Non-ST-Segment Elevation Myocardial Infarction (NSTEMI) Case File
Eugene C. Toy, Md, Michael d . Faulx, Md
Case 2
A 73-yearld woman presents to the emergency department with episodic. burning precordial chest pain occurring at rest. She reports that the pain began several hours ago while she was taking a shower and has been intermittent since. She initially attributed it to indigestion and took antacids without relief. She has a history of coronary artery disease treated with percutaneous coronary intervention (PCI) with a drug-eluting stent 3 years ago after she presented with exertional chest discomfort. She also has hypertension and hyperlipidemia. Her home medical regimen consists of aspirin 81 mg daily, atorvastatin 40 mg daily. and lisinopril 10 mg daily.
On examination she appears to be in mild discomfort with a heart rate of 95 bpm. Her blood pressure is 168/94 mmHg. respiratory rate is 20 breaths/min. and oxygen saturation is 99% on room air. Her jugular venous pressure is not elevated. Pulmonary exam is unrevealing. Chest auscultation reveals regular rhythm. normal S1 and S2 with a soft 2/6 systolic murmur at the right upper sternal border.
There are no rubs or gallops. Her abdominal exam is benign. Her lower extremities are without edema. and she has 2+ pulses in her upper and lower extremities. A bedside troponin T is positive. An electrocardiogram (ECO) is performed (see Figure 2-1).
c What is the most likely diagnosis?
c What is the immediate medical management for this patient?
c What is the best subsequent management for this patient?
Figure 2-1. Presenting ECG This patient has sinus rhythm with voltage criteria for left ventricular hypertrophy (LVH) and nonspecific ST segment depression that is likely due to her LVH, although one must also consider ischemia as a cause. (Reproduced with perimission of Michael Faulx, MD)
Answer to Case 2:
Non-ST-Segment Elevation Myocardial Infarction (NSTEMI)
Summary: This 73-year-old woman is presenting with unrelenting chest burning that was not relieved with antacids. She has an established history of coronary artery disease. Women, as well as the elderly and diabetic patients, can present with symptoms of burning or shortness of breath alone as their “angina equivalent,” and thus a high index of suspicion for coronary artery disease should be maintained in these patient populations. The diagnosis can be confirmed with positive laboratory tests for creatinine kinase myocardial band (CK-MB) and troponin T or I (TnT or TnI). If these tests are negative, the patient is said to be experiencing unstable angina (UA).
Other life-threatening conditions that can cause chest pain include aortic dissection and pulmonary embolism; the possibility for either of these diagnoses should be entertained and excluded if there is any clinical suspicion for their presence. Afterward, the patient should be loaded with aspirin 325 mg as well as an adenosine diphosphate (ADP) inhibitor. The patient should also receive parenteral anticoagulation. Nitroglycerin should be administered and titrated until the patient’s chest pain has resolved. If there is no evidence of heart failure or cardiogenic shock on exam, intravenous metoprolol can also be administered to reduce myocardial oxygen demand by decreasing heart rate, contractility, and blood pressure. If there are high-risk features present (eg, markedly elevated troponin, recurrent ischemic discomfort, dynamic ECG changes, or hemodynamic instability), a glycoprotein (GP) IIb/IIIa inhibitor can be considered. Finally, a decision to pursue an early invasive approach versus an initial conservative approach is needed.
• Most likely diagnosis: Non-ST-segment elevation myocardial infarction.
• The next step in this patient’s medical management: Immediate treatment with anticoagulation and antiplatelet therapy.
• Best subsequent management: After aspirin, ADP inhibitor, anticoagulation, and perhaps a GP IIb/IIIa inhibitor, this patient should undergo cardiac catheterization within 24 hours on the basis of the high-risk factors (see Table 2-1).
