**5. Risk assessment and outcomes**

perfusion defects or echocardiography to assess wall motion abnormalities. Stress imaging is preferred over exercise ECG due to its greater diagnostic accuracy and superior prognostic value [47]. While studies have shown that normal exercise or pharmacological stress echocardiograms have high negative predictive value for ischemia and are associated with excellent patient outcomes ECG [48–50]. The addition of contrast to improve endocardial border detec-

To evaluate the extent of the CAD, a functional assessment using a submaximal exercise testing can be performed at 4 to 7 days after myocardial infarction, while symptom limited testing can be performed at 14 to 21 days post-myocardial infarction, when the patient has been free

Cardiac magnetic resonance (CMR) can be used in the assessment of myocardial perfusion and wall motion abnormalities. Patients presenting with acute chest pain with a normal stress CMR have an excellent short and midterm prognosis [53]. CMR also permits detection of scar tissue (using late gadolinium enhancement) and can differentiate this from recent infarction (using T2-weighted imaging to delineate myocardial edema) [54, 55]. Moreover, CMR can facilitate the differential diagnosis between infarction and myocarditis or Takotsubo cardiomyopathy [56].

Nuclear myocardial perfusion imaging has been shown to be useful for risk stratification in patients with acute chest pain suggestive for ACS. The presence of an area of myocardium that becomes deprived of perfusion during increased myocardial demand and reperfuses on

Resting myocardial scintigraphy, can be helpful for the diagnosis of patients presenting with chest pain without ECG changes or elevated cardiac troponins [57]. Combined stress–rest imaging may further enhance assessment of ischemia, while a normal study is associated with

Multidetector computed tomography (MDCT) provide noninvasive evaluation of coronary anatomy and atherosclerosis. Due to the high negative predictive value of coronary computed tomography angiography (CCTA), evidence suggests that CCTA is useful in patients with low to moderate risk of NSTEMI where a normal scan excludes CAD. When compared with the standard care (observation, serial enzymes followed by stress testing) for low-risk patients, CCTA reduced time to diagnosis, reduced length of emergency department stay, and had similar safety [60]. CCTA had high negative predictive values to exclude ACS and excellent outcome in patients presenting to the emergency department with low to intermediate pre-test probability for ACS and a normal coronary CT angiogram [61]. CCTA was proven

stopping the activity on nuclear imaging stress tests is a reversible defect (**Figure 2**).

tion and facilitate detection of ischemia [51].

of active ischemic or heart failure symptoms [52].

*3.3.6. Cardiac magnetic resonance*

68 Myocardial Infarction

*3.3.7. Nuclear myocardial perfusion imaging*

excellent outcome [58, 59].

**4. Anatomical evaluation**

ACS management requires continuous risk stratification for death or recurrent MI. Quantitative assessment of ischemic risk by means of scores is superior to the clinical assessment alone to further triage and assist in the selection of treatment options [1]. A number of risk scores exist which incorporate a number of variables, the GRACE risk score and the TIMI risk score are examples.

The GRACE risk score provides the most accurate stratification of risk both on admission and at discharge [68, 69]. The GRACE 2.0 risk calculator provides a direct estimation, of mortality while in hospital, at 6 months, at 1 year and at 3 years. The combined risk of death or MI at 1 year is also provided [70]. Variables used in the GRACE 2.0 risk calculation include age, systolic blood pressure, pulse rate, serum creatinine, Killip class at presentation, cardiac arrest at admission, elevated cardiac biomarkers and ST deviation. The TIMI risk score uses seven variables in an additive scoring system: age ≥ 65 years, three or more CAD risk factors, known CAD, aspirin use in the past 7 days, severe angina (two or more episodes within 24 h), ST change ≥0.5 mm and positive cardiac marker [71]. Patients with a TIMI score of 0–2 are low risk, 3–4 are intermediate risk, and 5–7 are high risk. All-cause mortality, rate of MI, and rate of urgent revascularization at 14 days increase in proportion to the number of risk factors present on the TIMI score. It is simple to use, but its discriminative accuracy is inferior to that of the GRACE risk score [1, 71].

MI but without hypoxia. Guidelines now recommend supplemental oxygen therapy only in patients who are hypoxemic (arterial oxygen saturation < 90%), or in those who have respira-

Non-ST Elevation Myocardial Infarction: Diagnosis and Management

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

71

The goal of pharmacological anti-ischemic therapy is to decrease myocardial oxygen demand (secondary to a decrease in heart rate, blood pressure, preload or myocardial contractility) or to increase myocardial oxygen supply (by administration of oxygen or through coronary

Pain relief is indicated in the initial management of all patients. Those with ongoing ischemic discomfort should receive a trial of sublingual nitroglycerin (0. 4 mg) every 5 min for a total of three doses. Sublingual nitroglycerin reduces myocardial oxygen demand and enhances myocardial oxygen delivery. Intravenous nitroglycerin is recommended in patients with no symptom relief after sublingual nitroglycerin. Under careful blood pressure monitoring, the dose should be titrated upwards until symptoms are relieved, and in hypertensive patients until blood pressure is normalized, unless side effects (notably headache or hypotension) occur. Beyond symptom control, there is no indication for nitrate treatment [76]. In patients with recent intake of a phosphodiesterase type 5 inhibitor (i.e. within 24 h for sildenafil or vardenafil and 48 h for tadalafil), nitrates should not be administered due to the risk of severe hypotension. Nitroglycerin should not be given if systolic BP is <90 mmHg or there is a concern about right ventricular infarction [77]. If the patient does not respond to nitroglycerin, intravenous morphine can be administered in the absence of any contraindications [1]. Morphine causes vasodilation and may produce reductions in heart rate (through increased vagal tone) and systolic BP to further reduce myocardial oxygen demand. It should be given instead of nitroglycerin when nitroglycerin is contraindicated. Morphine should be used with caution, one randomized, double-blind trial found that morphine delays and attenu-

ates ticagrelor exposure and action in patients with myocardial infarction [78, 79].

of progression to MI with beta-blocker treatment [80].

tively with no increase in cardiogenic shock [81, 82].

be avoided in these patients if the ventricular function is unknown.

Oral beta-blockers are recommended for routine use in all patients unless contraindicated. Beta-blockers competitively inhibit the myocardial effects of circulating catecholamines and reduce myocardial oxygen consumption by lowering heart rate, blood pressure and myocardial contractility. Randomized trials with threatened or evolving MI have shown lower rates

The beneficial effects of beta-blockers derived from several meta-analyses were a significant 8 and 13% relative risk reduction for in-hospital and first week mortality following MI respec-

A registry study of NSTEMI patients found that the use of B-Blocker blockers within 24 h of hospital admission in patients at risk of developing cardiogenic shock (i.e. age > 70 years, heart rate > 110 beats/min, systolic blood pressure < 120 mmHg), the observed shock or death rate was significantly increased [83]. Therefore, early administration of beta-blockers should

tory distress or other high-risk features for hypoxemia [1, 15, 75].

**7.2. Pharmacological treatment of ischemia**

vasodilation).

*7.2.1. Beta-blockers*
