Acute Coronary Syndrome

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Author

Drew Evan Fenton, MD, FAAEM, Private Practice

Nothing to disclose.

Specialty Editor(s)

Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University

Nothing to disclose.

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

eMedicine Salary Employment

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Nothing to disclose.

Chief Editor

David FM Brown, MD, Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

Nothing to disclose.

Background

The initial diagnosis of acute coronary syndrome (ACS) is based on history, risk factors, and, to a lesser extent, ECG findings. The symptoms are due to myocardial ischemia, the underlying cause of which is an imbalance between supply and demand of myocardial oxygen.

Patients with ACS include those whose clinical presentations cover the following range of diagnoses: unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). This ACS spectrum concept is a useful framework for developing therapeutic strategies.


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A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a....


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A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complai....

Pathophysiology

Myocardial ischemia is most often due to atherosclerotic plaques, which reduce the blood supply to a portion of myocardium. Initially, the plaques allow sufficient blood flow to match myocardial demand. When myocardial demand increases, the areas of narrowing may become clinically significant and precipitate angina. Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest, and without recent change in frequency or severity of activity that produce symptoms, is called chronic stable angina. Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombus forms. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina.

Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery. Angiographic evidence of coronary thrombus formation may be seen in more than 90% of patients with STEMI but in only 1% of patients with stable angina and about 35-75% of patients with unstable angina or NSTEMI. However, not every STEMI evolves into a Q-wave myocardial infarction (MI); likewise, a patient with NSTEMI may develop Q waves.

The excessive mortality rate of coronary heart disease is primarily due to rupture and thrombosis of the atherosclerotic plaque. Inflammation plays a critical role in plaque destabilization and is widespread in the coronary and remote vascular beds. Systemic inflammatory, thrombotic, and hemodynamic factors are relevant to the outcome. Evidence indicates that platelets contribute to promoting plaque inflammation as well as thrombosis. A new theory of unbalanced cytokine-mediated inflammation is emerging, providing an opportunity for intervention.

A less common cause of angina is dynamic obstruction, which may be caused by intense focal spasm of a segment of an epicardial artery (Prinzmetal angina). Coronary vasospasm is a frequent complication in patients with connective tissue disease. Other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, such as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina as a baseline medical condition.

Spontaneous and cocaine-related coronary artery dissection remains an unusual cause of ACS and should be included in the differential diagnosis, especially when a younger female or cocaine user is being evaluated. An early clinical suspicion of this disease is necessary for a good outcome. Cardiology consultation should be obtained for consideration for urgent percutaneous coronary intervention.

Although rare, pediatric and adult ACS may result from the following (see Myocardial Infarction in Childhood):

Irrespective of the cause of unstable angina, the result of persistent ischemia is MI.

Epidemiology

Frequency

United States

Although the exact incidence of ACS is difficult to ascertain, hospital discharge data indicate that 1,680,000 unique discharges for ACS occurred in 2001.

International

In Britain, annual incidence rate of angina is estimated at 1.1 cases per 1000 males and 0.5 cases per 1000 females aged 31-70 years. In Sweden, chest pain of ischemic origin is thought to affect 5% of all males aged 50-57 years. In industrialized countries, annual incidence rate of unstable angina is approximately 6 cases per 10,000 people.

Mortality/Morbidity

When the only therapy for angina was nitroglycerin and limitation of activity, patients with newly diagnosed angina had a 40% incidence of MI and a 17% mortality rate within 3 months. A recent study shows that the 30-day mortality rate from ACS has decreased as treatment has improved, a statistically significant 47% relative decrease in 30-day mortality rate among newly diagnosed ACS from 1987-2000. This decrease in mortality rate is attributed to aspirin, glycoprotein (GP) IIb/IIIa blockers, and coronary revascularization via medical intervention or procedures.

Clinical characteristics associated with a poor prognosis include advanced age, male sex, prior MI, diabetes, hypertension, and multiple-vessel or left-mainstem disease.

Sex

Incidence is higher in males among all patients younger than 70 years. This is due to the cardioprotective effect of estrogen in females. At 15 years postmenopause, the incidence of angina occurs with equal frequency in both sexes. Evidence exists that women more often have coronary events without typical symptoms, which might explain the frequent failure to initially diagnose ACS in women.

