Acute Coronary Syndrome Treatment & Management

  • Author: David L Coven, MD, PhD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Feb 21, 2012
 

Approach Considerations

Initial therapy for acute coronary syndrome should focus on stabilizing the patient's condition, relieving ischemic pain, and providing antithrombotic therapy to reduce myocardial damage and prevent further ischemia. Morphine (or fentanyl) for pain control, oxygen, sublingual and/or IV nitroglycerin, soluble aspirin 162-325 mg, and clopidogrel with a 300- to 600-mg loading dose are given as initial treatment.

In complete vessel occlusion without collateralization of the infarct-related vessel, there is little utility in “pushing nitrates.”

High-risk patients with non-ST-segment elevation myocardial infarction (NSTEMI ACS) should receive aggressive care, including aspirin, clopidogrel, unfractionated heparin or low–molecular weight heparin (LMWH), intravenous platelet glycoprotein IIb/IIIa complex blockers (eg, tirofiban, eptifibatide), and a beta blocker. The goal is early revascularization.

Intermediate-risk patients with NSTEMI ACS should rapidly undergo diagnostic evaluation and further assessment to determine their appropriate risk category.

Low-risk patients with NSTEMI ACS should undergo further follow-up with biomarkers and clinical assessment. Optimal medical therapies include use of standard medical therapies, including beta blockers, aspirin, and unfractionated heparin or LMWH. The Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) study showed that clopidogrel would be beneficial even in low-risk patients.[49] If no further pain occurs, and follow-up studies are negative, a stress study should drive further management.

Monitor and immediately treat arrhythmias in the first 48 hours. Pay attention to exacerbating factors, such as disturbances in electrolytes (especially potassium and magnesium), hypoxemia, drugs, or acidosis. Correct these factors accordingly.

Humidified oxygen may reduce the risk of nosebleeds in patients with ACS who are receiving antiplatelet and antithrombin therapy.

Do not administer nitrates if the patient is hypotensive (systolic BP < 90 mm Hg); if RV infarction, large pericardial effusion, or severe aortic stenosis is suspected; or if the patient recently received phosphodiesterase-5 inhibitors (eg, sildenafil).

Patients with known hypersensitivity to antiplatelet agents, active internal bleeding, and bleeding disorders should not receive antiplatelet or antithrombotic therapy.

Some patients with intractable chest pain or severe hypotension may require the insertion of an intra-aortic balloon pump. The EuroHeart survey showed a nearly 40% reduction in the risk of death in patients with ACS who received support with an intra-aortic balloon pump. This benefit was independent of the status of the ST segment.

Congestive heart failure (CHF) can be due to systolic dysfunction or diastolic dysfunction in the setting of myocardial infarction. Aggressive treatment is indicated to prevent worsening of the situation.

Patients presenting with cardiogenic shock should undergo percutaneous coronary intervention (PCI) as soon as possible. Cardiogenic shock is associated with a high mortality rate. Pressor agents, such as dopamine, and inotropic agents, such as dobutamine, may be needed. In a prospective, natural-history study of coronary atherosclerosis, patients underwent 3-vessel coronary angiography and gray-scale and radiofrequency intravascular ultrasonographic imaging after PCI.[50]

Recurrent ischemia may be due to incomplete reperfusion. In the setting of PCI, consider stent thrombosis as a possible cause. Whether drug-eluting stents have an increased rate of thrombosis compared with bare metal stents is unclear.

Drug-eluting stents are linked with fewer periprocedural risks but tend to have high incidence of postprocedural complications including myocardial infarction, repeat procedures, and 12-month major adverse cardiac and brain complications, compared with coronary bypass surgery.[51]

One study by Ribichini et al suggests that prednisone treatment after bare metal stents or drug-eluting stent implantation results in a better event-free survival at 1 year.[52]

In the final report of the HORIZONS-AMI trial, which assessed the 3 year outcomes of the effectiveness and safety of bivalirudin monotherapy and paclitaxel-eluting stenting, outcomes were sustained for patients with STEMI undergoing primary PCI.[53]

