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AACN Advanced Critical Care:
doi: 10.1097/NCI.0b013e31820b24cf
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Non-ST-Segment Elevation Acute Coronary Syndrome: Impact of Nursing Care on Optimal Outcomes

Housholder-Hughes, Susan D. RN, MSN, CCRN, ANP-BC, FAHA, AACC

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Author Information

Susan D. Housholder-Hughes is Nurse Practitioner, UM-Multidisciplinary Aortic Program, Cardiovascular Center, Room 5124, University of Michigan Health System, and Adjunct Clinical Instructor, University of Michigan School of Nursing, 1500 E Medical Center Dr, Ann Arbor, MI 48109 (shoushol@med.umich.edu).

Disclosure: S.H. has received speaker honoraria from Schering-Plough Corp.

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Abstract

Of the nearly 1.4 million hospitalizations for acute coronary syndromes in 2006, approximately two-thirds were for unstable angina (UA) or non–ST-segment elevation myocardial infarction (NSTEMI). Given the high risk for in-hospital ischemic events and late mortality in patients with UA/NSTEMI, it is critical to accurately and rapidly diagnose these patients, stratify their level of risk, and provide appropriate pharmacologic and nonpharmacologic treatment that maximizes anti-ischemic benefit and minimizes risk of bleeding. Appropriate in-hospital care following intervention is critical for optimizing both short- and long-term outcomes. However, evidence suggests that up to 26% of opportunities to provide guidelines-recommended care are missed. Nurses can play a critical role in ensuring that patients receive guidelines-based care. This review examines the most recent recommendations for the diagnosis and pharmacologic management of patients with UA/NSTEMI and discusses ways in which nursing staff can contribute to minimizing patient risk and optimizing patient benefit.

Acute coronary syndromes (ACS) accounted for nearly 1.4 million hospitalizations in 2006, with approximately two-thirds of these hospitalizations for unstable angina (UA) or non–ST-segment elevation myocardial infarction (NSTEMI).1 Given the high risk for in-hospital ischemic events and late mortality in patients with UA/NSTEMI, it is critical to accurately and rapidly diagnose these patients, stratify their level of risk, and provide evidence-based therapies to optimize short- and long-term outcomes.2 Nurses play a key role in the care of ACS patients, using their triage and decision-making skills at every entry point into health care systems.

Risk factors associated with atherosclerosis and its progression include high levels of low-density lipoprotein cholesterol, elevated blood pressure, smoking, diabetes, inactivity, elevated body mass index, family history of cardiovascular disease, Western dietary patterns, and chronic stress.1 These risk factors are associated with atherosclerotic plaque formation and subsequent risk for ACS. Acute coronary syndromes occur when a “vulnerable” plaque ruptures, triggering a complex cascade of events that culminate in thrombi partially or completely occluding the coronary vasculature, compromised coronary blood flow, and subsequent injury and/or death of myocardial tissue.

Patients with UA/NSTEMI have an elevated incidence of ischemic events during hospitalization. These events dramatically increase the incidence of recurrent ischemia and late mortality.2 Coupled with the higher incidence of UA/NSTEMI, these data suggest that careful attention to appropriate care is warranted.

Notably, there is a gap between current recommendations for appropriate care as outlined in American College of Cardiology/American Heart Association (ACC/AHA) guidelines and “real world” care: Contemporary data indicate that up to 26% of opportunities to provide guidelines-recommended care are missed.3 Failure to adhere to national guidelines for best practice can have important clinical consequences. For example, guideline nonadherence rates are associated with in-hospital mortality; mortality rates in one study ranged from 6.31% at centers with the lowest guideline adherence to 4.15% at centers with the highest adherence (P < .001).3

Accurate diagnosis, risk stratification, and provision of appropriate pharmacologic and nonpharmacologic treatment that maximizes anti-ischemic benefit and minimizes bleeding risk are critical for optimal outcomes in patients with ACS. In addition, appropriate patient care following any intervention is critical for optimizing both short- and long-term outcomes and for minimizing length of hospital stay.