ANALYSIS
Objectives
1. Be able to distinguish UA from NSTEMI.
2. Be able to risk-stratify patients who present with UA/NSTEMI.
3. Be aware of other conditions that may precipitate secondary unstable angina or NSTEMI.
4. Understand when an early invasive approach rather than an initial conservative approach should be used.
5. Know which evidence-based therapies patients should receive for secondary prevention.
Note: low risk: 0–2; intermediate risk: 3–4; high risk: 5–7.
[Data from Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/ non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000;284(7):835.]
Considerations
This patient is presenting with unrelenting chest burning for the past several hours. The ECG shows subtle ST depressions with T wave inversions in the inferior leads. A bedside troponin T is positive. In this clinical scenario, the most likely diagnosis is NSTEMI. If the patient did not have positive cardiac biomarkers, the diagnosis would be unstable angina. After ruling out other potential life-threatening causes of chest pain such as aortic dissection, pneumothorax, or pulmonary embolism, the patient should be administered aspirin, ADP inhibitor, anticoagulation, and perhaps a GP IIb/IIIa inhibitor. Risk stratification (see Table 2-1) suggests that this patient has high-risk features and thus should undergo cardiac catheterization within 24 hours of presentation. Other testing to rule out secondary causes of UA/NSTEMI such as profound anemia, thyrotoxicosis, hypertensive emergency, sepsis, or tachyarrhythmias should be performed as clinically indicated.
Approach To:
Non-ST-Elevation Myocardial Infarction
DEFINITIONS
ADENOSINE DIPHOSPHATE (ADP) RECEPTOR INHIBITOR: Any of the antiplatelet medications used to inhibit platelet activation and aggregation by blocking the ADP receptor on platelet cell membranes. The most widely used ADP inhibitors include clopidogrel, prasugrel, and ticagrelor.
CARDIAC BIOMARKERS: Any serum marker that is specific for necrosis of myocardial tissue such as troponin T, troponin I, and CK-MB. When these markers are positive in the appropriate clinical setting, a patient has “ruled in” for myocardial infarction.
GLYCOPROTEIN IIb/IIIa (GP IIb/IIIa) INHIBITORS: Any of the intravenous antiplatelet medications that inhibit the IIb/IIIa platelet receptor, thus preventing platelet aggregation and subsequent thrombus formation. Typical GP IIb/IIIa inhibitors include abciximab, eptifibatide, and tirofiban.
NON-ST-ELEVATION MYOCARDIAL INFARCTION: Chest discomfort (or anginal equivalent) in a patient usually with ST segment depression or T wave inversion with positive cardiac biomarkers.
UNSTABLE ANGINA: Prolonged, resting (or increasing) chest discomfort (or anginal equivalent) in a patient usually with ST segment depression or T wave inversion with negative cardiac biomarkers.
CLINICAL APPROACH
Pathophysiology
The most common cause of NSTEMI or UA is reduced coronary blood flow with resultant myocardial ischemia or infarction due to a nonocclusive thrombus that develops on an atherosclerotic plaque. Microembolization of thrombus and plaque components may also occur, resulting in downstream occlusion and subsequent infarction. Alternatively, an occlusive thrombus in patients with extensive coronary collateralization may precipitate NSTEMI/UA. Coronary plaques become vulnerable as a result of arterial inflammation with activated macrophages and T lymphocytes upregulating enzymes that cause plaque thinning and disruption such as metalloproteinases. Subsequent disruption of the fibrous cap exposes its thrombogenic components, initiating platelet activation and aggregation with resultant thrombus formation. Other causes of NSTEMI/UA include coronary spasm, severe luminal narrowing without spasm or thrombus formation due to progressive coronary artery disease, coronary dissection, or mismatch of myocardial perfusion and demand due to external factors such as fever, tachycardia, thyrotoxicosis, hypotension, hypoxemia, or anemia.