In a study of 3031 patients, Mehta et al found that early intervention (coronary angiography < or = 24 h after randomization) in patients with ACS did not differ greatly from delayed intervention (coronary angiography > or = 36 h randomization) in the prevention of primary outcomes (ie, composite of death, myocardial infarction, or stroke at 6 mo). Early intervention did reduce the rate of secondary outcomes (ie, death, myocardial infarction, or refractory ischemia at 6 mo) and improved primary outcomes in patients who were at highest risk (ie, GRACE risk score >140).[54]

In a Swedish registry of patients with STEMI from 1996-2007, reported an increase in the prevalence of evidence-based treatments.[55] The use of aspirin, clopidogrel, beta blockers, statins, and ACE inhibitors all increased. Clopidogrel increased from 0% to 82%, statins increased from 23% to 83%, and various ACE inhibitors increased by a large margin. A decrease was reported in 30-day and 1-year mortality that was sustained during long-term follow-up. By following the proper guidelines, patients who have experienced STEMI have higher survival rates.

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Pharmacologic Anti-ischemic Therapy

Nitrates

Nitrates do not improve mortality.[56] However, they provide symptomatic relief by means of several mechanisms, including coronary vasodilation, improved collateral blood flow, decrease in preload (venodilation and reduced venous return), and decrease in afterload (arterial vasodilation). Care should be taken to avoid hypotension, because this can potentially reduce coronary perfusion pressure (diastolic BP - LV diastolic pressure).

Beta-blockers

Beta-blockers are indicated in all patients unless they have the following contraindications:

  • Systolic blood pressure less than 90 mm Hg
  • Cardiogenic shock
  • Severe bradycardia
  • Second- or third-degree heart block
  • Asthma or emphysema that is sensitive to beta agonists
  • Peripheral vascular disease
  • Uncompensated CHF

Beta blockers reduce oxygen demand and ventricular wall tension. They also decrease mortality and adverse cardiovascular events. These drugs may prevent mechanical complications of myocardial infarction, including rupture of the papillary muscle, left ventricular free wall, and ventricular septum. Beta blockers meliorate dynamic obstruction of the left ventricular outflow tract in patients with apical infarct and hyperdynamic basal segments.

The most frequently used regimen is IV metoprolol 2-5 mg given every 5 minutes (up to 15 mg total) followed by 25-100 mg given orally twice a day.

Beta-blockers should not be used acutely in patients with cardiogenic shock or signs of heart failure on presentation.

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Pharmacologic Antithrombotic Therapy

Aspirin

Aspirin permanently impairs the cyclooxygenase pathway of thromboxane A2 production in platelets, in this way inhibiting platelet function. Aspirin reduces morbidity and mortality and is continued indefinitely.[57]

Clopidogrel

Clopidogrel (thienopyridine) inhibits adenosine 5'-diphosphate (ADP)–dependent activation of the glycoprotein IIb/IIIa complex, a necessary step for platelet aggregation. This process results in intense inhibition of platelet function, particularly in combination with aspirin. In the CURE trial, thienopyridine reduced the rate of myocardial infarction by 20%.[49]

Clopidogrel is a class I recommendation for patients when an early noninterventional approach is planned in therapy for at least 1 month and ideally up to 1 year.[58] When percutaneous coronary intervention (PCI) is planned, clopidogrel 300-600 mg should be given as early as possible before or at the time of PCI.[58] Clopidogrel, 75 mg daily, is continued for at least 12 months after PCI, if the patient is not at high risk for bleeding, according to 2011 ACCF/AHA guidelines (class I recommendation).[58] Early discontinuation should be considered if the risk of bleeding-related morbidity outweighs the anticipated benefits.

The optimal loading dose for clopidogrel is still being evaluated. Reports show that a loading dose of 600 mg might be more beneficial than 300 mg. Withhold clopidogrel for at least 5 days before elective coronary artery bypass grafting (CABG). Since 12% of patients with non-ST elevation ACS have coronary anatomy that favors CABG, the use of clopidogrel is withheld until coronary angiography at some institutions.

