electrical reflections of a primary event viewed from either the other side of the heart, as in epicardial injury, or the other side of the ventricular wall, as in subendocardial injury.

Pathophysiology of acute myocardial infarction:
There is acute occlusion of a coronary artery by thrombus. In 7.5% of cases, there is vasospasm or abnormal thrombogenesis. The earliest signs of acute MI are manifested as myocardial injury.

Major steps in the diagnosis of myocardial infarction:
Below is a systematic method for the diagnosis of myocardial injury and/or infarction, arranged in seven steps. Following the steps will achieve the diagnosis in most cases.


Steps 1 & 2 - Identifying myocardial injury and defining the involved cardiac areas:

The six primary areas supplied by the major coronary arteries:
The GUSTO study enrolled patients with ST segment elevation in two contiguous leads and defined four affected areas as follows:

Area of ST segment elevation
Leads defining this area
Anterior
V1-4
Apical
V5-6
Lateral
I, aVL
Inferior
II, III, aVF

Additional primary areas not included in the GUSTO study:
Two other major areas of possible injury or infarction were not included in the GUSTO categorization above, because they do not produce ST elevation in two contiguous standard leads. These were:

  1. Posterior: The most commonly used sign of posterior injury is ST depression in leads V1-3, but posterior injury may best be diagnosed by obtaining posterior leads V7, V8 and V9.
  2. Right ventricle: The most sensitive sign of RV injury, ST segment elevation > 1 mm, is found in lead V4R. A very specific, but insensitive, sign of RV injury and/or infarction is ST elevation in V1, with concomitant ST segment depression in V2 in the setting of ST elevation in the inferior leads. This reflects the confounding effects of RV injury on lead V t in a person with posterior injury.
Step 3: Identifying the primary area of involvement and the culprit artery:

Primary anterior area:
ST elevation in two contiguous leads V 1-4 defines a primary anterior area of involvement. The LAD is the culprit artery. Areas contiguous to anterior (V t-4) include lateral (I & aVL) and apical (V5 & V6). ST elevation in these leads suggests more myocardium at risk and conveys more adverse outcomes.

Primary inferior area:
ST segment elevation in two contiguous leads (II, aVF or III) defines a primary inferior area of involvement and a probable RCA lesion. Areas contiguous to inferior (I1, aVF & III) include apical (V5 & V6), posterior (V1-3 or V7-9) and right ventricular (V4R). ST elevation in these contiguous leads suggests more myocardium at risk and conveys more adverse outcomes.

Identification of the culprit artery:
Prediction of the culprit artery involved in the acute infarction can be determined by extrapolating results of data in the table below, taken from a subset of 2,128 patients enrolled in the GUSTO study.

Location of ST segment elevation
(2 contiguous leads)
Total
(N)
LAD
(%)
RCA
(%)
LCx
(%)
Anterior ONLY
341
97.9
0.9
1.2
Ant + Ap ONLY
143
98.6
0.7
0.7
Ant + Lat ONLY
118
97.5
0.8
1.7
Ant + Ap + Lat
173
99.4
0.6
0.0
Ant + Inf + Ap
28
78.6
21.4
0.0
Ant + Inf + Ap + Lat
8
100.0
0.0
0.0
Ant+ Inf ONLY
34
47.1
52.9
0.0
Inferior ONLY
897
0.7
85.7
13.6
Inf + Ap ONLY
302
2.3
64.6
33.1
Inf + Lat ONLY
11
0.0
63.6
36.4
Apical ONLY
8
25.0
62.5
12.5
Lateral ONLY
30
63.3
0.0
36.7
Ap + Lat ONLY
24
41.7
0.0
58.3
Inf + Ap + Lat
11
18.2
9.1
72.7

Therefore, patients with ST segment elevation in any 2 contiguous leads V 1-4, either alone or with associated changes in leads V5-6 and/or I and aVL, had LAD obstruction in 98.3%. In patients with ST segment elevation only in leads II, aVF and III, there was RCA obstruction in 85.7%.

The anatomy of the coronary arteries:
The following diagram, adapted from Selvester's chapter in MacFarlane and Veitch Lawrie, shows a Mercator projection of the arteries to the left ventricle. Section A includes the septal branches of the left anterior descending (LAD) coronary artery; Section B includes the diagonal branches of the LAD; Section C includes the branches of the circumflex coronary artery and Section D includes the branches of the right coronary artery supplying the LV. Curved bold lines identify the distribution of each artery.

