2: Evaluation of myocardial ischaemia

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Topic 2 Evaluation of myocardial ischaemia

Markers of myocardial injury and infarction

A universal classification system for myocardial infarction (MI) was published in 2007.

It defines five types of MI:

1. Spontaneous MI due to a primary coronary event, e.g. plaque erosion, rupture, fissuring or dissection.

2. MI secondary to ischaemia due to increased oxygen demand or decreased supply.

3. Sudden unexpected cardiac death with pathological evidence of coronary artery thrombus.

4. MI associated with coronary stenting.

a. MI post percutaneous coronary intervention.

b. MI secondary to coronary stent thrombosis.

5. MI associated with coronary artery bypass surgery.

Myocardial damage results in release of proteins into the circulation that can be detected with laboratory assays. These include troponins, myoglobin and CK-MB. Cardiac troponins are currently the preferred biomarkers as their detection in blood is highly specific and sensitive for myocardial damage.

CK-MB is an isoenzyme of creatine kinase, which is present in skeletal and myocardial muscle. An elevated level is usually detectable within 4–6 h of myocardial injury. Reference range is 0–5 ng/mL.

Cardiac troponins are myocardial contractile proteins. An increased value for cardiac troponin is defined as a measurement exceeding the 99th percentile of a normal reference population upper reference limit, measured with a coefficient of variation <10%.

Cardiac troponin T (cTnT) assays have a relatively consistent sensitivity with a cutoff (including 10% coefficient of variation) of 0.03 μg/L. The lowest level of detectability is 0.01 μg/L. cTnT is expressed by skeletal muscle in patients with chronic renal failure, and therefore cTnT measurements during acute presentations must be compared to baseline values in this patient cohort.

Cardiac troponin I (cTnI) assays are more variable and therefore reference to local laboratory assay ranges and coefficient of variation is appropriate. As a guide, a serum cTnI value of >0.5 ng/ml is evidence of acute myocardial injury with significant prognostic implications. Serum cTnI levels <0.01 are normal. cTnI values between 0.01–0.04 ng/ml may reflect myocyte necrosis, but depend on specific sensitivities and variability of the local assay. cTnI values between 0.04 and 0.5 ng/ml are suggestive of acute myocardial injury, and need to be placed in clinical context.

Troponin values may remain elevated for 7–14 days following the onset of infarction.

Myocardial injury and troponin elevation can occur without coronary artery disease. Examples include:

• Acute decompensated heart failure.

• Tachyarrhythmias.

• Myocarditis.

• Cardiac contusion.

• DC cardioversion.

Troponin levels may also be elevated in noncardiac conditions such as in acute pulmonary embolism, renal failure, sepsis and following brain injury or burns.

Myocardial territories supplied by coronary arteries (Figure 2.1)

Figure 2.1 Left ventricular coronary artery territories on standard 2D echo views (16 segment).

Stress tests

Stress protocols

Several modalities can be used to noninvasively assess coronary artery disease. Many techniques induce a form of cardiac stress to enhance detection of physiologically significant coronary artery disease, and therefore provide functional information which complements anatomic methods of assessment such as coronary angiography.This may be achieved with exercise (typically treadmill or bicycle) or by pharmacological methods or a combination of both.

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