**1. Introduction**

#### **1.1. Definition of acute coronary syndrome**

Acute coronary syndrome (ACS) is a term that describes an acute ischemic insult to the myocardium resulting from sudden reduction in coronary blood flow. The findings on the ECG will help to categorize patients into two major subdivision of major diagnostic and therapeutic consequences [1]:

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**1.** Patients with acute chest pain and persistent >1 mm ST-segment elevation in ≥2 anatomically contiguous leads. This condition is termed ST-elevation ACS and generally reflects an acute total coronary occlusion. The mainstay of treatment in these patients is immediate reperfusion with primary angioplasty or fibrinolytic therapy [2]. While biomarkers are useful for confirmatory and prognostic purposes, they are not required for the diagnosis of STEMI and should not delay treatment.

**1.3. Classification of myocardial infarction**

particularly in women [8, 10, 11, 14].

**Type 4b MI**: MI associated with stent thrombosis.

**2. Epidemiology and pathogenesis**

**2.1. Epidemiology**

ischemia by any of the following possible etiologies [3, 8, 13]:

The development of myocardial tissue-specific biomarkers and sensitive cardiac imaging techniques allows for early detection of very small amounts of myocardial injury or necrosis. Consequently MI has been redefined to encompass any necrosis in the setting of myocardial

Non-ST Elevation Myocardial Infarction: Diagnosis and Management

http://dx.doi.org/10.5772/intechopen.76241

63

**Type 1 MI**: spontaneous MI caused by atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis. The patient may have underlying severe CAD but in 5–20% of cases there may be non-obstructive coronary atherosclerosis or no angiographic evidence of CAD,

**Type 2 MI**: MI secondary to an increase in oxygen demand or decrease in supply. The myocardial necrosis results from causes other than coronary plaque instability [8]. Mechanisms include coronary artery spasm, coronary endothelial dysfunction, tachyarrhythmias, bradyarrhythmias, anemia, respiratory failure, hypotension and severe hypertension. In addition, in critically ill patients and in patients undergoing major non-cardiac surgery, myocardial

**Type 4a MI**: MI associated with percutaneous coronary intervention (PCI) where there is a

**Type 5 MI**: MI associated with coronary bypass graft surgery (CABG), a greater than 10-fold rise from normal baseline levels in troponin during the first 48 h following the intervention [8].

Cardiovascular disease (CVD) is the number one cause of death worldwide, accounting for 17.5 million deaths per year. Coronary heart disease mortality is decreasing in many developed countries, but it is increasing in developing and transitional countries, partly as a result of increasing longevity, urbanization, and lifestyle changes. Epidemiological data have shown that acute coronary syndrome cases with STEMI appear to be declining and that NSTEMI occurs more frequently than STEMI [15, 16]. In the United States, it is estimated that >780,000 people will experience an ACS each year, and approximately 70% of these will have NSTEMI [17]. Trends from the world's largest database of patients with ACS show that the percentage of patients with a diagnosis of NSTEMI is rising dramatically [18]. This is likely to be due

necrosis may be related to injurious effects of pharmacological agents and toxins [9]. **Type 3 MI**: Sudden unexpected cardiac death before cardiac biomarkers obtained.

greater than 5-fold rise in troponin during the first 48 h following the intervention [8].

	- **1.** Non-ST elevation myocardial infarction (NSTEMI) which denote cardiomyocyte necrosis and death by a rise in serum troponin levels.
	- **2.** Unstable angina is defined as myocardial ischemia at rest or minimal exertion in the absence of cardiomyocyte necrosis (cardiac biomarkers are not increased) [3, 4].

The application of high-sensitivity cardiac troponin measurements in daily clinical practice instead standard troponin assays showed increased detection of MI (4% absolute and 20% relative increase) and decreased diagnosis of unstable angina [5–7]. In comparison with NSTEMI patients, unstable angina patients do not have necrosis in their myocardial tissue and have a substantially lower risk of death. Unstable angina patients benefit less from intensified antiplatelet therapy and early invasive strategy [5–12]. NSTEMI encompasses a broad spectrum of ischemic injury to the myocardium, which is detected by elevation of serum cardiac biomarkers. It can be distinguished from unstable angina pectoris by normal serial cardiac biomarkers [1].