PRIMARY ANTERIOR PROCESS: acute occlusion of the LAD coronary artery, producing changes in the anterior leads (V1-4).

Earliest findings of occlusion:

  • "Hyperacute" changes: (may not be seen in the E.D. setting)
    ST elevation (injury) with loss of normal ST segment concavity, commonly with tall peaked T waves.

  • Acute injury: ST elevation
    The ST segment commonly appears as though a thumb has been pushed up into it. 

Evolutionary changes of anterior infarction:

  • Development of pathologic Q waves (infarction): Pathologic Q waves may occur within the first hour after symptom onset in at least 30% of patients.

  • ST segment elevation decreases. T wave inversion, usually occurs, in the 2nd 24 hour period of the infarction.

  • Fully evolved pattern: pathologic Q waves, rounded upward ST segment, inverted T waves.

A patient who presents to the E.D. with cardiac-type chest pain who hag T wave inversion in. leads with pathologic Q waves is most likely in the evolutionary or completed phase of infarct.

Successful revascularization usually causes prompt resolution of the acute signs of injury or infarction and results in the ECG signs of a Fully evolved infarction.

PRIMARY INFERIOR PROCESS: usually acute occlusion of the right coronary artery, producing changes in the inferior leads (II, aVF & III)

  • Earliest findings:
    Acute injury: (ST segment elevation) The J point may "climb up the back" of the R wave (a), or the ST segment may rise up into the T wave (b).

  • Evolutionary changes:
    ST segment elevation decreases and pathologic Q waves develop. T wave inversion may occur int he 1st 12 hours of an infeior MI, in contrast to that in anterior MI.

  • Right ventricular involvement:
    There is ST segment elevation, best seen in lead V4R, either with or without a QS complex signifying infarction.

  • Normal morphology of the QRS complex in lead V4R:
    The normal morphology of the QRS complex in lead V4R is shown below. The normal J point averages + 0.2 mm.

Identification of the culprit artery in patients with inferior injury based upon the QRS-ST-T morphology in lead V4R:
Bract studied patients with ST segment elevation in leads II, aVF, & III, all of whom had an acute MI. They determined the culprit artery and site of occlusion and related the ECG waveforms to the anatomy, as follows, with the performances cited.

POSTERIOR INJURY OR INFARCTION: commonly due to acute occlusion of the left circumflex coronary artery, producing changes in the posterior leads (V7, V8, V9), or reciprocal ST segment depression in leads V1-3.

  • Acute patterns: ST segment depression in V1-3, and possibly also V4, usually with upright, often prominent T waves.

  • Chronic pattern: Pathologic R waves with prominent tall T waves in leads V1-3.

Indications for obtaining posterior chest ECG leads
Whenever a patient presents with cardiac pain and only ST depression on the standard 12-lead ECG, especially in leads V 1-4, you should obtain posterior leads V7-9. These may reveal ST segment elevation reflective of an occluded artery, for which the treatment is relief of the occlusion. Diffuse ST segment depression due to subendocardial injury, shown below, will not produce ST segment elevation in� the, posterior leads, but will show the expected ST segment depression.

Placement of the posterior lead electrodes:
All electrodes are on the same horizontal plane as lead V4: Place V7 at the posterior axillary line, V8 under the scapular tip, and V9 in the left paraspinous recess.

Normal QRS morphology in the posterior leads (V8 illustrated):
The normal morphology of V8 resembles that of lead V6, but its amplitude is diminished because of the attenuating effects of lung tissue. Examples of waveforms are shown below.

Subendocardial injury: As illustrated by a positive exercise stress test
Lead aVR is the only lead that consistently views the endocardial surface of the left ventricle. Subendocardial injury produces ST segment elevation in aVR. On initial inspection of the 12-lead ECG, however, the finding that one should notice is diffuse ST segment depression, a reciprocal change. Other conditions, namely LVH, digitalis and hypokalemia, may produce ST elevation in aVR but are not examples of subendocardial injury. One of the most potent causes of significant depression of the ST segment is acute anemia.

