Classification, diagnosis and definitions of acute coronary syndromes (ACS) and acute myocardial infarction (AMI)

Acute coronary syndromes are subdivided into STE-ACS and NSTE-ACS. STE-ACS is the acronym for ST Elevation Acute Coronary Syndrome. All acute coronary syndromes which exhibit significant ST segment elevations on the ECG are classified as STE-ACS. NSTE-ACS is the acronym for Non-ST Elevation Acute Coronary Syndrome. This category includes all acute coronary syndromes which does not exhibit significant ST segment elevations. NSTE-ACS typically presents with ST segment depressions and/or T-wave inversions. Hence, the difference between STE-ACS and NSTE-ACS is merely the presence of ST segment elevations in the former. A diagnosis of myocardial infarction is made only after blood analyses confirm elevated levels of proteins specific to myocardial cells. These proteins are cardiac troponins (henceforth referred to only as troponins).

When elevated troponin levels are confirmed in patients with STE-ACS, the condition is classified as STEMI (ST elevation myocardial infarction). When elevated troponin levels are confirmed in patients with NSTE-ACS, the condition is classified as Non-STEMI (Non-ST elevation myocardial infarction).

The following flow-chart illustrates the natural course of coronary artery disease, from risk factors to myocardial infarction. It also displays classification of acute coronary syndromes and myocardial infarctions.

Figure 1. Classification of coronary heart disease (ischemic heart disease).

Figure 1. Classification of coronary heart disease (ischemic heart disease).

STE-ACS (ST Elevation Acute Coronary Syndrome) and STEMI (ST Elevation Myocardial Infarction)

Acute coronary syndromes with significant ST segment elevations are classified as STE-ACS. Virtually all cases of STE-ACS lead to myocardial infarction (elevated troponin levels), whereafter the condition is classified as ST Elevation Myocardial Infarction (STEMI). The thrombus causing STE-ACS is located proximally in the coronary artery and it occludes the entire artery lumen (i.e no blood passes the thrombus). The ensuing ischemia is transmural, implying that it is extensive and stretches from the endocardium to the epicardium (Figures 1 and 2).

ECG in STE-ACS (STEMI)

The ECG leads which displays ST segment elevations reflects the ischemic area. This means that ST segment elevations in leads V3 and V4 (anterior chest leads) reflect transmural anterior ischemia. ST elevations must exist in at least two anatomically contiguous leads in order to fulfill criteria for STE-ACS. Anatomically contiguous implies that the leads must be anatomically juxtaposed; for example V1 and V2; V5 and V6; V4 and V5; aVF and III and so on. In most cases the ST segment elevations are accompanied by reciprocal ST segment depressions. Such ST segment depressions occur in leads which detect the ischemic vectors from the opposite angle, compared with the leads showing ST segment elevations. The ST segment elevations are gradually normalized and followed by T-wave inversions. The latter may persist for a month, or even longer.

Pathological Q-waves may appear if the infarct area is large. These Q-waves are abnormally wide and deep. They testify that the heart has suffered a large infarction. Infarctions that leave pathological Q-waves are referred to as Q-wave infarctions.

On rare occasions the thrombus may resolve (either spontaneously or due to expedite reperfusion treatment) before the infarction process begins. In this case the troponin levels are not elevated and the condition is classified as unstable angina pectoris (or aborted myocardial infarction). This is, however, rare because virtually all cases of STE-ACS progress to STEMI.

Patients with STE-ACS (STEMI) have pronounced symptoms and high risk of ventricular arrhythmias in the acute phase. Ventricular tachycardia and ventricular fibrillation cause virtually all deaths in the acute phase of myocardial infarction/ischemia. Death due to pumping failure (cardiogenic shock) is much less common in the acute phase.

STE-ACS (STEMI) is treated with anti-ischemic and antithrombotic medications, as well as immediate coronary angiography with the purpose of performing PCI (percutaneous coronary intervention). Anti-thrombotic medications and PCI reduces mortality markedly by counteracting thrombus formation and restoring coronary blood flow, respectively.

NSTE-ACS (Non ST Elevation Acute Coronary Syndrome) and Non-STEMI (Non-ST Elevation Myocardial Infarction)

All acute coronary syndromes which do not fulfill criteria for STE-ACS are classified as NSTE-ACS. The artery occlusion is partial (not complete) and thus some blood flow remains in the artery. The occlusion is typically located proximally (along the epicardial course of the artery).

Because the occlusion is partial the ischemia will primarily affect the subendocardium, which has the poorest prerequisites in case of ischemia. The remaining layers of the myocardial wall (i.e endocardium and epicardium) will overcome the ischemia without damage.