Clinical Presentation
Patients with NSTEMI or UA can have a variable presentation from recent-onset angina to progressively worsening angina within the past 48 hours to resting anginal pain (>20 minutes). Pain from UA/NSTEMI is more severe and of longer duration when compared to stable angina. NSTEMI is differentiated from UA by the presence of positive cardiac biomarkers. In general, patients with UA/NSTEMI are older and have more cardiac risk factors such as hypertension, hyperlipidemia, or diabetes when compared to patients with ST elevation myocardial infarction (STEMI). They are also more likely to have a prior history of myocardial infarction or to have undergone revascularization with PCI or coronary artery bypass grafting (CABG).
Associated symptoms include dyspnea, diaphoresis, palpitations, nausea, or vomiting. Diabetic patients, females, or the elderly may present without chest pain, describing only a nonspecific discomfort in combination with one of the aforementioned associated symptoms such as dyspnea or diaphoresis. The physical exam seldom adds to the diagnosis of UA/NSTEMI. Patients who present with signs of heart failure on exam (elevated jugular venous pressure, S3 gallop, or rales) are at increased risk for in-hospital morbidity and mortality. Documentation of the baseline physical exam is very important to recognize potential complications that may arise during their hospital stay, particularly the presence or absence of cardiac murmurs as a new murmur may indicate a mechanical complication related to myocardial infarction.
An ECG should be performed within 10 minutes of presentation and is helpful in risk-stratifying patients. Patients with ST segment depression of ≥0.5 mm or transient ST segment elevation as well as those with a preexisting left bundle branch block are at increased risk of death or myocardial infarction within 1 year. Other patients may present with new T wave inversions alone, which are less specific, although new, deep T wave inversions of ≥2 mm across the precordium usually are associated with ischemia, generally due to a severe lesion of the proximal left anterior descending artery (Wellens’ syndrome). Importantly, many patients do not present with any ischemic ECG changes, so lack of ECG changes is insufficient to rule out a diagnosis of UA/NSTEMI. In patients with ongoing chest pain suspicious for acute coronary syndrome (ACS), serial ECGs should be obtained every 15–30 minutes to monitor for the development of ST segment deviation.
Laboratory investigation is critical to differentiate between UA and NSTEMI. Clinically, UA and NSTEMI are indistinguishable. A diagnosis of NSTEMI is confirmed by the presence of positive cardiac biomarkers. Importantly, there is a time delay between when symptoms first start and the development of positive biomarkers. Contemporary cardiac biomarkers include creatine kinase (CK), creatine kinase myocardial band (CK-MB), troponin I (TnI), and troponin T (TnT). CK is present throughout skeletal tissue, whereas CK-MB is more specific to cardiac muscle. Both are released during NSTEMI and are measureable within 4–6 hours, peak within the first 24 hours, and normalize by 48–72 hours. TnI and TnT are both specific and sensitive for acute myocardial infarction. They are released within 4–8 hours after symptom onset and generally peak by 12–36 hours. Troponins may stay elevated for up to a week after an acute event. Given the aforementioned time delay, patients with negative cardiac biomarkers within 6 hours of symptom onset should have biomarkers remeasured within 8–12 hours after symptom onset. It is also common to trend biomarkers at 6–8-hour intervals 3 times or until levels have peaked to provide a measure of infarct size.
Differential Diagnosis
The differential for UA/NSTEMI is similar to STEMI that was discussed in Case 1. However, in this patient population, it is also important to explore for causes of secondary UA/NSTEMI, that is, disease that precipitates myocardial ischemia due to instigating a mismatch between myocardial oxygen supply and demand. For example, patients with an underlying high-grade coronary artery stenosis that is generally asymptomatic may present with anginal chest pain if they become tachycardic with increasing oxygen demand. This can be observed in patients who present with a supraventricular tachycardia or in patients who are septic with relative hypovolemia and compensatory tachycardia. Likewise, a patient with significant acute blood loss with resultant anemia may also develop supply demand mismatch due to hypovolemia with tachycardia as well as decreased oxygen-carrying capacity from loss of red blood cells. Other potential diagnoses that can cause supply demand mismatch include thyrotoxicosis, hypotension, or hypoxemia. In these cases of secondary UA/ NSTEMI, the primary goal is treatment of the underlying disease state. Once the patient has recovered from the acute illness, a search for significant coronary artery disease can be considered.