Pathophysiology of subendocardial injury:
Usually a transient supply-demand mismatch caused by elevated blood pressure and/or heart rate in a patient with a fixed coronary artery lesion. Clinical presentation: typical angina.

Reciprocal changes in the setting of acute MI:
A recent study of patients who had continuous ST segment monitoring in the setting of acute MI showed that in 66% of patients, there was ST depression in leads remote from the primary site of injury. With successful reperfusion, the ST depression resolved. This was felt to be a purely reciprocal change. In another 23% of patients, there were no reciprocal changes seen on the 12lead ECG. In another 11% of patients, when the ST segment elevation resolved, there was persistent ST segment depression in leads remote from the acute injury. In this latter group, the mortality was significantly increased, compared with the other two groups. These patients had more significant three-vessel disease, and had so-called "ischemia at a distance."


Step 4 - Identifying the location of the lesion within the artery:

Identifying the location of the lesion within the coronary artery is important for the purposes of risk stratification. Start by locating the primary area of myocardium involved.

Primary anterior process:
Aside from an acute occlusion of the left main coronary artery, occlusion of the proximal left anterior descending coronary artery conveys the greatest adverse outcomes. Four ECG signs indicate proximal LAD occlusion:

  1. ST elevation >1 mm in either lead I, aVL, or both
  2. New right bundle branch block
  3. New left anterior fascicular block
  4. New first degree A-V block

Primary inferior process:
Nearly 50% of patients with IMI will have distinguishing features that may produce complications or adverse outcomes unless successfully managed. These include:

  1. Precordial ST segment depression in V1-3, suggestive of concomitant posterior wall involvement
  2. Right ventricular injury or infarction, which identifies a proximal RCA lesion,
  3. A-V block, which conveys a greater amount of involved myocardium, and
  4. The sum of ST segment depression in leads V4-6 which exceeds that of the sum of ST segment depression in leads V1-3 (which suggests multivessel disease).
Step 5 - The ECG diagnosis of infarction:

The screening mantra for waves of infarction: a quick and simple method for learning the widths of pathologic Q or R waves.

The 12-lead ECG shown below contains numbers corresponding to pathologic widths for Q waves and R waves for selected leads.

One can memorize the criteria above by using a simple scheme whose numbers represent the durations of Q waves or R waves which, if present, denote a pathologic wave (Q or R). Begin with lead V 1 and repeat the numbers in the box below in the following order. The numbers increase from "any" to 50.

Any
Q wave in lead V1, for anterior MI
Any
Q wave in lead V2, for anterior MI
Any
Q wave in lead V3, for anterior MI
20
Q wave > 20 msec in lead V4, for anterior MI
30
Q wave > 20 msec in lead V5, for apical MI
30
Q wave > 20 msec in lead V6, for apical MI
30
Q wave > 30 msec in lead I, for lateral MI
30
Q wave > 30 msec in lead aVL, for lateral MI
30
Q wave > 30 msec in lead II, for inferior MI
30
Q wave > 30 msec in lead aVF, for inferior MI
R40
R wave > 40 msec in lead v1, for posterior MI
R50
R wave > 50 msec in lead v2, for posterior MI

Notice that leads III and aVR are not listed. This is because lead III may normally have Q waves that are both wide and deep and lead aVR may commonly have a wide Q wave.


Step 6 - Defining the age of an infarction:

An acute infarction manifests ST segment elevation in a lead with a pathologic Q wave. The T waves may be either upright or inverted.

An old or age Indeterminate infarction manifests a pathologic Q wave, with or without slight ST segment elevation or T wave abnormalities.

Step 7 - Combine all observations into a single ECG diagnosis:

There are two possibilities for the major ECG diagnosis: myocardial infarction or acute injury.

  • If there are no pathological changes in the QRS complex, diagnose acute injury of the affected segments, beginning with the primary area, followed by any contiguous areas.
  • If there are ECG criteria for infarction, based upon pathologic changes in the QRS complex, diagnose infarction, beginning with the primary area, followed by any contiguous areas, and state the age of the infarction.

Persistent ST segment elevation after acute MI
Persistent ST segment elevation > 1 mm after a myocardial infarction was a sign of dyskinetic wall motion in the area of infarct in 100% of patients in one echocardiographic study. One-half of these patients had echocardiographically defined aneurysm.

 

 

 

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