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Pathophysiology of Acute Coronary Syndromes

Acute coronary syndromes refer to any constellation of symptoms suggesting acute myocardial ischemia and include UA, NSTEMI, and STEMI. ST-segment elevation myocardial infarction, which occurs when a thrombus totally occludes the coronary artery lumen, results in acute injury and/or death of myocardial tissue if reperfusion strategies are not successful in restoring blood flow. This article contains a discussion of UA/NSTEMI only. UA/NSTEMI results from an imbalance in oxygen supply and demand; most commonly, myocardial blood flow is compromised by a nonocclusive thrombus. Less common causes include dynamic obstruction due to focal spasm of an epicardial vessel,4 arterial inflammation (infection), induction of coronary spasms from cocaine/methamphetamine use, or secondary causes of increased myocardial stress, such as thyrotoxicosis, anemia, hypoxemia, or fever.5

In healthy individuals, the endothelium—the inner lining of the blood vessel—produces substances that inhibit platelet injury and activation.6 Damage to the endothelium exposes collagen and von Willebrand factor, which are subsequently bound by platelet-surface receptor complexes. Subsequently, bound platelets are activated by a series of intracellular events (calcium mobilization, alterations in the cytoskeleton, and intracellular release of prothrombotic factors). Platelet activation is characterized by activation of the glycoprotein IIb/IIIa receptor, induced mainly by collagen, thrombin, adenosine diphosphate (ADP), and thromboxane A2.6

Platelets then form aggregates that contribute to the formation of a vessel-blocking thrombus. This platelet-rich thrombus is the underlying cause of ischemic events in patients with ACS. Partial blockage results in myocardial ischemia and UA; complete blockage of smaller myocardial vessels results in NSTEMI. Platelets also spontaneously disaggregate during thrombus formation; therefore, thrombi release microemboli composed of platelet aggregates and activated platelets. Release of microemboli from the site of plaque disruption, resulting in microvascular obstructions in the myocardium, brain, or periphery, can continue for days to weeks.7

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Diagnosis of UA/NSTEMI

Early diagnosis of UA/NSTEMI is critical to achieve rapid initiation of appropriate treatment, particularly in light of the often-significant delay between initial symptom onset and presentation to a hospital.8 Strategies for diagnosing ACS include symptom assessment, electrocardiographic (ECG) analysis for ST-segment shifts or T-wave inversion, and analysis of cardiac biomarkers. The first task when a patient enters the health care facility is to assess whether symptoms are a manifestation of ACS. Recommendations for initial identification of ACS are summarized in Table 1.

Table 1: Guidelines ...
Table 1: Guidelines ...
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The 12-lead ECG is an important tool in the diagnosis of ACS5 (and in risk stratification, discussed later). ST-segment changes (≥0.5 mm in 2 contiguous leads) when a patient is experiencing symptoms suggest acute myocardial ischemia; ST-segment depression and/or inverted T waves may indicate either UA or NSTEMI. These are differentiated by the absence or presence, respectively, of cardiac biomarkers; the presence of these biomarkers indicates myocardial ischemia, injury, and/or necrosis. The presence of Q waves suggests prior myocardial infarction and indicates a high likelihood of coronary artery disease.

As a general rule, the cardiac enzymes troponin T and I are the preferred biomarkers for diagnosis5; however, although troponin levels can often be detected in the blood as early as 2 to 4 hours after symptoms begin, in some patients, elevation can be delayed for 8 to 12 hours (Figure).5 For this reason, patients with negative biomarker readouts within 6 hours of symptom onset should have a repeat measurement between 8 and 12 hours after symptom onset.5 Levels of creatine kinase-MB fraction and myoglobin can also be measured at the same time as troponin levels.9 However, both troponin and creatine kinase-MB fraction elevations can be caused by a variety of other conditions, so these biomarkers cannot be used alone to diagnose ACS.9

Figure:. Timing of b...
Figure:. Timing of b...
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Risk Stratification

Along with rapid diagnosis, risk stratification is important to optimize long-term outcomes in patients with UA/NSTEMI. Many factors, including patient medical history, physical examination and ECG findings, renal function, and cardiac biomarker measurements, must be integrated to estimate ischemic risk and select the best pharmacologic and nonpharmacologic management options.

Numerous studies have demonstrated that the benefits of aggressive therapy, such as early intervention and administration of glycoprotein IIb/IIIa inhibitors, are greatest in patients at moderate or high risk (determined by levels of markers of myocardial necrosis and global risk scores).10-13 Patients at elevated risk levels represent at least half of the population admitted to hospitals for UA/NSTEMI.10 Therapies must be accurately assigned to patients who are likely to receive the most benefit from them, because aggressive therapy also raises the risk for bleeding.

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Risk-Scoring Systems

Three scoring methods help to stratify risk in patients with UA/NSTEMI: the TIMI (Thrombolysis In Myocardial Infarction),14 GRACE (Global Registry of Acute Coronary Events),15 and PURSUIT (Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy)16 systems. These systems help to identify high-risk patients; current UA/NSTEMI guidelines assign a class IIa (level of evidence B) recommendation for their use.5 In the author's experience, the TIMI model, which can estimate risk up to 1 year after an event, is the most commonly used in clinical practice.14,17,18 High scores for the 7 risk factors that contribute to TIMI rating (Table 2) are associated with significant increases in all-cause mortality, myocardial infarction, and recurrent ischemia requiring urgent revascularization.14 This tool is simple, quick, and easily incorporated into hospital ACS triaging processes. (Further details on the TIMI risk-scoring system can be found online at http://www.TIMI.org.)