TREATMENT OF UA/NSTEMI
After diagnosis of UA/NSTEMI with the aforementioned criteria, the initial treatment goals include alleviation of ischemic pain, optimization of the patient’s hemodynamics, cardiac risk stratification, choosing a management strategy, and initiation of antithrombotic therapy. For relief of ischemic pain, sublingual nitroglycerin should be administered, and if pain continues after three tablets, intravenous nitroglycerin can be infused and titrated for pain relief. Intravenous nitroglycerin can also be administered to treat any concomitant hypertension. Likewise, beta-blockers can be used for those with suboptimal hemodynamics, such as hypertension or tachycardia, to decrease myocardial oxygen demand. Beta-blockers are also helpful for those with ongoing chest pain; however, they should be avoided in the acute setting when signs and symptoms of cardiogenic shock or hemodynamic compromise are present. Oxygen can be given to those with hypoxia or respiratory distress.
Various risk stratification models have been developed to identify patients who are at high risk and thus may benefit from an early invasive approach with cardiac catheterization. The “thrombolysis in myocardial infarction” (TIMI) risk score (see Table 2-1) is frequently used to help identify patients at high risk. Importantly, some factors in this risk score carry more weight than others. For example, patients with ST segment depression or elevated cardiac biomarkers are considered high risk regardless of the patient’s TIMI score.
Another important decision to be made when the patient initially presents is whether to pursue early invasive therapy versus an initially conservative approach. This decision depends on various factors and is summarized in Table 2-2. Patients undergoing an early invasive approach should undergo cardiac catheterization
[Data from Jneid H, Anderson JL, Wright RS, et al. 2012 ACCF/AHA focused update incorporated into the ACCF/AHA 2007 guidelines for the management of patients with unstable angina/ non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2012;61(23):e179–e347.]
within 24 hours of presentation. Patients for whom a conservative strategy is chosen should be optimized medically and undergo catheterization only should they develop recurrent ischemia or symptoms on optimized therapy. Low- and intermediate-risk patients who are initially managed conservatively should also undergo cardiac stress testing. If high-risk features are present on functional testing, cardiac catheterization should be considered.
With regard to antithrombotic therapy, all patients should be loaded with aspirin 325 mg. Patients who undergo an initially conservative approach should be loaded with clopidogrel 600 mg or ticagrelor 180 mg (preferred). Anticoagulation with low-molecular-weight heparin or fondaparinux is preferred, although unfractionated heparin can also be employed if needed. Patients treated with fondaparinux have a higher incidence of catheter- associated thrombosis, so if a patient treated with this agent ultimately undergoes catheterization, another anticoagulant should be used. In patients who are at higher risk (recurrent ischemic discomfort, dynamic ECG changes, or hemodynamic instability), a 48–72-hour GP IIb/IIIa (eptifibatide or tirofiban) infusion can be considered. It should be noted that most of these higherrisk patients should then proceed to catheterization.
Patients in whom an initial invasive approach is chosen should receive anticoagulation with unfractionated heparin, enoxaparin, or bivalirudin (preferred because of lower bleeding risk). They should also receive ADP inhibition with clopidogrel, ticagrelor, or prasugrel. GP IIb/IIIa inhibitors can be reserved for use during catheterization, although if bivalirudin is used as the anticoagulant, they are not necessary. Finally, it is important to note that there is no role for fibrinolytic agents in patients with UA/NSTEMI.
In addition to antiplatelet therapy described previously, a high-dose HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitor (statin), such as atorvastatin 80 mg daily, should be prescribed on presentation even if lipids are the goal. Beta-blockers should be started as soon as feasible and maintained indefinitely. An angiotensin-converting enzyme inhibitor (ACEI) should also be prescribed indefinitely in all patients with UA/NSTEMI and heart failure, an ejection fraction <40%, hypertension, or diabetes. Angiotensin receptor blockers (ARBs) are an alternative for those intolerant to ACEIs. Eplerenone, an aldosterone antagonist, also reduces morbidity and mortality in post-infarct patients with an EF <40%, even when added in combination with ACEIs, ARBs, and beta-blockers. Low-dose aspirin should be continued indefinitely, and ADP inhibitors should be maintained for at least a year.
