**5. Diagnosis**

The diagnosis of acute MI depends on both clinical and laboratory findings including electrocardiogram, and cardiac biomarkers for myocyte injury [32]. Biochemical cardiac markers are the signals from the injured myocardium (**Figure 1**) and are released in case of damage at the cardiac muscle. The most common causes of injury are acute coronary syndromes (MI, non Q-wave MI, unstable angina pectoris) and other conditions affecting cardiac muscle including trauma, cardiac surgery, myocarditis etc. The level of cardiac biomarkers can be detected/ measured in blood samples in these cases [33–35].

Patients with elevated cardiac troponin levels but negative CK-MB who were previously diagnosed as unstable angina or minor myocardial injury are now re-stratified as non–ST-segment

The Diagnostic Value of Biochemical Cardiac Markers in Acute Myocardial Infarction

http://dx.doi.org/10.5772/intechopen.76150

27

The term MI should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. Under these conditions any one of the following criteria

• Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit (URL) together with evidence

• ECG changes indicative of new ischemia (new ST-T changes or new left bundle branch

• Imaging evidence of new loss of viable myocardium or new regional wall motion abnor-

• Type 1: Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection. This would be the

• Type 2: Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, ar-

• Type 3: Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the

• Type 4: MI associated with percutaneous coronary interventions, and there are two types of this category: one associated with the procedure itself, and one associated with subse-

elevation MI (NSTEMI) even in the absence of diagnostic ECG changes [43].

**5.1. Operational definition for acute myocardial infarction**

of myocardial ischemia with at least one of the following:

The most recent guidelines recognize five distinct types of MI [43–48].

• Development of pathological Q waves in the ECG;

typical ST elevation or non-ST elevation MI.

rhythmias, hypertension, or hypotension.

appearance of cardiac biomarkers in the blood.

• Type 5: Myocardial infarction associated with CABG [43–48].

quently verified stent thrombosis.

meets the diagnosis for myocardial infarction:

• Symptoms of ischemia;

block [LBBB]);

mality [43–46].

**5.2. Types of myocardial infarctions**

The role of cardiac biomarkers in the process of diagnosis, risk evaluation, and management of patients with chest pain has continued to evolve. The initial electrocardiogram (ECG) may be non-diagnostic. Although physicians awareness and diagnostic utilities increase the rate of missed MI continues to remain between 1.5 and 2%. Determination of cardiac biomarkers plays an increasingly important role for the evaluation and diagnosis of patients with chest pain. The guidelines for the diagnosis of MI have recently been upgraded and have incorporated the results of cardiac marker estimation in the clinical definition of MI [36–39]. Creatine kinase-MB (CK-MB), cardiac troponin T (cTnT), cardiac troponin I (cTnI), myoglobin, homocysteine and C-reactive protein (CRP) are all used for evaluation of the suspected acute MI. CK-MB, cTnT, and cTnI may also be used to detect and manage highrisk patients [36–39].

In early 1990s, the diagnosis of MI was primarily based on an elevated serum CK-MB level. Though, the introduction of troponin markers significantly increased the sensitivity and specificity for the diagnosis of myocardial injury and for this reason succeeded CK-MB as the gold standard for the diagnosis. A consensus guideline from both the American College of Cardiology (ACC) and the European Society of Cardiology (ESC) has redefined acute MI [40]. According to these associations, acute MI is now typically termed as a typical rise and fall of serum biochemical markers (e.g., Troponin, CK-MB), associated with symptoms of ischemic injury, new pathologic Q waves on ECG, ischemic ECG changes (ST-segment elevation or depression), coronary artery intervention or histologic findings of AMI [41, 42].

**Figure 1.** Cardiac muscle cell. Biochemical markers (troponin T, CK-MB, and myoglobin) in myocardium; adopted by Cummins.

Patients with elevated cardiac troponin levels but negative CK-MB who were previously diagnosed as unstable angina or minor myocardial injury are now re-stratified as non–ST-segment elevation MI (NSTEMI) even in the absence of diagnostic ECG changes [43].

#### **5.1. Operational definition for acute myocardial infarction**

The term MI should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. Under these conditions any one of the following criteria meets the diagnosis for myocardial infarction:


cardiac muscle. The most common causes of injury are acute coronary syndromes (MI, non Q-wave MI, unstable angina pectoris) and other conditions affecting cardiac muscle including trauma, cardiac surgery, myocarditis etc. The level of cardiac biomarkers can be detected/

The role of cardiac biomarkers in the process of diagnosis, risk evaluation, and management of patients with chest pain has continued to evolve. The initial electrocardiogram (ECG) may be non-diagnostic. Although physicians awareness and diagnostic utilities increase the rate of missed MI continues to remain between 1.5 and 2%. Determination of cardiac biomarkers plays an increasingly important role for the evaluation and diagnosis of patients with chest pain. The guidelines for the diagnosis of MI have recently been upgraded and have incorporated the results of cardiac marker estimation in the clinical definition of MI [36–39]. Creatine kinase-MB (CK-MB), cardiac troponin T (cTnT), cardiac troponin I (cTnI), myoglobin, homocysteine and C-reactive protein (CRP) are all used for evaluation of the suspected acute MI. CK-MB, cTnT, and cTnI may also be used to detect and manage high-

In early 1990s, the diagnosis of MI was primarily based on an elevated serum CK-MB level. Though, the introduction of troponin markers significantly increased the sensitivity and specificity for the diagnosis of myocardial injury and for this reason succeeded CK-MB as the gold standard for the diagnosis. A consensus guideline from both the American College of Cardiology (ACC) and the European Society of Cardiology (ESC) has redefined acute MI [40]. According to these associations, acute MI is now typically termed as a typical rise and fall of serum biochemical markers (e.g., Troponin, CK-MB), associated with symptoms of ischemic injury, new pathologic Q waves on ECG, ischemic ECG changes (ST-segment elevation or depression), coronary artery intervention or histologic findings of AMI [41, 42].

**Figure 1.** Cardiac muscle cell. Biochemical markers (troponin T, CK-MB, and myoglobin) in myocardium; adopted by

measured in blood samples in these cases [33–35].

risk patients [36–39].

26 Myocardial Infarction

Cummins.


#### **5.2. Types of myocardial infarctions**

The most recent guidelines recognize five distinct types of MI [43–48].