Table 2: The TIMI Ri...
Table 2: The TIMI Ri...
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Electrocardiographic Findings

Nurses caring for patients with ACS are responsible for continuous dysrhythmia/ECG monitoring and for reporting and documenting findings. Initial ECG readings can be inconclusive or misleading; in one study, 16% of patients with UA/NSTEMI were found to have normal ECG readings at presentation.19 Thus, increased use of continuous ST-segment monitoring may provide considerable additional value in the setting of ACS. Nurses using telemetry or hardwire monitoring systems can immediately initiate the continuous ST-segment software and set the appropriate alarm.

Continuous ST-segment monitoring is a well-established adjunct to static 12-lead ECGs in detecting dynamic ST-segment shifts, thus assisting in the identification of patients at high risk for adverse outcomes. Moreover, a high prevalence of silent ischemic events (without symptoms but indicated by ST changes) has been reported in patients with UA. An early study of continuous ECG within 2 days of admission to a coronary care unit detected silent ischemic episodes in more than half of patients with ACS symptoms; more than 90% of these episodes were asymptomatic.20 In a substudy of the PURSUIT trial, patients with UA/NSTEMI whose 24-hour continuous readings with a 12-lead ECG21 showed 2 or more ST-deviation episodes had higher mortality (P = .008) at 6-month follow-up. In a more recent study, patients with non–ST-segment elevation ACS with ST-segment shifts during the first 48 hours after admission had a higher risk of death (17.7% vs 5.8%; P < .001) and of combined death and myocardial infarction (24.6% vs 11.1%; P < .001) than those without ST-segment shifts.22

Continuous ST-segment monitoring is underutilized throughout health care systems across the country.23-25 Potential reasons for underutilization include physician disinterest, physician lack of awareness, lack of use by staff nurses, concern for frequent false-positive alarms, and lack of institutional protocols for use.23-25 Continuous ST-segment monitoring has now been established in the ACC/AHA guidelines as a class I, level of evidence B recommendation for patients with probable or possible ACS whose initial ECG readings are normal on presentation.5

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Estimating and Minimizing Bleeding Risk

In contrast to ischemic risk stratification, formal methods for estimating bleeding risk are in their infancy. One bleeding risk–scoring method has recently been designed and validated using data from the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) quality improvement initiative.26 Recognition of potential bleeding risk factors is critical for appropriate use of pharmacologic therapy, because all agents that reduce ischemic risk inevitably increase bleeding risk.

Nurses can make meaningful contributions to patient care by performing a thorough assessment to identify patients who have higher bleeding risk. Factors associated with increased risk for bleeding include older age, female gender, lower body weight, renal insufficiency, prolonged or complicated interventional procedures, use of an intra-aortic balloon pump, presence of anemia, and excessive dosing of antithrombotics.27-29

Bleeding is frequently related to excess dosing of antithrombotic or antiplatelet agents. An analysis of data from the CRUSADE program found that patients who received excess dosages tended toward or had increased risks for major bleeding, mortality, and longer hospital stay.30 Although not all risk factors are controllable, dosing of antiplatelet/antithrombotic medications can be individualized in response to these variables. Perhaps most important, dosing should be carefully individualized on the basis of renal function (Table 3).

Table 3: Dosage Adju...
Table 3: Dosage Adju...
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Downstream Management: Overview

The 2007 ACC/AHA guidelines for the management of UA/NSTEMI have moved toward preferential use of an early invasive strategy, in which patients who are receiving evidence-based anti-ischemic, antithrombotic, and antiplatelet medications undergo diagnostic angiography from 4 to 24 hours after admission with the intent to perform revascularization.5 Guidelines for the management of UA/NSTEMI include a classification system based on the size and certainty of the treatment effect (Table 4). The early invasive strategy approach—which is used in most patients at moderate to high risk for clinical events—is differentiated from a selectively invasive strategy, which involves invasive evaluation only if optimal medical management fails. Selectively invasive strategy is warranted only in patients with low risk scores.5

Table 4: Categories ...
Table 4: Categories ...
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Pharmacologic Management of Acute Coronary Syndromes

According to CRUSADE data, nearly 50% of patients with UA/NSTEMI who present to hospitals without facilities for revascularization are not transferred to tertiary hospitals.37 When patients with NSTEMI are managed using early invasive strategy at hospitals that have this capability, coronary angiography is typically performed within 24 to 48 hours of admission (although guidelines call for it within 24 hours).5,38 Most of these patients undergo revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass grafting. All coronary interventions carry significant risk for periprocedural thromboembolic complications. As a result, adjunctive pharmacologic therapy, targeted at reducing ischemia, inhibiting the coagulation cascade, and reducing platelet aggregation, is required in all patients who undergo these procedures. Although nurses may not be the final decision makers regarding choice of pharmacotherapy, familiarity with guideline recommendations (Tables 5 through 7) is another tool that can further nurses' understanding and expectations when working with patients who undergo PCI, thereby ensuring rapid communication to physician colleagues when necessary.

