Definition of acute myocardial infarction

A diagnosis of myocardial infarction is based on the following three components:

  • Troponins – mandatory
  • ECG
  • Symptoms


A diagnosis of myocardial infarction is made when elevated levels of troponins is verified and the patient displays either symptoms or ECG changes consistent with myocardial infarction/ischemia. Elevated troponin levels are mandatory. As for symptoms and ECG changes, only one of them is sufficient. Most patients will however display both symptoms and ECG changes.

Troponins and other biomarkers of myocardial necrosis

Myocardial cells may endure 20 to 30 minutes of complete ischemia. After this period the cells die and the cell membranes collapse whereby intracellular proteins leak into the circulation. It is possible to detect elevated levels of myocardial proteins in the blood within a few hours after onset of myocardial infarction. Elevated levels of myocardial proteins is evidence of myocardial necrosis. This is because there is no (or very little) turnover of myocardial cells and therefore myocardial proteins are usually not detected in blood (other than at very low levels).

Current immunoassays for detection of myocardial proteins are extremely sensitive. They may actually detect elevated levels of myocardial proteins after long distance run. Indeed, it is now possible to detect myocardial infarctions that are 100 times smaller than what was possible to detect in the year 2000. This implies that – among patients with acute coronary syndromes – many who would previously have been diagnosed with unstable angina pectoris are now diagnosed with myocardial infarction (interested readers are referred to E. Braunwald: Unstable angina: is it time for a requiem? Circulation, 2013).

North American (ACC, AHA) and European (ESC) guidelines recommend the use of cardiac specific troponin, which has almost 100% specificity for myocardial cells. There are three types of troponins: T, C and I. Conventional assays allow for detection of troponin T down to 0.005 ng/mL.


Reference limit for troponins

Troponin levels higher than the upper reference limit are considered to be elevated (abnormal) and thus indicate myocardial necrosis. The upper reference limit is currently the 99th percentile in a healthy population. Thus, a troponin level higher than the 99th percentile of a normal population is considered elevated.


Criteria for elevated troponins

A diagnosis of myocardial infarction requires at least two troponin analyses. One of these must be elevated and there should be a change between the two analyses; either an increase or a decrease in troponin levels between the two tests. A change in troponin levels between the two analyses is necessary to differentiate acutely elevated troponin levels (due to acute myocardial infarction) from chronically elevated troponin levels (e.g chronic kidney disease, which leads to diminished elimination of troponins from the blood).

In clinical practice it is conventional to draw the first analysis directly upon arrival to the hospital and then repeat the test after 6 to 8 hours. If the first two analyses are negative/inconclusive but the suspicion of infarction persists, a third test may be done after 12 to 24 hours. Besides troponins, it is possible to analyze CK-MB, total CK and MB, but these biomarkers have much lower specificity than cardiac troponins (CK-MB, CK and MB are abundant in skeletal muscle). Figure 1 shows how the blood levels of these proteins change during the course of myocardial infarction.


Figure 1. Levels of myocardial proteins in the circulation following myocardial infarction.

Figure 1. Levels of myocardial proteins in the circulation following myocardial infarction.


Specific cardiac biomarkers


Troponin T levels increase within 6 hours after onset of myocardial necrosis. Levels are normalized within 7 days (Figure 1). The slow normalization is due to slow ongoing leakage of troponin T from necrotic cells. A negative (i.e normal) troponin T 6 hours after the latest episode of symptoms rules out myocardial infarction with high certainty (it does not rule out unstable angina). Troponin levels (T, C or I) 16 to 24 hours after onset of symptoms may be used to estimate the size of the infarction.