Age

ACS becomes progressively more common with increasing age. In persons aged 40-70 years, ACS is diagnosed more often in men than in women. In persons older than 70 years, men and women are affected about equally.

History

Physical

Causes

Laboratory Studies

Imaging Studies

Chest radiograph may demonstrate complications of ischemia, such as pulmonary edema, or it may provide clues to alternative causes of symptoms, such as thoracic aneurysm or pneumonia.

Echocardiogram often demonstrates wall motion abnormalities due to ischemia. It is of limited value in patients whose symptoms have resolved or in those with preexisting wall motion abnormalities. However, echocardiogram may be useful in identifying precipitants for ischemia, such as ventricular hypertrophy and valvular disease.

Radionuclide myocardial perfusion imaging has been shown to have favorable diagnostic and prognostic value in this setting, with an excellent early sensitivity to detect acute myocardial infarction (MI) not achieved by other testing modalities.

Recent advances include CT coronary angiography and CT coronary artery calcium scoring.

Technetium-99m (99mTc) tetrofosmin single-photon emission computed tomography (SPECT) is a useful method to exclude high-risk patients among patients with chest pain in the emergency department.

Resting cardiac magnetic resonance imaging (MRI) has exhibited diagnostic operating characteristics suitable for triage of patients with chest pain in the ED. Performed urgently to evaluate chest pain, MRI accurately detected a high fraction of patients with ACS, including patients with enzyme-negative unstable angina. MRI can identify wall thinning, scar, delayed enhancement (infarction), and wall motion abnormalities (ischemia). Coronary artery assessment may be coupled with magnetic resonance (MR) angiography in the future.

Other Tests

Prehospital Care

Generally, patients transported with chest pain should initially be managed under the assumption that the pain is ischemic in origin. Prehospital interventions should be guided by the nature of the presenting complaint, individual risk factors, and associated symptoms (eg, breathing difficulty, hemodynamic instability, appearance of ectopy). Airway, breathing, and circulation should be rapidly assessed with institution of CPR, ACLS-guided interventions, or other measures as indicated for the unstable patient.

Emergency Department Care

The ACS spectrum concept is a useful framework for developing therapeutic strategies. Antithrombin therapy and antiplatelet therapy should be administered to all patients with an ACS regardless of the presence or the absence of ST-segment elevation. Patients presenting with persistent ST-segment elevation are candidates for reperfusion therapy (either pharmacological or catheter based) to restore flow promptly in the occluded epicardial infarct-related artery. Patients presenting without ST-segment elevation are not candidates for immediate pharmacological reperfusion but should receive anti-ischemic therapy and PCI when appropriate. "Time is myocardium" is a dictum to be remembered as survival has been shown to correlate with time to reperfusion in patients with acute MI. Many centers set goals for, and routinely record, door-to-ECG, door-to-needle (thrombolytic therapy), or door-to-vascular access (for patients receiving PCI) times as measures of quality of care provided.

Rathore et al found that any delay in primary percutaneous coronary intervention after a patient with ST-elevation myocardial infarction (STEMI) arrives at hospital is associated with higher mortality.[9] In a prospective cohort study of 43,801 patients enrolled in the American College of Cardiology National Cardiovascular Data Registry, 2005-2006, longer door-to-balloon times were associated with a higher adjusted risk of in-hospital mortality, in a continuous nonlinear fashion (30 min = 3%, 60 min = 3.5%, 90 min = 4.3%, 120 min = 5.6%, 150 min = 7%, 180 min = 8.4%, P< 0.001). A reduction in door-to-balloon time from 90 minutes to 60 minutes was associated with 0.8% lower mortality, and a reduction from 60 minutes to 30 minutes was associated with a 0.5% lower mortality.

A recent study by Ryan et al sought to determine if point-of-care cardiac marker testing decreased length of stay in patients being evaluated for acute coronary syndrome in the ED.[10] Patients were randomized to 2 groups, with 1000 patients in each group: one having point-of-care markers and central laboratory markers and one having central laboratory markers only. Median time to discharge home was 4.6 hours (3.5-6.1 h) in central laboratory only patients and 4.5 hours (3.5-6.1 h) in the point-of-care patients.