A meta-analysis of 34 studies analyzed the safety of CABG among patients with ACS continuing clopidogrel. The investigators found that although mortality is increased in those receiving clopidogrel, it is influenced by ACS status and case urgency in primarily nonrandomized studies. Among patients with ACS, no differences in mortality or postoperative myocardial infarction or stroke rates were found. This suggests that in patients with ACS who require urgent CABG, proceeding despite the continuation of clopidogrel is likely safe.[59]

Clopidogrel can be considered an alternative to aspirin in patients with aspirin intolerance or who are allergic to aspirin.

Patients with chronic kidney disease who have low platelet response to clopidogrel tend to have worse outcomes after PCI.[60]

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.[61]

Evidence has shown that dexlansoprazole and lansoprazole do not significantly reduce the conversion of clopidogrel to its active metabolite (reduced by 9% and 14%, respectively), and no dose adjustment of clopidogrel is required.[62, 63]

The group’s findings and recommendations are listed below.

  • Clopidogrel reduces major CV events compared with placebo or aspirin.
  • Dual antiplatelet therapy with clopidogrel and aspirin, compared with aspirin alone, reduces major CV events in patients with established ischemic heart disease, and it reduces coronary stent thrombosis but is not routinely recommended for patients with prior ischemic stroke because of the risk of bleeding.[64]
  • Clopidogrel alone, aspirin alone, and their combination are all associated with increased risk of GI bleeding.
  • Clopidogrel requires metabolic activation by cytochrome P450 2C19 (CYP2C19). PPIs that inhibit CYP2C19 are commonly coadministered with clopidogrel to reduce the risk of GI bleeding. A study by Simon et al showed that PPI use is not associated with an increased risk of cardiovascular events or mortality in patients who have been treated with clopidogrel for a recent MI, regardless of CYP2C19 genotype.[65]
  • Patients with prior GI bleeding are at highest risk for recurrent bleeding on antiplatelet therapy; other risk factors include advanced age, concurrent use of anticoagulants, steroids, or NSAIDs including aspirin, and Helicobacter pylori infection; risk increases as the number of risk factors increases.
  • Use of PPIs or histamine H2 receptor antagonists (H2RAs) reduces the risk of upper GI bleeding compared with no therapy; PPIs reduce upper GI bleeding to a greater degree than do H2Ras.
  • PPIs are recommended to reduce GI bleeding among patients with a history of upper GI bleeding; PPIs are appropriate in patients with multiple risk factors for GI bleeding who require antiplatelet therapy.
  • Routine use of either a PPI or an H2RA is not recommended for patients at lower risk of upper GI bleeding, who have much less potential to benefit from prophylactic therapy.
  • Clinical decisions regarding concomitant use of PPIs and thienopyridines must balance overall risks and benefits, considering both CV and GI complications.
  • Pharmacokinetic and pharmacodynamic studies, using platelet assays as surrogate endpoints, suggest that concomitant use of clopidogrel and a PPI reduces the antiplatelet effects of clopidogrel; the strongest evidence for an interaction is between omeprazole and clopidogrel; it is not established that changes in these surrogate endpoints translate into clinically meaningful differences.
  • Observational studies and a single randomized clinical trial have shown inconsistent effects on CV outcomes of concomitant use of thienopyridines and PPIs; a clinically important interaction cannot be excluded, particularly in certain subgroups, such as poor metabolizers of clopidogrel.
  • The role of either pharmacogenomic testing or platelet function testing in managing therapy with thienopyridines and PPIs has not yet been established.

Prasugrel

Like clopidogrel, prasugrel is a thienopyridine ADP receptor inhibitor that inhibits platelet aggregation. It has been approved in the United States and has been shown to reduce new and recurrent myocardial infarctions.[66] The loading dose is 60 mg PO once and maintenance is 10 mg PO qd (given with aspirin 75-325 mg/d). Prasugrel is indicated for the reduction of thrombotic cardiovascular events (including stent thrombosis) with ACS that is managed with PCI.

The 2011 ACF/AHA guidelines advise that a loading dose of prasugrel be given as soon as possible, once coronary anatomy is defined and a decision is made to proceed with PCI. Prasugrel should be administered no later than 1 hour after PCI. Maintenance therapy with prasugrel is continued for at least 1 year after PCI.[58] Early discontinuation should be considered if the risk of bleeding-related morbidity outweighs the anticipated benefits.