Although cardiac troponins are highly specific to myocardial cells, elevated levels do not tell the cause of the elevation. Any condition that causes damage to myocardial cells will lead to elevated troponin levels. A common cause of steadily elevated troponin levels is chronic kidney disease. Individuals with reduced glomerular filtration rate will eliminate troponin slower, which leads to higher baseline levels of troponins. It is wise to analyze troponin I in patients with chronic kidney disease because troponin I is less affected by glomerular filtration. Nevertheless, even in individuals with chronic kidney disease it is possible to analyze any type of cardiac troponin because if the individual has suffered a myocardial infarction, the troponin levels will display dynamics (i.e change) between the two tests. There are many other causes of elevated troponin levels. A rather exhaustive list follows:

  • Myocardial infarction
  • Chronic and acute kidney failure
  • Cardiac contusion or trauma
  • Acute or chronic heart failure
  • Electrical cardioversion
  • Takotsubo cardiomyopathy
  • Pericarditis and myocarditis (perimyocarditis)
  • Ablation procedures
  • Supraventricular tachyarrhythmia
  • Ventricular tachyarrhythmia
  • Bradyarrhythmia
  • Stroke, subarachnoidal hemorrhage
  • Sepsis (septic shock)
  • Intoxication
  • Extreme physical exercise
  • Aortic dissection
  • Rhabdomyolysis with myocardial damage
  • Pulmonary embolism
  • Severe pulmonary hypertension
  • Amyloidosis
  • Burn injury
  • Severely ill patients

CK-MB and MB

CK-MB (Creatinin-Kinase MB) is the best alternative if troponin assays are not available. The upper reference limit (99th percentile) and decision process is identical to troponin. CK-MB is, however, less specific than troponin because it is abundant in skeletal muscle. CK-MB has two advantages over troponin: CK-MB is released into the circulation faster (may be detected earlier) and it is normalized earlier (which makes it useful for diagnosing re-infarctions). Refer to Figure 1.

MB (myoglobin) is even less specific but may be detected even earlier than CK-MB. Normal MB levels 3 to 4 hours after the last episode of symptoms rules out myocardial infarction.


ECG in ischemia and infarction

ECG in myocardial ischemia

Acute ischemia manifests on the ECG as ST deviation (ST segment elevation or depression) and T-wave changes. ST deviation and T-wave changes are collectively referred to as ST-T changes. ST segment deviation indicates acute (ongoing) ischemia. In most cases ST deviations are accompanied by T-wave changes. The latter manifests as T-wave inversions (negative T-waves), flat T-waves (T-waves with low amplitude) or hyperacute T-waves (very large T-waves). As for the T-waves, the following must be noted:

  • Isolated T-wave inversion is never a sign of acute (ongoing) ischemia. Isolated T-wave inversion occurs after the ischemic episode. These T-wave changes are often called post-ischemic T-wave inversions. The same is true for flat T-waves.
  • Hyperacute T-waves may, however, be an isolated sign of myocardial ischemia. These T-waves are very broad and very high.


ECG in myocardial infarction

Myocardial infarction manifests as pathological Q-waves, reduced R-wave amplitude or fragmented QRS complexes.

The ECG in guidelines

Current guidelines include ECG criteria for ST deviation, T-wave inversion, Q-waves, and R-waves. Hyperacute T-waves and fragmented QRS complexes are not included as criteria for myocardial infarction. The reason for this will be discussed later. The ECG criteria for ischemia/infarction must always be evident in at least two anatomically contiguous leads. This is required because it is unlikely that ischemia/infarction will be localized to just one ECG lead.

It should also be noted that guidelines recommend that patients with chest pain and a newly discovered left bundle branch block on the ECG be treated as patients with STE-ACS (STEMI). This will also be discussed in detail later on.


Angina pectoris is the hallmark of myocardial ischemia. It is described as a retrosternal chest discomfort (pressure, heaviness, squeezing, burning or chocking sensation). It is commonly accompanied by radiation of the pain to the left shoulder and/or arm. Pain localized in the epigastrium, back, jaw, or neck is also common. Autonomic symptoms such as paleness, cold sweat, anxiety, vomiting is also common. Dyspnea is very common and actually equally common as chest discomfort in older patients (particularly women). The pain lasts longer than 20 minutes in myocardial infarction. Shorter durations are usually episodes of unstable angina. As compared with stable angina pectoris, the symptoms during acute coronary syndromes are more pronounced, present at rest and do not respond to nitroglycerin.