Median time to transfer to an inpatient setting for admitted patients was 5.5 hours (4.2-7.5 h) in the central laboratory patients, and 5.4 hours (4.1-7.3 h) in point-of-care group patients. Time to transfer to the floor was reduced in the point-of-care group at one site, compared with the laboratory group (difference in medians 0.45 h; 95% confidence interval [CI] -0.14 to 1.04 h). Time to ED departure for discharged patients was higher in the point-of-care group than in the laboratory group (difference in medians 1.25 h; 95% CI 0.13 to 2.36 h) at one site.[10]

Results between the EDs varied, with one showing that point-of-care testing decreased time to admission, and another showing that point-of-care testing increased time to discharge. Ryan et al concluded that the potential effects of point-of-care testing in the ED for patient throughput should be considered in the full context of ED operations.

Treatment and evaluation guidelines are available from various sources including the American College of Emergency Physicians, American College of Chest Physicians, and National Academy of Clinical Biochemistry.[11, 12, 13]

Consultations

Cardiology or interventional cardiology consultation may be indicated for patients with any of the following:

The Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial studied the impact of age on outcomes in moderate- and high-risk non-ST-segment elevation acute coronary syndrome (NSTE-ACS). Outcomes were analyzed at 30 days and 1 year in 4 age groups, overall and among those undergoing percutaneous coronary intervention (PCI). Of 13,819 patients in the ACUITY trial, 3,655 (26.4%) were younger than 55 years of age, 3,940 (28.5%) were aged 55-64 years, 3,783 (27.4%) were aged 65-74 years, and 2,441 (17.7%) were 75 years or older. Older patients had more cardiovascular risk factors and had a higher acuity at presentation. Patients aged 75 years or older treated with bivalirudin alone had similar ischemic outcomes but significantly lower rates of bleeding compared with those treated with heparin and glycoprotein IIb/IIIa inhibitors overall and in the PCI subset.[14]

Another analysis from the ACUITY study data found patients with more than a 24-hour delay to cardiac catheterization had increased 30-day and 1-year mortality rates.[15]

Medication Summary

The goals of treatment are to preserve patency of the coronary artery, augment blood flow through stenotic lesions, and reduce myocardial oxygen demand. All patients should receive antiplatelet agents, and patients with evidence of ongoing ischemia should receive aggressive medical intervention until signs of ischemia, as determined by symptoms and ECG, resolve.

The value of aspirin in primary prophylaxis for cardiovascular diseases was challenged in the Aspirin for Asymptomatic Atherosclerosis trial. In this double-blind randomized controlled trial, 28,980 men and women aged 50-75 years living in central Scotland, and recruited from a community health registry, who were free of clinical cardiovascular disease, but at higher risk of atherosclerosis and an increased risk of cardiovascular and cerebrovascular events based on low ankle brachial index (ABI), were given 100 mg aspirin (enteric coated) or placebo.

The primary end point was a composite of initial fatal or nonfatal coronary event or stroke or revascularization. Secondary end points included angina, intermittent claudication, or transient ischemic attack; as well as all-cause mortality. After a mean (SD) follow-up of 8.2 (1.6) years, none of the study end points showed statistically significant difference between groups. The rate of an initial event of major hemorrhage requiring admission to hospital was not also statistically different between the groups. Note though that this study was powered to detect a 25% proportional risk reduction in events, which may not have been achieved.[16, 17]

Class Summary

These agents inhibit the cyclooxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator. Antiplatelet therapy has been shown to reduce mortality rates by reducing the risk of fatal strokes and fatal myocardial infarctions.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Clinical Context:  Early administration of aspirin in patients with AMI may reduce cardiac mortality in first month.

Class Summary

These agents oppose coronary artery spasm and reduce myocardial oxygen demand by reducing both preload and afterload.

Nitroglycerin (Nitro-Bid)

Clinical Context:  Causes relaxation of the vascular smooth muscle via stimulation of intracellular cyclic guanosine monophosphate production, causing a decrease in blood pressure.

Class Summary

These agents reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

Clinical Context:  DOC for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone.

Morphine sulfate administered IV may be dosed in a number of ways and commonly titrated until desired effect obtained.

Class Summary

These agents are used to prevent recurrence of clot after a spontaneous fibrinolysis.

Heparin

Clinical Context:  Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents recurrence of a clot after spontaneous fibrinolysis.

Class Summary

These agents have antiarrhythmic and antihypertensive properties as well as ability to reduce ischemia. They minimize the imbalance between myocardial supply and demand by reducing afterload and wall stress. In patients with acute MI, they have been shown to decrease infarct size as well as short- and long-term mortality, which is a function of their anti-ischemic and antiarrhythmic properties.