One study, however, found that significant, sometimes fatal, bleeding occurred more frequently with prasugrel than with clopidogrel, although the overall mortality rate did not differ significantly between a treatment group receiving prasugrel and another receiving clopidogrel.[67, 66]

Ticagrelor

Ticagrelor (Brilinta) was approved by the US Food and Drug Administration in July 2011 and is the first reversible oral P2Y receptor antagonist. Results from the platelet inhibition and patient outcomes (PLATO) trial showed ticagrelor provides faster, greater, and more consistent ADP-receptor inhibition than clopidogrel.[68]

The difference between treatments on the composite resulted from effects on CV death and MI; each was statistically significant when considered as a secondary endpoint and there was no beneficial effect on strokes. For all-cause mortality, the benefit was also statistically significant of 9.8% for ticagrelor and 11.7% for clopidogrel (p = 0.0003) with a hazard ratio of 0.78.

Bleeding risk was assessed in the PLATO trial and ticagrelor increased the overall risk of bleeding (major + minor) to a somewhat greater extent than did clopidogrel. The increase was seen for non-CABG-related bleeding but not for CABG-related bleeding. Fatal and life-threatening bleeding rates were not increased.

Abciximab, eptifibatide, and tirofiban

Glycoprotein IIb/IIIa receptor antagonists include abciximab[69, 70] , eptifibatide[71] , and tirofiban[72] . These drugs inhibit the glycoprotein IIb/IIIa receptor, which is involved in the final common pathway for platelet adhesion and aggregation. (See the image below.)

Use of cardiac markers in the ED. Effect of time tUse of cardiac markers in the ED. Effect of time to treatment in patients with acute coronary syndrome (ACS) who are treated with the GIIb/IIIa inhibitor eptifibatide.

Use eptifibatide or tirofiban in patients with high-risk features in whom invasive treatment is not planned.

The use of eptifibatide 12 hours or more before angiography was not superior to the provisional use of eptifibatide after angiography, according to results from the EARLY ACS trial. The study compared a strategy of early, routine administration of eptifibatide with delayed, provisional administration in patients who had ACS without ST-segment elevation and who were assigned to an invasive strategy. The study also found that early use of eptifibatide was associated with an increased risk of non–life-threatening bleeding and the need for transfusion.[73]

Two trials with tirofiban and 1 trial with eptifibatide documented their efficacy in unstable angina/NSTEMI patients, only some of whom underwent interventions. These antagonists are a class I recommendation in patients in whom catheterization and PCI are planned. Intermediate- and high-risk patients appear to respond favorably to glycoprotein IIb/IIIa inhibitors.[74] They include patients with ST-segment depression, elevated risk scores, elevated serum troponin levels[75] , and/or diabetes mellitus.

Currently, IIb/IIIb antagonists in combination with aspirin are considered standard antiplatelet therapy for patients at high risk for unstable angina.

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Pharmacologic Anticoagulation Therapy

Unfractionated heparin

A study by Oler et al found that unfractionated heparin was associated with a 33% reduction in the risk of myocardial infarction or death in patients with unstable angina who were treated with aspirin plus heparin, compared with patients who were treated with aspirin alone.[76] The FUTURA/OASIS-8 randomized trial found that low-dose unfractionated heparin, 50 U/kg (regardless of use of glycoprotein IIb/IIIa inhibitors), compared with standard-dose unfractionated heparin, 85 U/kg (60 U/kg with Gp IIb/IIIa inhibitors), did not reduce major peri-PCI bleeding and vascular access-site complications.[77]

Low–molecular-weight heparin

LMWHs might be superior to unfractionated heparin in reducing cardiovascular outcomes, with a safety profile similar to that of heparin in patients receiving medical care.

Conflicting results emerged from 9 randomized trials directly comparing LMWH with unfractionated heparin. Two trials evaluated dalteparin, another evaluated nadroparin, and 6 evaluated enoxaparin.[78, 79] Trials with dalteparin and nadroparin reported similar rates of nonfatal myocardial infarction or death compared with heparin, whereas 5 of 6 trials of enoxaparin found point estimates for death or nonfatal myocardial infarction that favored enoxaparin over heparin. The benefit of enoxaparin appeared to be driven largely by a reduction in nonfatal myocardial infarction, especially in the cohort of patients who had not received any open-label anticoagulant therapy before randomization.