COMPLICATIONS OF UA/NSTEMI
Complications of UA/NSTEMI are similar to those of STEMI discussed in Case 1, except that they occur much less frequently. In addition, complications that are observed more frequently in transmural infarction such as free wall rupture and ventricular septal rupture are much less common in patients with NSTEMI. Cardiogenic shock, however, can occur in up to 5% of patients with NSTEMI and is associated with greater than 60% mortality. Please refer to Case 1 for further discussion regarding complications of myocardial infarction.
SECONDARY PREVENTION
In addition to the long-term medical therapy discussed previously, other cardiac risk factors should be modified. Smoking cessation is imperative and is the most important action that a patient can take to prevent further cardiovascular morbidity and mortality. Many post–myocardial infarction patients are receptive to smoking cessation efforts and significant time should be spent engaging them in this endeavor. If the patient has hypertension or diabetes, their blood pressure and glucose levels should be optimized. Finally, for any patient on optimal medical therapy whose ejection fraction remains depressed 40 days after the event, an implantable cardioverter defibrillator (ICD) should be considered.
CASE CORRELATION
• See also Case 1 (acute coronary syndrome/STEMI).
COMPREHENSION QUESTIONS
2.1 An 83-year-old man with a medical history of coronary artery disease with three-vessel CABG, hypertension, and hyperlipidemia presents to the emergency department with lightheadedness and chest pain radiating down his left arm. The pain began approximately 2 hours ago and has progressively worsened throughout the day. He took one sublingual nitroglycerin at home that did not seem to help. He reports having several episodes of loose, dark stools earlier in the day. He appears to be in moderate distress. Pertinent findings on exam include a blood pressure of 94/52 mmHg, heart rate of 116 bpm, and oxygen saturation of 97%. His neck veins are flat. There is a left carotid bruit present. Lungs are clear to auscultation. Cardiac exam reveals a regular tachycardia with a soft systolic murmur at the right upper sterna border. There is mild epigastric tenderness on abdominal palpation. His extremities are cool to touch; there is no edema. A stat ECG is performed and shows sinus tachycardia with 2-mm ST depressions across the precordium. Currently, the patient reports an urge to defecate.
What is the next best step?
A. Obtain stat cardiac biomarkers
B. Administer aspirin, heparin, and ADP inhibitor
C. Activate the cardiac catheterization laboratory for immediate revascularization
D. Place two large-bore IVs
E. Initiate IV nitroglycerin and titrate until chest pain is relieved
2.2 A 68-year-old woman with a medical history of coronary artery disease with coronary artery stenting 4 months ago in a setting of inferior STEMI presents to the emergency department for evaluation of recurrent chest pain at rest that is unrelieved with nitroglycerin. She reports that the pain began about 45 minutes ago, is similar to her prior presentation with STEMI, and isn’t relieved with nitroglycerin. She reports faithful compliance with her cardioprotective medical regimen, including aspirin, clopidogrel, lisinopril, atorvastatin, and carvedilol. A recent follow-up echocardiogram showed an ejection fraction of 35%. Telemetry shows occasional nonsustained ventricular tachycardia. Stat ECG reveals 1.5 mm of ST depression in the lateral leads. Which feature of her presentation is not an indication for an early invasive approach in this patient with UA/NSTEMI?