Metoprolol (Lopressor)

Clinical Context:  Selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions.

During IV administration, carefully monitor blood pressure, heart rate, and ECG. Goal of treatment is to reduce heart rate to 60-90 beats/min.

Esmolol (Brevibloc)

Clinical Context:  Excellent drug for use in patients at risk for complications from beta-blockers, particularly reactive airway disease, mild-to-moderate LV dysfunction, and peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect with ability to stop quickly prn.

Class Summary

Glycoprotein (GP) IIb/IIIa antagonists prevent the binding of fibrinogen, thereby blocking platelet aggregation. Studies to date suggest that as a class, the addition of intravenous GP IIb/IIIa inhibitors to aspirin and heparin improves both early and late outcomes, including mortality, Q-wave MI, need for revascularization procedures, and length of hospital stay.

Currently, IIb/IIIb antagonists in combination with aspirin are considered standard antiplatelet therapy for patients at high risk for unstable angina. Adenosine diphosphate (ADP) antagonists are not considered standard therapy but may be used in patients unable to tolerate aspirin.

Abciximab (ReoPro)

Clinical Context:  Chimeric human-murine monoclonal antibody. Binds to receptor with high affinity and reduces platelet aggregation by 80%. Inhibition of platelet aggregation persists for up to 48 h after end of infusion.

Abciximab has been approved for use in elective/urgent/emergent percutaneous coronary intervention.

Eptifibatide (Integrilin)

Clinical Context:  Antagonist of the platelet GP IIb/IIIa receptor, which reversibly prevents von Willebrand factor, fibrinogen, and other adhesion ligands from binding to the GP IIb/IIIa receptor. End effect is the inhibition of platelet aggregation. Effects persist over duration of maintenance infusion and are reversed when infusion ends.

Tirofiban (Aggrastat)

Clinical Context:  Nonpeptide antagonist of GP IIb/IIIa receptor. Reversible antagonist of fibrinogen binding. When administered IV, more than 90% of platelet aggregation inhibited.

Approved for use in combination with heparin for patients with unstable angina who are being treated medically and for those undergoing PCI.

Class Summary

Low molecular weight heparin (enoxaparin) has been shown to reduce cardiac ischemic events and death by as much as 15% in patients with unstable angina. The benefits appear to be sustained at 1 year, with a 13% reduction in patients requiring coronary artery bypass graft (CABG) or percutaneous transluminal coronary angioplasty (PTCA) and a 15% reduction in death or AMI. These clinical effects have been reported with all patients also receiving aspirin.

One systematic review comparing low molecular weight heparin (LMWH) with unfractionated heparin found no significant difference in benefits between the two. The advantages of using LMWH over unfractionated heparin are ease of administration, absence of need for anticoagulation monitoring, safety profile, and potential for overall cost savings. Although 3 LMWHs are approved for use in the United States, only enoxaparin is currently approved for use in unstable angina. Lev et al found that the combination of eptifibatide with enoxaparin appears to have a more potent antithrombotic effect than that of eptifibatide and unfractionated heparin (UFH).[18]

Enoxaparin (Lovenox)

Clinical Context:  LMWH is produced by partial chemical or enzymatic depolymerization of UFH. Binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). LMWH differs from unfractionated heparin by having a higher ratio of antifactor Xa to antifactor IIa compared with UFH. Maximum antifactor Xa and antithrombin activities occur 3-5 h after administration.

Indicated for treatment of acute ST-segment elevation myocardial infarction (STEMI) managed medically or with subsequent percutaneous coronary intervention (PCI). Also indicated as prophylaxis of ischemic complications caused by unstable angina and non-Q-wave MI.

Class Summary

Hirudin is the prototype of direct thrombin inhibitors. Hirudin binds directly to the anion binding site and the catalytic sites of thrombin to produce potent and predictable anticoagulation.

Hirudin (Lepirudin, Refludan)

Clinical Context:  When compared with unfractionated heparin in unstable angina trials, hirudin demonstrated a modest short-term reduction in the composite end point of death or nonfatal MI. Risk of bleeding is increased modestly. Currently, hirudin is indicated only in patients unable to receive heparin because of heparin-induced thrombocytopenia.