Table 5: Anti-ischem...
Table 5: Anti-ischem...
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Symptoms of ischemia may be relieved with treatments that increase oxygen supply or reduce oxygen demands of the heart; these include supplemental oxygen, nitrates, morphine, and β-blockers and are summarized in Table 5.39 β-blockers lower heart rate and blood pressure by blocking β-1 receptors, which ultimately lowers myocardial oxygen demands. To decrease risk of cardiogenic shock, early intravenous administration of β-blockers should be avoided in ACS patients who are hemodynamically unstable or show signs of heart failure.40 Nitrates decrease oxygen demand by reducing preload while increasing coronary blood flow via vasodilatory properties.5 Nitrate therapy is useful in treating ischemic pain during ACS. Morphine sulfate can be used to assist with pain management in patients unresponsive to nitrates. Morphine also has beneficial hemodynamic effects via properties of venodilation, with resultant reduction in myocardial oxygen demand.5 As a result of considerable evidence from placebo-controlled trials showing that aspirin has a profound positive impact on outcomes in patients with ACS, aspirin is an integral part of the pharmacologic regimen for nearly all such patients (Table 6).

Table 6: Antiplatele...
Table 6: Antiplatele...
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P2Y12 Inhibitors

Clopidogrel, ticlopidine (an older agent, rarely used because of potential adverse effects), and prasugrel (approved by the US Food and Drug Administration in 2009)41 are thienopyridine agents that act by irreversibly inhibiting the platelet P2Y12 ADP receptor and ADP-mediated platelet aggregation.5 However, clopidogrel has a slow onset of action, and glycoprotein IIb/IIIa inhibitors are frequently needed to provide adequate antiplatelet coverage in patients undergoing urgent procedures. Clopidogrel is strongly recommended in the guidelines for many indications in patients with NSTEMI and ACS (Table 6); however, if coronary artery bypass grafting is anticipated, clopidogrel should be withheld for at least 5 days before surgery (class I, level of evidence C).5

Data suggest that the use of prasugrel is associated with significantly reduced rates of ischemic events compared with clopidogrel.42 Prasugrel may have a role in the treatment of high-risk ACS patients undergoing PCI and/or those undergoing complex stent deployment.43 However, prasugrel increases the risk of bleeding, including fatal bleeding events; this risk is increased in patients with a history of stroke or transient ischemic attack, low body weight (under 60 kg), or age greater than 75 years.42

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Glycoprotein IIb/IIIa Inhibitors

The efficacy of glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, and tirofiban) in patients with ACS and undergoing PCI has been documented extensively in clinical trials.1113,1452 As a result, these agents carry class I or IIa recommendations in various indications for ACS (Table 5); in current practice, they are nearly always used with heparin.

The benefit of glycoprotein IIb/IIIa inhibition may be limited in low- to moderate-risk patients but significant in patients at higher risk.13,50, However, anatomic features—which drive procedural complexity—may also determine risk, and recent evidence indicates that patients undergoing complex stenting procedures who might traditionally have been considered at low or moderate risk actually experience significant benefits from more aggressive antiplatelet intervention.53

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Heparin

Heparin has important benefits: Its anticoagulant effect can be reversed rapidly with intravenous administration of protamine, it is not subject to renal elimination, and it can be used, with appropriate caution, in patients with severe kidney impairment.54 However, the anticoagulant activity of heparin must be monitored closely,54 and patients receiving unfractionated heparin should be monitored for heparin-induced thrombocytopenia, a potentially prothrombotic state. Heparin-induced thrombocytopenia should be considered with the occurrence of any unexplained fall in platelet count, evidence of bleeding, or signs and symptoms of vascular occlusion (eg, confusion, chest pain, tachypnea, and loss of pulse sensation or motor function).55-57

The low-molecular-weight heparins are directly derived from heparin.58 Because of their near-100% bioavailability and low plasma protein binding, consistent anticoagulation is achieved without the need for laboratory monitoring.59 Although a number of low-molecular-weight heparins are available, current guidelines recommend enoxaparin as the agent of choice (Table 7).4

Table 7: Antithrombo...
Table 7: Antithrombo...
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Fondaparinux, a factor Xa inhibitor that is administered subcutaneously, has decreased plasma protein binding and dose-independent clearance compared with unfractionated heparin, and a longer half-life.5 As with low-molecular-weight heparin, fondaparinux does not require monitoring. The 2007 guidelines are the first to recommend its use in patients with UA/NSTEMI (Table 7).