In addition, a systematic review comparing LMWH with unfractionated heparin found no significant difference in benefits between the 2 drugs.

Aside from the possible medical benefits of using LMWH in place of unfractionated heparin, advantages of LMWH include ease of administration, absence of need for anticoagulation monitoring, 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.[80]

The role of LMWHs in patients for whom PCI is scheduled is relatively ill defined. However, it is likely to be at least equivalent to that of heparin. It appears reasonable to minimize the risk of excessive anticoagulation during PCI by avoiding crossover of anticoagulants (ie, maintain consistent anticoagulant therapy from the pre-PCI phase throughout the procedure itself). Additional experience with regard to the safety and efficacy of the concomitant administration of LMWHs with Gp IIb/IIIa antagonists and fibrinolytic agents is currently being acquired.

Adding apixaban (5 mg twice daily) to antiplatelet therapy in high-risk patients after ACS may increase the number of major bleeding events without significantly reducing recurrent ischemic events.[81, 82]

Factor Xa inhibitors

Use of the oral Xa inhibitor, rivaroxaban (Xarelto), in addition to dual antiplatelet therapy in patients with ACS was recently investigated in the ATLAS ACS2-TIMI 51 trial. Low-dose rivaroxaban (2.5 mg twice daily) resulted in a significant reduction in overall and cardiac mortality whereas use of the higher dose (5 mg twice daily) did not result in a significant mortality reduction. However, both doses were associated with an increased risk of bleeding compared with placebo. Rivaroxaban is not currently approved by the US Food and Drug Administration (FDA) for use in ACS.

Another factor Xda inhibitor, fondaparinux (Arixtra), has been studied for use in patients with STEMI who do not undergo PCI.[83] In the Fifth Organization to Assess Strategies in Ischemic Syndromes (OASIS-5) trial, fondaparinux reduced major bleeding and improved net clinical outcome compared with enoxaparin in patients receiving GP IIb/IIIa inhibitors or thienopyridines for ACS.[84] Fondaparinux is not currently FDA approved for use in ACS.

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Thrombolysis

Prehospital thrombolysis allows eligible patients to receive thrombolysis 30-60 minutes sooner than if treatment were given in the ED; however, prehospital thrombolysis is still under investigation and has not become a trend, as a result of unproven benefit and an increase in the availability of PCI in many medical centers as an alternative to thrombolysis for STEMI.

The Remodeling With Erythropoietin After Large Myocardial Infarction (REVEAL) trial evaluated the safety and efficacy of a single intravenous bolus of epoetin alfa in patients with STEMI who had successful reperfusion with primary or rescue PCI.[85] A single intravenous bolus of epoetin alfa within 4 hours of PCI did not reduce infarct size and was associated with higher rates of adverse cardiovascular events.

Although PCI is the preferred treatment for STEMI, the distance to primary PCI centers and the inherent time delay in delivering primary PCI limits widespread use of this treatment. Prehospital electrocardiographic (ECG) diagnosis and direct referral for primary PCI enables patients with STEMI living far from a PCI center to achieve a system delay comparable to patients who are closer to a PCI center.[86]

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Coronary Interventions

An early invasive strategy (ie, diagnostic angiography with intent to perform revascularization) is indicated in unstable angina/NSTEMI patients who have refractory angina or hemodynamic or electrical instability without serious comorbidities or contraindications to such procedures.[29] An early invasive strategy is also indicated in initially stabilized unstable angina/NSTEMI patients who do not have serious comorbidities or contraindications to such procedures and who have an elevated risk for clinical events.

According to the 2011 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines, an early invasive strategy (ie, within 12-24 hours of admission) is a reasonable choice for initially stabilized high-risk patients with unstable angina/NSTEMI; for patients not at high risk , a delayed invasive approach is also reasonable (class IIa recommendation).[58]

In NSTEMI ACS, early revascularization reduces myocardial infarction and death rates compared with a more selective strategy, particularly in high-risk patients. Use of Gp IIb/IIIa blockers followed by early invasive catheterization is the most logical approach. An early invasive strategy should be considered in patients with large myocardial infarction, hypotension, shock, RV infarction, and refractory chest pain.