Bivalirudin (Angiomax)

Clinical Context:  Synthetic analogue of recombinant hirudin. Inhibits thrombin. Used for anticoagulation in unstable angina undergoing PTCA. With provisional use of glycoprotein IIb/IIIa inhibitor (GPIIb/IIIa inhibitor) indicated for use as anticoagulant in patients undergoing PCI. Potential advantages over conventional heparin therapy include more predictable and precise levels of anticoagulation, activity against clot-bound thrombin, absence of natural inhibitors (eg, platelet factor 4, heparinase), and continued efficacy following clearance from plasma (because of binding to thrombin).

Class Summary

Two thienopyridines, clopidogrel and ticlopidine, are ADP antagonists that are approved for antiplatelet activity. Both have irreversible antiplatelet activity but take several days to manifest. A potential additive benefit exists when ADP antagonists are used in conjunction with aspirin.

These drugs may be considered alternatives to aspirin in patients intolerant or allergic to aspirin.

Literature continues to emerge regarding whether the use of proton pump inhibitors (PPIs) interferes with clopidogrel following MI.

Results from the Clopidogrel and the Optimization of Gastrointestinal Events Trial (COGENT) found no apparent cardiovascular interaction between clopidogrel and omeprazole, even in high-risk subgroups. This study did not rule out a clinically meaningful difference in cardiovascular events resulting from PPI use. The authors noted several limitations of the study. The study was prematurely halted, and it used an investigational combination product of omeprazole and clopidogrel, therefore limiting its power to fully evaluate anticipated end results. Additionally, the confidence interval of the hazard ratio for cardiovascular events is wide; thus, the absence of omeprazole interacting with clopidogrel cannot be definitively determined.[19]

Some concern exists about possible interaction between proton pump inhibitors (PPIs) and clopidogrel, resulting in decreased effectiveness of clopidogrel. This concern was addressed in a nationwide retrospective cohort study in Denmark. Charlot et al found that combined use of PPIs and clopidogrel was not associated with increased adverse cardiovascular events over that observed for patients prescribed PPI alone.[20] For concomitant use of a PPI and clopidogrel among the cohort assembled at day 30 after discharge, the hazard ratio was 1.29 (95% confidence interval [CI], 1.17-1.42) for cardiovascular death or rehospitalization for MI or stroke. For use of a PPI in patients who did not receive clopidogrel, the hazard ratio was 1.29 (CI, 1.21-1.37). No statistically significant interaction between a PPI and clopidogrel (P = 0.72) was noted.

The cause of increased cardiovascular risk in all patients who received PPI may be explained by significant differences in baseline comorbid conditions. Although the authors used 2 different methods for statistical analysis trying to adjust for known differences, other unmeasured confounders as well as proxy assumptions may not have been accounted for.

The use of observational studies did not show clinical evidence for PPIs interfering with the effectiveness of clopidogrel, although the potential for observational studies to be misleading should be kept in mind. Use of ex vivo antiplatelet testing to examine the interaction may be potentially misleading.[21]

A consensus statement issued by the American College of Cardiology, American College of Gastroenterology, and American Heart Association in November 2010 addresses the issue of concomitant use of proton pump inhibitors (PPIs) and thienopyridine antiplatelet drugs.[22]

The group's findings and recommendations are listed below.

Clopidogrel (Plavix)

Clinical Context:  Generally preferred over ticlopidine because it more rapidly inhibits platelets and appears to have a more favorable safety profile.

Ticlopidine (Ticlid)

Clinical Context:  Beneficial effects were noted in patients with UA after 2 wk of use in one randomized trial. When compared to controls, ticlopidine use decreased vascular deaths and nonfatal MIs.

Further Inpatient Care

Patients with unstable angina, ECG changes, or both should be admitted to a telemetry bed. A certain subset of patients with stable angina may be treated as outpatients with antianginal agents, but close follow-up is necessary.

Patients with symptoms refractory to aggressive medical treatment, shock, suspected or known aortic stenosis, or new or worsening mitral regurgitation are at high risk. Management for these patients should include the following: admission to an intensive care unit setting and cardiology consultation.

Intra-aortic balloon pump (IABP) and early angiography to delineate anatomy should be considered.

Antiplatelet and antianginal medications initiated in the ED should be continued. Subsequent dosing is determined by symptomatic response and tolerance of side effects.