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Bivalirudin

The 2007 ACC/AHA guidelines incorporate recommendations for the use of bivalirudin, an anticoagulant that directly inhibits thrombin (Table 7). Bivalirudin is also indicated for use in patients with or at risk of heparin-induced thrombocytopenia. Activated clotting time (ACT) should be assessed 5 minutes after bolus injection. Some practitioners may continue administration of bivalirudin for up to 4 hours post-PCI.60

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Minimizing Vascular Access Site Complications

When patients undergo PCI, nurses are actively involved in managing the vascular access site, with the goal of minimizing complications (hematoma, pseudoaneurysm, arteriovenous fistula, acute arterial occlusion, cholesterol embolus, and infection). These events, which occur in 5% to 10% of patients,61 can complicate downstream management, increase hospital stays, and—importantly in today's constrained health care environment—increase the cost of care.

Mechanisms for reducing femoral access site complications were evaluated in the SANDBAG (Standards of Angioplasty Nursing techniques to Diminish Bleeding Around the Groin) substudy62 of the IMPACT II (Integrilin to Manage Platelet Aggregation to prevent Coronary Thrombosis) trial,47 which examined the effects of the glycoprotein IIb/IIIa inhibitor eptifibatide on ischemic complications in patients undergoing PCI. Factors that did not appear to influence bleeding were complete bed rest, log rolling, head elevation, frequent assessments of vascular access site, type of wound dressing used after sheath removal, and patient medication.62 Factors identified as highly significant predictors of increased bleeding included having a nurse (rather than a technician) remove the sheath and apply manual pressure; prolonged time between removal of the sheath and patient ambulation; and patient complaints of nausea, vomiting, and back pain.62 Although it would seem counterintuitive, the SANDBAG investigators reported reduced bleeding in patients who had early sheath removal while eptifibatide was still being infused.62

Risk factors associated with bleeding at the access site were also evaluated in a retrospective study reviewing data from 17 901 patients who underwent PCI at the Mayo Clinic from 1994 to 2005.63 Procedural factors significantly associated with major femoral bleeding were greater sheath size, glycoprotein IIb/IIIa inhibitor use, lower peak ACT values, use of heparin after procedure, longer procedure duration, and use of a vascular closure device (VCD). Significantly associated patient factors included older age, female sex, severe renal impairment, and normal (vs elevated) body mass index. Diabetes was significantly associated with lower bleeding risk.

Vascular closure devices (VCDs) were developed because of concerns regarding high rates of access site bleeding in individuals undergoing PCI.64 Since the development of VCDs, many technologic advances have been made in hopes of creating a device that will secure hemostasis with few complications. Currently available VCDs include those using a collagen plug, clips, or suture for closing the artery.65 Although VCDs have been shown to reduce the time to hemostasis compared with manual compression, concerns remain regarding their potential for serious complications including pseudoaneurysm, bleeding, hematoma, arterial laceration, arteriovenous fistula, device embolization, arterial thrombosis, and infection.64-66 More clinical research is needed to evaluate the safety and efficacy of VCDs before their superiority over manual compression is proven.

The main goals following sheath removal are to achieve hemostasis and assess for vascular complications. Hospitals can be encouraged to implement sheath removal protocols that are collaboratively developed with appropriate disciplines involved. Currently, protocols vary from organization to organization; no “standard of care” exists in this area. The following are recommendations for best practices surrounding sheath removal:

1. Nurses must perform and document individualized assessments of risk of bleeding, on the basis of the type of anticoagulation the patient receives, procedure duration and complexity, use of an intra-aortic balloon pump, and dosing of antithrombotics.

2. The type of closure device used varies on the basis of hospital/physician choice; the ramifications of this choice must be understood by all caregivers.

3. Data support early sheath removal as a way to decrease bleeding complications and enhance patients' comfort level.62

4. Duration and degree of response to heparin in a given patient must be assessed by ACT testing. Unfortunately, results can vary by instrument used, calibration of the instrument, use of venous versus arterial blood, and operator technique.67 This uncertainty must be considered when using ACT to determine hemostasis and optimal time of sheath removal.