A. Nonsustained ventricular tachycardia
B. Recent coronary artery stenting
C. Resting angina unrelieved with nitroglycerin
D. Left ventricular ejection fraction of 35%
E. ST segment depression
2.3 A 78-year-old woman is recovering after receiving percutaneous coronary intervention for NSTEMI approximately 6 hours ago. She received aspirin 325 mg, ticagrelor 180 mg, metoprolol 25 mg 3 times daily, atorvastatin 80 mg, and unfractionated heparin, and has eptifibatide infusing for another 8 hours. You are called to the bedside to assess the patient, who is complaining of moderate lower back pain and lightheadedness after sitting up from bed rest. Her current blood pressure is 88/57 mmHg with a heart rate of 87 bpm. Her neck veins are flat and her chest is clear to auscultation. Cardiac exam reveals regular rate and rhythm without murmurs, rubs, or gallops. The right femoral artery catheterization site is soft and nontender. Her extremities are cool, but all pulses are palpable. ECG shows sinus rhythm with nonspecific T wave changes similar to prior ECG.
What is the next best step?
A. Order an analgesic
B. Administer intravenous fluids
C. Return to cardiac catheterization laboratory
D. Obtain an echocardiogram
E. Order a noncontrast abdominal CT scan
2.4 A 58-year-old man with a medical history of coronary artery disease treated with PCI to the LAD 2 years ago and hyperlipidemia presents to the emergency room with precordial chest pain radiating down his left arm for the past 2 hours. Physical exam shows blood pressure of 136/77 mmHg, heart rate of 96 bpm, and oxygen saturation of 98%. His JVD is flat and pulmonary exam is unremarkable. Cardiac exam reveals regular rate and rhythm with an S4 gallop. Abdominal exam is benign, and his peripheries are warm. ECG shows 2-mm ST segment depressions in the anterior leads. He is administered aspirin 325 mg, ticagrelor 180 mg, and unfractionated heparin, and is started on a nitroglycerin infusion that has to be titrated to a high dose to achieve resolution of his chest pain. He is scheduled for cardiac catheterization at the end of the day. Just before he is transported out of the emergency department, he begins to experience long runs of ventricular tachycardia associated with lightheadedness. Blood pressure obtained during one of these long runs is 89/54 mmHg. He reports that his chest pain is beginning to return.
What is the next best step?
A. Continue to titrate nitroglycerin for pain relief
B. Obtain an echocardiogram
C. Proceed immediately to the catheterization laboratory for angiography
D. Administer IV metoprolol
E. Administer IV dobutamine
ANSWERS
2.1 D. This patient is most likely presenting with UA/NSTEMI due to acute blood loss from a gastrointestinal bleed with a resultant mismatch in myocardial oxygen supply versus demand. The most important action is to place two large-bore IVs in preparation for volume resuscitation. A stat complete blood count and type and screen should be performed immediately, followed by packed red blood cell transfusion. The patient has no signs or symptoms of heart failure, and thus normal saline can be administered while waiting for blood. His volume status could be further investigated by carefully performing orthostatic vital signs, which would likely be markedly positive. An intravenous proton pump inhibitor should be administered, and the patient should undergo urgent evaluation by a gastroenterologist for likely endoscopy. Cardiac biomarkers are likely to be positive in this patient, although this would not affect your management in the acute setting. Likewise, sending the patient to the catheterization laboratory is not indicated as he is unlikely to be experiencing myocardial ischemia due to an occluded coronary artery. In a patient with active gastrointestinal bleeding, antiplatetet agents and anticoagulants are contraindicated. Furthermore, this patient is volume-depleted, and thus administration of nitroglycerin is not indicated and may even exacerbate his symptoms.
2.2 A. Patients presenting with UA/NSTEMI deemed high risk should be considered for an early invasive approach. Sustained ventricular tachycardia, not nonsustained ventricular tachycardia, is considered a high-risk feature, as are the other possible answer choices. Please refer to Table 2-2 to review factors that favor an early invasive strategy.