The routine use of lidocaine as prophylaxis for ventricular arrhythmias in patients with ACS is not indicated. In MI, it has been shown to increase mortality rates. Lidocaine may be used for patients with complex ventricular ectopy or for patients with hemodynamically significant, nonsustained, or sustained ventricular tachycardia.

Mehta et al studied 3031 patients with acute coronary syndromes. Early intervention (coronary angiography ≤ 24 h after randomization; median time 14 h) in acute coronary syndromes did not differ greatly from delayed intervention (coronary angiography >24 h randomization; median time 50 h) in preventing the primary outcome (ie, composite of death, myocardial infarction, or stroke at 6 mo). Early intervention did reduce the rate of the secondary outcome (ie, death, myocardial infarction, or refractory ischemia at 6 mo) and improved the primary outcome in patients who were at highest risk (ie, Global Registry of Acute Coronary Events [GRACE] risk score >140).[23]

Further Outpatient Care

Patients with chronic stable angina may be considered for discharge after occurrence of the following:

When in doubt, admit. The usual reason for a patient with chronic stable angina to present to the ED is a change in pattern or severity of symptoms, which makes their angina unstable.

A study by Bartholomew et al may be helpful in making the decision to admit or discharge. This prospective thrombolysis in myocardial infarction risk score (TIMI-RS) used 7 variables in patients with suspected ACS: (1) age older than 65 years, (2) 3 or more cardiac risk factors, (3) ST deviation, (4) aspirin use within 7 days, (5) 2 or more anginal events over 24 hours, (6) history of coronary stenosis, and (7) elevated troponin levels. Patients were contacted at 30 days, and data were collected concerning major adverse cardiac events.[24]

In patients presenting with chest pain, a higher TIMI-RS was associated with an increase in major adverse cardiac events within 30 days. The authors concluded that the 30-day event rate was 0% for a score of 1, 20% for a score of 2, 24% for a score of 3, 42% for a score of 4, 52% for a score of 5, and 70% for a score of 6 or 7 (p < 0.0001).

The TIMI-RS successfully differentiates early risk for major adverse cardiac events in a general population presenting with symptoms suggestive of ACS. A simple bedside calculation of the TIMI-RS provides rapid risk stratification, allowing facilitation of therapeutic decision-making in patients with symptoms suggestive of ACS and may be helpful with the patient's disposition.

Inpatient & Outpatient Medications

Inpatient and outpatient medications may include the following:

Transfer

Consider transfer only for patients at particularly high risk and for those who are being evaluated in a center without access to timely cardiac catheterization, PTCA, or bypass.

High-risk criteria include the following:

The risks of transferring these unstable patients must be carefully weighed against the benefits of transfer.

Deterrence/Prevention

Deterrence/prevention of ACS may include the following:

Complications

Complications of ACS may include the following:

Prognosis

Patients with angina either proceed to infarct or have their disease stabilized by medical and/or interventional therapies. Patients with angina are a heterogeneous group; therefore, prognosis varies with respect to stability of disease, demographics, comorbidity, and current intervention.

Patients with ACS with atrial fibrillation (AF) are associated with increased morbidity and mortality.[26]

Patients with ACS and diabetes mellitus, especially those with ST elevation, had increased in-hospital mortality rates. Among patients with ACS and diabetes mellitus, those receiving insulin had worse outcomes. Outcomes were similar for those on hypoglycemic medication or on diet alone.[27]

In chronic stable angina, prognosis is generally excellent. Factors that have been shown to impact prognosis include the following:

In unstable angina, prognosis is determined by the ability to control symptoms acutely, preventing progression to AMI. Factors associated with a poorer prognosis include the following:

References

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  14. [Best Evidence] Lopes RD, Alexander KP, Manoukian SV, Bertrand ME, Feit F, White HD, et al. Advanced age, antithrombotic strategy, and bleeding in non-ST-segment elevation acute coronary syndromes: results from the ACUITY (Acute Catheterization and Urgent Intervention Triage Strategy) trial. J Am Coll Cardiol. Mar 24 2009;53(12):1021-30.[View Abstract]
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A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and ECG changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta-blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.

A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure 140/90 mm Hg and heart rate is 98. Her ECG is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.

A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and ECG changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta-blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.

A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure 140/90 mm Hg and heart rate is 98. Her ECG is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.