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Conclusions

Nurses play an integral role in the assessment and care of patients with ACS. Early recognition of symptoms and ECG changes that may be indicative of acute myocardial ischemia is essential to the delivery of evidence-based therapies and achievement of best possible patient outcomes. A thorough understanding of the benefits and risks of pharmacotherapeutic options is essential. Use of risk stratification tools, continuous ST-segment monitoring, and rapid communication to physician colleagues will improve patient outcomes and assist in the prevention of adverse outcomes in those with UA/NSTEMI.

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Acknowledgments

Editorial assistance was provided by Rina Kleege, MS, and was funded by Schering Corp, now Merck & Co.

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REFERENCES

1. Lloyd-Jones D, Adams R, Carnethon M, et al. Heart disease and stroke statistics—2009 update. A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009 119(3): 480–486.

2. Armstrong PW, Fu Y, Chang WC, et al. Acute coronary syndromes in the GUSTO-IIb trial: prognostic insights and impact of recurrent ischemia. The GUSTO-IIb investigators. Circulation. 1998 98(18): 1860–1868.

3. Peterson ED, Roe MT, Mulgund J, et al. Association between hospital process performance and outcomes among patients with acute coronary syndromes. JAMA. 2006 295(16): 1912–1920.

4. Ong P, Athanasiadis A, Hill S, Vogelsberg H, Voehringer M, Sechtem U Coronary artery spasm as a frequent cause of acute coronary syndrome: the CASPAR (Coronary Artery Spasm in Patients With Acute Coronary Syndrome) study. J Am Coll Cardiol. 2008 52(7): 523–527.

5. Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. J Am Coll Cardiol. 2007 50(7): e1–e157.

6. Gurbel PA, Bliden KP, Hayes KM, Tantry U Platelet activation in myocardial ischemic syndromes. Expert Rev Cardiovasc Ther. 2004 2(4): 535–545.

7. Drouet L Atherothrombosis as a systemic disease. Cerebrovasc Dis. 2002 13(suppl 1): 1–6.

8. Goff DC Jr, Feldman HA, McGovern PG, et al. Prehospital delay in patients hospitalized with heart attack symptoms in the United States: the REACT trial. Rapid Early Action for Coronary Treatment (REACT) Study Group. Am Heart J. 1999 138(16, pt 1): 1046–1057.

9. Casey PE Markers of myocardial injury and dysfunction. AACN Clin Issues. 2004 15(4): 547–557.

10. Kastrati A, Mehilli J, Neumann FJ, et al. Abciximab in patients with acute coronary syndromes undergoing percutaneous coronary intervention after clopidogrel pretreatment: the ISAR-REACT 2 randomized trial. JAMA. 2006 295(13): 1531–1538.

11. PURSUIT Trial Investigators Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients with acute coronary syndromes. The PURSUIT trial investigators. Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy. N Engl J Med. 1998 339(7): 436–443.

12. ESPRIT Investigators Novel dosing regimen of eptifibatide in planned coronary stent implantation (ESPRIT): a randomised, placebo-controlled trial. Lancet. 2000 356(9247): 2037–2044.
13. PRISM-PLUS Investigators Inhibition of the platelet glycoprotein IIb/IIIa receptor with tirofiban in unstable angina and non-Q-wave myocardial infarction. Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) Study Investigators. N Engl J Med. 1998 338(21): 1488–1497.

14. 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): 835–842.

15. Granger CB, Goldberg RJ, Dabbous O, et al. Predictors of hospital mortality in the global registry of acute coronary events. Arch Intern Med. 2003 163(19): 2345–2353.

16. Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation. 2000 101(22): 2557–2567.

17. Pollack CV Jr, Braunwald E 2007 update to the ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: implications for emergency department practice. Ann Emerg Med. 2008 51(5): 591–606.

18. Scirica BM, Cannon CP, Antman EM, et al. Validation of the thrombolysis in myocardial infarction (TIMI) risk score for unstable angina pectoris and non-ST-elevation myocardial infarction in the TIMI III registry. Am J Cardiol. 2002 90(3): 303–305.

19. Collinson J, Bakhai A, Taneja A, Wang D, Flather MD Admission ECG predicts long-term outcome in acute coronary syndromes without ST elevation. QJM. 2006 99(9): 601–607.

20. Gottlieb SO, Weisfeldt ML, Ouyang P, Mellits ED, Gerstenblith G Silent ischemia as a marker for early unfavorable outcomes in patients with unstable angina. N Engl J Med. 1986 314(19): 1214–1219.

21. Akkerhuis KM, Maas AC, Klootwijk PA Recurrent ischemia during continuous 12-lead ECG-ischemia monitoring in patients with acute coronary syndromes treated with eptifibatide: relation with death and myocardial infarction. PURSUIT ECG-ischemia monitoring substudy investigators. Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy. J Electrocardiol. 2000 33(2): 127–136.