In the Invasive Versus Conservative Treatment in Unstable Coronary Syndromes (ICTUS) trial, an early invasive strategy had no apparent long-term benefit in reducing death or myocardial infarction. After stratification for risk, analysis of 5-year clinical outcomes in patients presenting with non-ST-segment elevation ACS and elevated troponin T (TnT) level showed that cumulative myocardial infarction or death rates were 22.3% in the early invasive group versus 18.1% in the selective invasive group. No difference was observed in mortality or myocardial infarction.[87]

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Concomitant Therapy

Current guidelines for patients with moderate- or high-risk ACS recommend an early invasive approach with concomitant antithrombotic therapy, including aspirin, clopidogrel, and unfractionated or LMWH. The Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial evaluated the role of thrombin-specific anticoagulation with bivalirudin in this patient population. In patients with moderate- or high-risk ACS who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associated with rates of ischemia and bleeding that were similar to those with heparin. Bivalirudin alone was associated with similar rates of ischemia and significantly lower rates of bleeding.[88] Further, glycoprotein IIb/IIIa inhibitors can be initiated at the time of angiography; routine administration 12-24 hours before the procedure carries an increased risk of bleeding and no improvement in outcome.

Kastrati et al compared the combination of glycoprotein IIb/IIIa inhibitors and heparin with bivalirudin, specifically among patients with NSTEMI undergoing PCI. In a double-blind manner, 1721 patients with acute NSTEMI were randomly assigned to receive abciximab plus unfractionated heparin (861 patients) or bivalirudin (860 patients). The study concluded that abciximab and unfractionated heparin, compared with bivalirudin, failed to reduce death, large recurrent myocardial infarction, urgent target-vessel revascularization, or major bleeding within 30 days. It also increased the risk of bleeding among patients with NSTEMI who were undergoing PCI.[89]

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Contributor Information and Disclosures
Author

David L Coven, MD, PhD  Assistant Professor of Medicine, Columbia University College of Physicians and Surgeons; Attending Physician in Interventional Cardiology, St Luke's-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

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

Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Arun Kalyanasundaram, MD, MPH  Interventional Cardiology Fellow, Department of Cardiology, Cleveland Clinic

Arun Kalyanasundaram, MD, MPH is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiac Angiography and Interventions, Society of General Internal Medicine, Society of Hospital Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

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

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

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

Jamshid Shirani, MD  Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, St Luke's Hospital and Health Network

Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Echocardiography, and Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Specialty Editor Board

Craig T Basson, MD, PhD  Gladys and Roland Harriman Professor of Medicine, Director of the Center for Molecular Cardiology, Director of Cardiovascular Research, Division of Cardiology, Department of Medicine, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Steven J Compton, MD, FACC, FACP  Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

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

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital, University of North Carolina at Chapel Hill School of Medicine

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

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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 electrocardiogram (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 = 98. Her electrocardiogram (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.
This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.
Suggested algorithm for triaging patients with chest pain. ACS = ACS; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).
Use of cardiac markers in the ED. Studies on troponins in ACS.
Use of cardiac markers in the ED. Troponin I levels and cardiac mortality in ACS.
Use of cardiac markers in the ED. Cardiac event rates in the platelet receptor inhibition for ischemic syndrome (PRISM) study based on troponin I results.
Use of cardiac markers in the ED. Effect of time to treatment in patients with acute coronary syndrome (ACS) who are treated with the GIIb/IIIa inhibitor eptifibatide.
Table. TIMI Risk Score for Unstable Angina and NSTEMI[43]
Characteristic Risk Score
History
Age ≥65 years1
At least 3 risk factors for coronary heart disease1
Previous coronary stenosis ≥50%1
Use of aspirin in previous 7 days1
Presentation
At least 2 anginal episodes in the previous 24 hours1
ST-segment elevation on admission ECG1
Elevated levels of serum biomarkers1
Total Score0-7
Note: Event rates significantly increased as the TIMI risk score increased in the test cohort in the TIMI IIB study. Rates were 4.7% for a score of 0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for 6/7 (P < .001, χ2 test for the trend). The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P < .001).
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