#### **1.2. Non-ST elevation myocardial infarction**

NSTEMI is an acute ischemic event causing cardiomyocyte death by necrosis in a clinical setting consistent with acute myocardial ischemia [8]. The leading symptom that initiates the diagnostic and therapeutic cascade in patients with suspected ACS is chest pain but to make a diagnosis of NTEMI, one major criteria is typical rise and gradual fall in cardiac biomarkers (troponin or CKMB) in addition to one or more of the following:


## **1.3. Classification of myocardial infarction**

**1.** Patients with acute chest pain and persistent >1 mm ST-segment elevation in ≥2 anatomically contiguous leads. This condition is termed ST-elevation ACS and generally reflects an acute total coronary occlusion. The mainstay of treatment in these patients is immediate reperfusion with primary angioplasty or fibrinolytic therapy [2]. While biomarkers are useful for confirmatory and prognostic purposes, they are not required for the diagnosis

**2.** Patients with acute chest pain but no persistent ST-segment elevation. This condition is termed non-ST elevation ACS (NSTE-ACS). The ECG may be normal or there may be transient ST-segment elevation, persistent or transient ST-segment depression, T-wave inversion, flat T waves or pseudo-normalization of T waves. The NSTE-ACS can be sub-

**1.** Non-ST elevation myocardial infarction (NSTEMI) which denote cardiomyocyte ne-

**2.** Unstable angina is defined as myocardial ischemia at rest or minimal exertion in the absence of cardiomyocyte necrosis (cardiac biomarkers are not increased) [3, 4]. The application of high-sensitivity cardiac troponin measurements in daily clinical practice instead standard troponin assays showed increased detection of MI (4% absolute and 20% relative increase) and decreased diagnosis of unstable angina [5–7]. In comparison with NSTEMI patients, unstable angina patients do not have necrosis in their myocardial tissue and have a substantially lower risk of death. Unstable angina patients benefit less from intensified antiplatelet therapy and early invasive strategy [5–12]. NSTEMI encompasses a broad spectrum of ischemic injury to the myocardium, which is detected by elevation of serum cardiac biomarkers. It can be distinguished from unstable angina pectoris by normal serial cardiac bio-

NSTEMI is an acute ischemic event causing cardiomyocyte death by necrosis in a clinical setting consistent with acute myocardial ischemia [8]. The leading symptom that initiates the diagnostic and therapeutic cascade in patients with suspected ACS is chest pain but to make a diagnosis of NTEMI, one major criteria is typical rise and gradual fall in cardiac biomarkers

**3.** Imaging evidence of new or presumed new loss of viable myocardium or regional wall

of STEMI and should not delay treatment.

**1.2. Non-ST elevation myocardial infarction**

crosis and death by a rise in serum troponin levels.

(troponin or CKMB) in addition to one or more of the following:

**4.** Intracoronary thrombus detected on angiography or autopsy [8].

classified to:

62 Myocardial Infarction

markers [1].

**1.** Symptoms of ischemia.

motion abnormality.

**2.** ECG changes.

The development of myocardial tissue-specific biomarkers and sensitive cardiac imaging techniques allows for early detection of very small amounts of myocardial injury or necrosis. Consequently MI has been redefined to encompass any necrosis in the setting of myocardial ischemia by any of the following possible etiologies [3, 8, 13]:

**Type 1 MI**: spontaneous MI caused by atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis. The patient may have underlying severe CAD but in 5–20% of cases there may be non-obstructive coronary atherosclerosis or no angiographic evidence of CAD, particularly in women [8, 10, 11, 14].

**Type 2 MI**: MI secondary to an increase in oxygen demand or decrease in supply. The myocardial necrosis results from causes other than coronary plaque instability [8]. Mechanisms include coronary artery spasm, coronary endothelial dysfunction, tachyarrhythmias, bradyarrhythmias, anemia, respiratory failure, hypotension and severe hypertension. In addition, in critically ill patients and in patients undergoing major non-cardiac surgery, myocardial necrosis may be related to injurious effects of pharmacological agents and toxins [9].

**Type 3 MI**: Sudden unexpected cardiac death before cardiac biomarkers obtained.

**Type 4a MI**: MI associated with percutaneous coronary intervention (PCI) where there is a greater than 5-fold rise in troponin during the first 48 h following the intervention [8].

**Type 4b MI**: MI associated with stent thrombosis.

**Type 5 MI**: MI associated with coronary bypass graft surgery (CABG), a greater than 10-fold rise from normal baseline levels in troponin during the first 48 h following the intervention [8].