22. Yan AT, Yan RT, Tan M, et al. Long-term prognostic value and therapeutic implications of continuous ST-segment monitoring in acute coronary syndrome. Am Heart J. 2007 153(4): 500–506.

23. Patton J, Funk M Survey of use of ST-segment monitoring in patients with acute coronary syndromes. Am J Crit Care. 2001 10(1): 23–34.

24. Sandau K, Sendelbach S, Frederickson J, Doran K National survey of cardiologists' standard of practice for continuous ST-segment monitoring. Am J Crit Care. 2010 19(2): 112–123.
25. Daleiden AM, Schell H Setting a new gold standard Am J Nurs. 2001 (suppl 2): 4–8.

26. Subherwal S, Bach RG, Chen AY, et al. Baseline risk of major bleeding in non-ST-segment-elevation myocardial infarction: the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) bleeding score. Circulation. 2009 119(14): 1873–1882.

27. Chew DP, Lincoff AM, Gurm H, et al. Bivalirudin versus heparin and glycoprotein IIb/IIIa inhibition among patients with renal impairment undergoing percutaneous coronary intervention (a subanalysis of the REPLACE-2 trial). Am J Cardiol. 2005 95(5): 581–585.

28. Aguirre FV, Topol EJ, Ferguson JJ, et al. Bleeding complications with the chimeric antibody to platelet glycoprotein IIb/IIIa integrin in patients undergoing percutaneous coronary intervention. EPIC investigators. Circulation. 1995 91(12): 2882–2890.

29. Kinnaird TD, Stabile E, Mintz GS, et al. Incidence, predictors, and prognostic implications of bleeding and blood transfusion following percutaneous coronary interventions. Am J Cardiol. 2003 92(8): 930–935.

30. Alexander KP, Chen AY, Roe MT, et al. Excess dosing of antiplatelet and antithrombin agents in the treatment of non-ST-segment elevation acute coronary syndromes. JAMA. 2005 294(24): 3108–3116.

31. Plavix [package insert] Bridgewater, NJ: Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership; 2009.
32. Lovenox [package insert] Greenville, NC: sanofi-aventis; 2009.
33. Fragmin [package insert] New York, NY: Pfizer Inc; 2010.
34. Integrilin [package insert] Kenilworth, NJ: Schering Corporation, a subsidiary of Schering-Plough Corporation; 2010.
35. Aggrastat [package insert] Somerset, NJ: Medicure Pharma Inc; 2008.
36. Cohen M, Hoekstra J, Giugliano R, et al. Treatment strategies in non-ST-elevation acute coronary syndromes in patients undergoing percutaneous coronary intervention: an evidence-based review of clinical trial results and treatment guidelines: report on a roundtable discussion. J Interv Cardiol. 2008 21: 283–299.

37. Roe MT, Chen AY, Delong ER, et al. Patterns of transfer for patients with non-ST-segment elevation acute coronary syndrome from community to tertiary care hospitals. Am Heart J. 2008 156(1): 185–192.

38. Chandra A, Glickman SW, Ou FS, et al. An analysis ofthe Association of Society of Chest Pain Centers Accreditation to American College of Cardiology/American Heart Association non-ST-segment elevation myocardial infarction guideline adherence. Ann Emerg Med. 2009 54(1): 17–25.

39. Housholder-Hughes SD Non-ST-segment elevation acute coronary syndromes: management strategies for optimal outcomes. Crit Care Nurse 2006 (suppl): 8–10, 12, 14 passim; quiz 36.

40. Chen ZM, Pan HC, Chen YP, et al. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomized, placebo-controlled trial. Lancet. 2005 366(9497): 1622–1632.

41. Effient [package insert] Indianapolis, IN: Eli Lilly and Company; 2009.

42. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007 357(20): 2001–2015.

43. Holmes D, Kereiakes D, Kleiman N, Moliterno D, Giuseppe P, Gines C Combining antiplatelet and anticoagulant therapies. J Am Coll Cardiol. 2009 54(2): 95–109.

44. EPIC Investigators Use of a monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor in high-risk coronary angioplasty. N Engl J Med. 1994 330(14): 956–961.
45. EPILOG Investigators Platelet glycoprotein IIb/IIIa receptor blockade and low-dose heparin during percutaneous coronary revascularization. N Engl J Med. 1997 336(24): 1689–1696.
46. CAPTURE Investigators Randomised placebo-controlled trial of abciximab before and during coronary intervention in refractory unstable angina: the CAPTURE Study. Lancet. 1997 349(9063): 1429–1435.
47. IMPACT-II Investigators Randomised placebo-controlled trial of effect of eptifibatide on complications of percutaneous coronary intervention: IMPACT-II. Integrilin to minimise platelet aggregation and coronary thrombosis-II. Lancet. 1997 349(9063): 1422–1428.

