**2. Epidemiology and pathogenesis**

#### **2.1. Epidemiology**

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 to the advent of more sensitive assays for myocardial injury, earlier pharmacotherapy, and reperfusion (and prevention) of STEMI [13, 18].

in jeopardy or cardiac arrest secondary to malignant ventricular ischemia. Therefore, it is essential to establish if the patient has ACS and if so, what is the likelihood the patient will have adverse clinical event [1]. Physicians will need to stratify the patients according to their risk status and according to the initial risk assessment to choose an appropriate management strategy. The initial

Non-ST Elevation Myocardial Infarction: Diagnosis and Management

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Angina pectoris is a kind of pain described as a sensation of tightness, heaviness, aching, burning, pressure, or squeezing typically localized at the retrosternal region. The pain can often radiate to the left arm but may also radiate to the lower jaw, neck, both arms, back, and epigastrium. It is associated with exertion or emotional stress and relieved by rest or admin-

In ACS patients other symptoms including sweating, nausea, abdominal pain, dyspnea and syncope may be present. Atypical presentations are also possible and characterized by epigastric pain, indigestion-like symptoms and isolated dyspnea. Atypical complaints are more often observed in the elderly, in women and in patients with diabetes mellitus, chronic renal disease or dementia [24, 25]. The relief of pain at rest increase the probability of myocardial ischemia while the relief of symptoms after nitrates administration is not specific for angina pectoris [25]. In patients presenting with suspected MI to the emergency department, overall,

Risk factors increase the likelihood of NSTEMI include: Older age, male gender, family history of CAD, diabetes, hyperlipidemia, hypertension, renal insufficiency, previous manifesta-

Physical examination is frequently unremarkable in patients with suspected NSTEMI but may reveal HTN or hypotension, the presence of third and fourth heart sounds, and paradoxical splitting of the second heart sound. Cardiac auscultation may reveal a systolic murmur due to ischemic mitral regurgitation, which is associated with poor prognosis [26] or a mechanical complication (i.e. papillary muscle rupture or ventricular septal defect) of a subacute and possibly undetected MI. Signs of heart failure (raised jugular venous pressure, bilateral crepitation on auscultation of the lungs) or cardiogenic shock may also be present, and these signify

Resting 12-lead ECG is the first diagnostic test for patients with chest pain and should be performed and interpreted within the first 10 min of the initial admission to the hospital [27]. ECG is critical for the diagnosis of STEMI as the cause for the chest pain, this has a tremen-

While the ECG in the setting of NSTEMI may be normal in more than one-third of patients, a serial ECG at 15- to 30-min intervals should be performed to detect the developing abnormalities.

the diagnostic performance of chest pain characteristics for MI is limited [25].

tion of CAD as well as peripheral or carotid artery disease.

risk assessment includes the history, examination, ECG, and cardiac biomarkers [1, 23].

**3.2. History and examination**

a worse prognosis.

*3.3.1. Electrocardiogram*

dous therapeutic implication for the patient.

**3.3. Initial tests**

istration of sublingual nitroglycerin [1].

#### **2.2. Pathophysiology**

NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion. Type 1 MI is most commonly caused by a non-occlusive thrombus that develops in a disrupted atherosclerotic plaque, and leads to non-occlusive or near-complete thrombosis of a vessel supplying the myocardium.

Plaque rupture usually occurs at the weakest and thinnest part of the atherosclerotic cap (often at the shoulder region). Ruptured plaques contain large numbers of inflammatory cells including monocytes, macrophages, and T lymphocytes [19, 20]. Although one third of occlusions occur at a site with the greatest stenosis, most (66–78%) arise from lesions with <50% stenosis, and <5% arise from lesions exhibiting >70% stenosis [19]. It is thought that the lack of ST elevation is because the infarct does not involve the full thickness of the myocardium (not a transmural infarction). The severity of myocardial damage in NSTEMI depends on:


Classically it is thought that NSTEMI patients ultimately have a diagnosis of a non-Q-wave MI; however, 25% of patients with NSTEMI and elevated biomarkers go on to develop Q-wave MI in the weeks to follow [21]. In addition, approximately 25% of patients with a diagnosis of NSTEMI have a 100% occlusion of the affected artery on coronary angiography [22].

NSTEMI may also be caused by other mechanisms, such as dynamic obstruction (i.e., focal coronary artery spasm or Prinzmetal angina), severe progressive atherosclerosis, restenosis following percutaneous coronary intervention, recreational drug use (e.g., cocaine or other stimulants), arterial inflammation (i.e., vasculitis), or extrinsic causes leading to myocardial supply–demand mismatch (such as hypotension, hypovolemia, or hypoxia) [1].