2.3 B. This patient has symptoms suggesting a retroperitoneal bleed with hypotension, lightheadedness with position change, and cool extremities. Her heart rate remains relatively low because she is treated with a beta-blocker. This is a potential complication of cardiac catheterization, and one must always consider this diagnosis in the postcatheterization patient with back pain, especially when there are also signs of hypovolemia. This is a potentially life-threatening diagnosis that should be immediately treated empirically with volume resuscitation. A stat hemoglobin and type and screen should be also obtained. Only after the patient is stabilized and volume-resuscitated should a confirmatory noncontrast abdominal CT scan be obtained. Should the patient not respond to IV fluids and/or blood transfusion, vascular surgery should be consulted. While patients can develop back discomfort due to prolonged bedrest after a cardiac catheterization, it is important to first rule out a more ominous etiology for the patient’s pain. The patient is not experiencing any signs or symptoms of ischemia and repeat ECG is unremarkable; thus, a return to the catheterization laboratory is not indicated. There is no evidence of tamponade (which might occur if there were a coronary artery perforation during the catheterization), JVD is flat, and there are no new cardiac findings on physical exam, so an echocardiogram is not likely to be helpful.
2.4 C. Any patient with UA/NSTEMI who develops or presents with hemodynamic instability, cardiogenic shock, ongoing chest pain despite aggressive medical therapy, new or worsening mitral regurgitation, or sustained ventricular arrhythmias should proceed immediately to the catheterization laboratory for coronary angiography. This patient has now developed sustained ventricular tachycardia associated with hemodynamic instability and thus should be referred for emergent angiography. The patient is already on a high dose of nitroglycerin, and thus further titration will unlikely be helpful. Furthermore, his blood pressure is now tenuous, so this agent should be used carefully. Likewise, intravenous metoprolol in a patient with hemodynamic instability is unlikely to be helpful, although one could consider loading with intravenous amiodarone to try to suppress his arrhythmia. Dobutamine administration would not definitively address this patient’s underlying problem and might exacerbate it by further precipitating arrhythmias and increasing myocardial oxygen demand. An echocardiogram is unlikely to provide any additional pertinent information at this time.
CLINICAL PEARLS
C UA/NSTEMI is typically dite to reduced blood flow with subsequent myo cardial ischernia or infarction in the setting of a nonocclusive thrombus that forms on an atherosclerotic plaque.
C UA and NSTEMI are clinically indistinguishable. NSTEMI is characterized by the presence of positive cardiac biomarkers. whereas patients with UA have negative cardiac biomarkers.
C UA/NSTEMI may present with ST segment depression. T wave inversion, or no ECG changes at all. Patients in this later group who have ongoing chest pain concerning for ACS should receive a repeat ECG every 15—30 minutes to monitor for ischemic changes.
C UA/NSTEMI patients should be risk-stratified and referred for an early invasive therapy if indicated (seel Tables 2-1 and 2-2).
C Post-NSTEMI care includes monitoring for potential electrical or mechanical complications of ACS.
C risk factor modification and maintenance of an evidence-based medical regimen are essential for secondary prevention.
References
Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000;284(7):835.
Cannon CP, Braunwald E. Unstable angina and non-ST elevation myocardial infarction. In: Bonow RO, Mann DL, Zipes DP, Libby P, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia, PA: Saunders/Elsevier; 2012:1178–1209.
Harvey JE. Unstable angina and non-ST-segment elevation myocardial infarction. In: Griffin BP, ed. Manual of Cardiovascular Medicine. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012: 36–59.
Jneid H, Anderson JL, Wright RS, et al. 2012 ACCF/AHA focused update incorporated into the ACCF/ AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction. J Am Coll Cardiol. 2012;61(23):e179–e347.
May CH, Lincoff AM. Antiplatelet agents in ischemic heart disease. In: Gresele P, Born GVR, Patrono C, Page CP, eds. Antiplatelet Agents. London, UK: Springer; 2012:495–518.
Smith SC Jr, Benjamin EJ, Bonow RO, et al. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update. J Am Coll Cardiol. 2011;58(23):2432–2446.
 Case File Eugene C. Toy, Md, Michael d . Faulx, Md Case 2 A 73-yearld woman presen...){kind=link}
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