48. RESTORE Investigators Effects of platelet glycoprotein IIb/IIIa blockade with tirofiban on adverse cardiac events in patients with unstable angina or acute myocardial infarction undergoing coronary angioplasty. The RESTORE Investigators. Randomized efficacy study of tirofiban for outcomes and restenosis. Circulation. 1997 96(5): 1445–1453.

49. EPISTENT Investigators Randomised placebo-controlled and balloon-angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein-IIb/IIIa blockade. Lancet. 1998 352(9122): 87–92.
50. Kastrati A, Mehilli J, Schuhlen H, et al. A clinical trial of abciximab in elective percutaneous coronary intervention after pretreatment with clopidogrel. N Engl J Med. 2004 350(3): 232–238.

51. PRISM Investigators A comparison of aspirin plus tirofiban with aspirin plus heparin for unstable angina. Platelet Receptor Inhibition in Ischemic Syndrome Management (PRISM) study investigators. N Engl J Med. 1998 338(21): 1498–1505.
52. Mukherjee D, Mahaffey KW, Moliterno DJ, et al. Promise of combined low-molecular-weight heparin and platelet glycoprotein IIb/IIIa inhibition: results from platelet IIb/IIIa antagonist for the reduction of acute coronary syndrome events in a global organization network B (PARAGON B). Am Heart J. 2002 144(6): 995–1002.

53. Tcheng JE, Lim IH, Srinivasan S, et al. Stent parameters predict adverse clinical outcomes and response to platelet glycoprotein IIb/IIIa blockade: findings of the ESPRIT trial. Circ Cardiovasc Interv. 2009 2(1): 43–51.

54. Hirsh J, Bauer KA, Donati MB, Gould M, Samama MM, Weitz JI Parenteral anticoagulants: American College of Chest Physicians evidence-based clinical practice guidelines. 8th ed. Chest. 2008 133(6)(suppl): 141S–159S.

55. Cooney M Heparin-induced thrombocytopenia: advances in diagnosis and treatment. Crit Care Nurse. 2006 26(6): 30–37.

56. Housholder-Hughes S, Bennett J The Nurse's Role in Managing HIT. Wayne, NJ: Health Learning Systems; 2003.
57. Warkentin TE, Kelton JG Temporal aspects of heparin-induced thrombocytopenia. N Engl J Med. 2001 344(7): 1286–1292.

58. Weitz JI Low-molecular-weight heparins. N Engl J Med. 1997 337(10): 688–698.

59. Hirsh J, Raschke R Heparin and low-molecular-weight heparin: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004 126(3)(suppl): 188S–203S.

60. Angiomax [package insert] Parsippany, NJ: The Medicines Company; 2005.

61. Legrand V, Doneux P, Martinez C, et al. Femoral access management: comparison between two different vascular closure devices after percutaneous coronary intervention. Acta Cardiol. 2005 60(5): 482–488.

62. Juran NB, Rouse CL, Smith DD, et al. Nursing interventions to decrease bleeding at the femoral access site after percutaneous coronary intervention. SANDBAG Nursing Coordinators. Standards of Angioplasty Nursing Techniques to Diminish Bleeding Around the Groin. Am J Crit Care. 1999 8(5): 303–313.

63. Doyle BJ, Ting HH, Bell MR, et al. Major femoral bleeding complications after percutaneous coronary intervention: incidence, predictors, and impact on long-term survival among 17,901 patients treated at the Mayo Clinic from 1994 to 2005. JACC Cardiovasc Interv. 2008 1(2): 202–209.

64. Dauerman H, Applegate R, Cohen D Vascular closure devices: the second decade. J Am Coll Cardiol. 2007 50(17): 1617–1626.

65. Hon LQ, Ganeshan A, Thomas SM, Warakaulle D, Jagdish J, Uberoi R An overview of vascular closure devices: what every radiologist should know. Eur J Radiol. 2010 73(1): 181–190.

66. Meyerson SL, Feldman T, Desai TR, et al. Angiographic access site complications in the era of arterial closure devices. Vasc Endovascular Surg. 2002 36(2): 137–144.

67. Galli A, Palatnik A Ask the experts. Crit Care Nurse. 2005 25(2): 88–95.

acute coronary syndrome; antiplatelet medications; anticoagulants; myocardial infarction; non–ST-segment elevation MI; unstable angina

© 2011 American Association of Critical–Care Nurses

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