Chest discomfort may be explained by a wide range of conditions which must be included as differential diagnoses. In patients presenting with chest discomfort, the following differential diagnoses must be considered:

  • Cardiac: Stable angina pectoris. Acute coronary syndromes. Perimyocarditis. Aortic dissection. Arrhythmias. Valvular disease. Prinzmetal’s angina (vasospasm). Syndrome X (angina without vasospasm but with normal coronary arteries).
  • Pulmonary: Pneumonia. Pleuritis. Pneumothorax. Pulmonary embolism. Pulmonary infarction.
  • Gastrointestinal: Ventricular ulcer. Esophageal reflux. Esophageal rupture. Esophageal spasm. Pancreatitis. Cholecystitis.
  • Musculoskeletal: Tietze’s syndrom. Rib fracture. Trauma/contusion. Post-thoracotomy. Neurogenic pain.
  • Psychiatric: Acute/chronic stress. Anxiety. Depression.
  • Other: Herpes Zoster. Anemia with secondary ischemia.



Classification of myocardial infarction according to the ESC

The entire discussion so far has been devoted to myocardial infarction as a result of coronary atherothrombosis, which is indeed the most common cause of myocardial infarction. However, there are other types of myocardial infarction and the European Society for Cardiology has defined five types:

Type 1: Spontaneous myocardial infarction – Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD but on occasion non-obstructive or no CAD.

Type 2: Myocardial infarction secondary to an ischaemic imbalance – In instances of myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g. coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anaemia, respiratory failure, hypotension, and hypertension with or without LVH.

Type 3: Myocardial infarction resulting in death when biomarker values are unavailable – Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in rare cases cardiac biomarkers were not collected.

Type 4a: Myocardial infarction related to percutaneous coronary intervention (PCI): Myocardial infarction associated with PCI is arbitrarily defined by elevation of cTn values >5 x 99th percentile URL in patients with normal baseline values (≤99th percentile URL) or a rise of cTn values >20% if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial ischaemia, or (ii) new ischaemic ECG changes or new LBBB, or (iii) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no-flow or embolization, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

Type 4b: Myocardial infarction related to stent thrombosis – Myocardial infarction associated with stent thrombosis is detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/ or fall of cardiac biomarkers values with at least one value above the 99th percentile URL.

Type 5: Myocardial infarction related to coronary artery bypass grafting (CABG) – Myocardial infarction associated with CABG is arbitrarily defined by elevation of cardiac biomarker values >10 x 99th percentile URL in patients with normal baseline cTn values (≤99th percentile URL). In addition, either (i) new pathological Q waves or new LBBB, or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. 


Risk stratification using the ECG

Among patients with chest discomfort the ECG correlates strongly with the risk of acute myocardial infarction and 30-days mortality. Table 1 below presents 7 variants of ECG changes; the risk of infarction and 30-days mortality increase gradually from 1 to 7.

Table 1

  ECG Classification in case of myocardial infarction
1 Normal or inconclusive ECG NSTEMI
2 Isolated T-wave inversions NSTEMI
3 ST-segment depressions NSTEMI
4 ST-segment depressions and T-wave inversions NSTEMI
5 New or presumed new left bundle branch block This group of patients is managed as patients with STEMI because a significant portion of these patients also have a complete occlusion and the prognosis of the whole group is improved if they are referred to PCI immediately.
6 ST-segment elevations STEMI
7 ST-segment elevations and ST-segment depressions STEMI


In patients with acute coronary syndromes, the association between ECG changes and mortality has been examined in several studies. Figure 2 shows results from the legendary GUSTO-II study. As seen in Figure 2, isolated T-wave inversions carry the lowest mortality. Short term mortality is higher in STEMI than non-STEMI, but long term mortality is higher in the non-STEMI group which is usually explained by the fact that patients with Non-STEMI are older and have more comorbidities. As seen in Figure 2, roughly 7% of patients with STEMI die within 30 days, as compared with 3–5 % of patients with non-STEMI.


Figure 2. The GUSTO-II study.

Figure 2. The GUSTO-II study.

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