NSTE-ACS is classified as Non-ST Elevation Myocardial Infarction (Non-STEMI) if troponin levels are elevated. If cardiac troponin levels are normal, then the condition is classified as unstable angina pectoris, which thus can be viewed as an impending myocardial infarction (Figures 1 and 2).

ECG in NSTE-ACS (Non-STEMI)

The hallmark of NSTE-ACS (Non-STEMI) is ST segment depressions which are often accompanied by T-wave changes. The latter may be T-wave inversions or flat T-waves. Importantly, the leads displaying ST segment depressions are not indicative of the ischemic area. This means that ST segment depressions in lead V3–V4 are not necessarily due to anterior wall ischemia. Similarly, ST segment depressions in leads II, aVF and III does not suggest that the ischemia is located to the inferior wall. Hence, ST-segment depressions cannot localize the ischemic area.

Pathological Q-waves usually does not develop, which is explained by the fact that NSTEMI are generally smaller infarctions than STEMI. However, extensive subendocardial infarctions may certainly lead to pathological Q-waves. It is actually a widespread misunderstanding that infarctions must be transmural in order to cause pathological Q-waves.

T-wave inversions are also frequently misunderstood. Isolated T-wave inversions, i.e T-wave inversions without concomitant ST segment deviations, are never indicative of acute (ongoing) ischemia. T-wave inversions that are accompanied by ST segment depressions, however, are indicative of acute (ongoing ischemia), but in that scenario it is actually the ST segment deviation that reflects the ischemia. Isolated T-wave inversions are post-ischemic, i.e they occur after the ischemic episode has surmounted.

A minority of patients with NSTE-ACS (Non-STEMI) display normal ECG on arrival. It is unusual, however, to display a normal ECG throughout the course; the majority of patients with normal ECG on arrival will develop some ECG changes during the course. Moreover, normal ECGs on arrival cannot be used to rule out myocardial ischemia/infarction. There are infarctions which do not cause ECG changes (typically smaller infarctions) and there are cases in which the thrombus is dynamic in size. The thrombus may become larger or smaller, with minute-to-minute variation, and thus cause varying ECG changes.

NSTE-ACS (Non-STEMI) is treated with anti-ischemic, anti-thrombotic medications. Most patients undergo coronary angiography with the purpose of performing PCI. Angiography is performed within 24 hours but sooner if the patient is a high risk patient. ECG changes, troponin levels, clinical status and comorbidities will dictate if angiography must be performed promptly. Note that acute angiography (as is done in STE-ACS/STEMI) has never proven to reduce mortality or morbidity in NSTE-ACS (Non-STEMI), which is why it is not recommended in any guidelines.

Last but not least, NSTE-ACS may actually occur due to a proximal and complete occlusion (which usually leads to STE-ACS) if the affected myocardium has extensive collateral circulation. Collateral circulation, which is common among patients with ischemic heart disease, implies that the ischemic area obtains blood flow from two coronary arteries/branches of arteries. This type of circulation arise when ischemic myocardium stimulates surrounding arteries to sprout out vessels to the ischemic area (VEGF [Vascular Endothelial Growth Factor] plays a critical role in the development of collateral circulation).

Figur 2. NSTE-ACS is caused by a partial occlusion, which means that there is some residual flow in the artery. The ischemia will affect the subendocardium which has poorest prerequisites in case of ischemia. The subendocardium is too far away from the blood in the ventricular cavity and the oxygen level in the coronary artery is reduced because oxygen has been extracted during the passage through the myocardiuam. In case of STE-ACS, the entire cross section becomes ischemic/infarcted.

Figure 2. NSTE-ACS (Non-STEMI) is caused by a partial occlusion, which means that there is some residual flow in the artery. The ischemia will affect the subendocardium which has poorest prerequisites in case of ischemia. The subendocardium is too far away from the blood in the ventricular cavity and the oxygen level in the coronary artery is reduced because oxygen has been extracted during the passage through the myocardium. In case of STE-ACS, the entire cross section becomes ischemic/infarcted.

Normalization of ECG changes

ST-T changes are normalized within days or weeks. The duration is longer if ischemia results in infarction. QRS changes are mostly permanent, particularly Q-waves. Note that treatment and reperfusion therapy may modify the speed by which the ECG normalizes.

Risk stratification in the acute setting

Risk stratification must always be made in patients presenting with acute coronary syndromes. Risk stratification is based on patient data, anamnesis, ECG and troponin levels. There are numerous risk calculators available for acute coronary syndromes. These calculators assist the clinician in estimating the risk of in-hospital mortality, death within 6 months, 12 months and 3 years. Examples of such calculators are FRISC II, TIMI, PURSUIT and GRACE. TIMI and GRACE are the best validated risk calculators and you can find them here:

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