Recognizing and Managing Asymptomatic Left Ventricular Dysfunction: After Myocardial Infarction Nancy M. Albert and Connie Lewis Crit Care Nurse 2008, 28:20-37. © 2008 American Association of Critical-Care Nurses Published online http://www.cconline.org Subscription Information http://ccn.aacnjournals.org/subscriptions Information for authors http://ccn.aacnjournals.org/misc/ifora.xhtml Submit Manuscript www.editorialmanager.com/ccn E-mail alerts http://ccn.aacnjournals.org/subscriptions/etoc.xhtml Critical Care Nurse is the official peer-reviewed clinical journal of the American Association ofCritical-Care Nurses, published bi-monthly by The InnoVision Group 101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949) 362-2049. Copyright © 2011 by AACN. All rights reserved. Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 Cover Article Recognizing and Managing Asymptomatic Left Ventricular Dysfunction After Myocardial Infarction PRIME POINTS Nancy M. Albert, PhD, CCNS, CCRN, CNA Connie Lewis, MSN, ACNP, ANP, CCRN • MI survivors should be assessed for asymptomatic LVSD. • Patients with asymptomatic LVSD after MI have worse outcomes than do patients without this dysfunction. A pproximately 865 000 myocardial infarctions occur each year in the United States; of these, approximately 565 000 are new cases.1 Despite advances in treatment, disabling heart failure develops in 46% of women and 22% of men within 6 • Improve survival and quality of life in these patients by recognizing the problem and promoting prompt use of evidence-based treatments. • Teach patients how to provide self-care before they leave the hospital. CEContinuing Education This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives: 1. Identify the definitive measurement for the diagnosis of asymptomatic left ventricular systolic dysfunction (LVSD) after myocardial infarction 2. Describe the pathophysiology of asymptomatic LVSD after myocardial infarction 3. Discuss the pharmacologic management of asymptomatic LVSD after myocardial infarction years after myocardial infarction.2 Approximately 40% of myocardial infarctions are accompanied by left ventricular systolic dysfunction (LVSD), with or without clinical (ie, symptomatic) heart failure.3 Although current management of myocardial infarction is improving patients’ survival, a markedly compromised heart decreases quality of life and functional capacity and increases hospitalization and mortality. With such a high proportion of survivors of myocardial infarction, especially women, in whom heart failure is likely to develop within a few years of the acute event, detection of LVSD should be a priority. During hospitalization, nurse clinicians should promote advocacy for patients, coordination of care, and 20 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org health-related education. Once cardiac damage due to a myocardial infarction is detected, the risk for clinical heart failure can be reduced by using medications selected on the basis of current clinical evidence. Building on disease management models that have been successful in patients with chronic heart failure, nurse clinicians should ensure that patients who have had a myocardial infarction receive the right medications, comprehensive self-care education to decrease the risk for new cardiac events, and an appointment for follow-up after discharge (eg, at a nurse-led clinic).4 It is crucial to organize hospital care structures to ensure that all cases of LVSD after myocardial infarction are detected and managed appropriately. Asymptomatic LVSD Many patients may not immediately have signs and symptoms of heart failure after myocardial infarction but may have LVSD due to injury of cardiomyocytes. Asymptomatic LVSD is classified as a form of structural heart disease that is strongly associated with development of heart failure but without signs or symptoms, also known as pre–heart failure or stage B heart failure5 (Figure 1). Asymptomatic LVSD is often undiagnosed and undertreated, even though its mortality and morbidity are high and similar to those in patients with clinical heart failure.5 Moreover, undiagnosed impaired cardiac function may confer an even higher risk for poor outcomes because patients are medically undertreated and do not understand their role in self-care. In this review, we discuss patients with asymptomatic LVSD after myocardial infarction in the context of progressive disease, presenting data supporting an aggressive diagnostic and therapeutic approach for this commonly overlooked and undertreated problem, and describe the role of nurse clinicians in improving care. Epidemiology In the United States, coronary artery disease is the most common cause of LVSD leading to heart failure among whites.6 Ischemic cardiomyopathy is the etiology of heart failure in approximately 61% of patients with mild to severe signs and symptoms.7 In the Survival and Ventricular Enlargement (SAVE) trial, asymptomatic LVSD was present in 58% of patients after myocardial infarction.8 Data on the percentage of patients in whom asymptomatic LVSD develops after myocardial infarction are limited. Authors Nancy M. Albert is director of nursing research and innovation for the Nursing Institute and a clinical nurse specialist at George M. and Linda H. Kaufman Center for Heart Failure, Cleveland Clinic Foundation in Cleveland, Ohio. Connie Lewis is a heart failure coordinator at Centennial Medical Center in Nashville, Tennessee. Corresponding author: Nancy M. Albert, RN, PhD, Cleveland Clinic Foundation, 9500 Euclid Ave, Mail Code P32, Cleveland, OH 44195 (e-mail: [email protected]). To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected]. http://ccn.aacnjournals.org Data from Europe indicate that only about 60% of patients with myocardial infarction have their ventricular function assessed.9,10 In a systematic review of 33 studies of heart failure after myocardial infarction between 1978 and 2000, Hellermann et al11 found that the incidence of heart failure was reported in only a few clinical trials, and generally, the criteria for diagnosis of heart failure were not provided. If the Killip class (a risk stratification system for patients after myocardial infarction that uses signs such as rales, S3 gallop, elevated jugular venous pressure, pulmonary edema, and cardiogenic shock) had been used as the classification measure, patients with asymptomatic LVSD would have been classified as Killip class 1, reflecting no clinical signs of heart failure. The registry for the Trandolapril Cardiac Evaluation (TRACE) study,12 a randomized controlled trial in which placebo and trandolapril were compared in patients with myocardial infarction, provides the best database for examining the occurrence of asymptomatic LVSD after myocardial infarction. Of 6676 patients in whom wall motion index (the degree of motion of the left ventricular wall during systole, which correlates with ejection fraction) could be determined, major LVSD developed in 2606 patients (39%). Among those with LVSD, clinical heart failure developed in 74%.12 TRACE researchers found that 30% of all patients had both LVSD and clinical heart failure and 54% of patients had features of heart failure but not LVSD, reflecting heart failure with preserved systolic function.12 Overall, 64% of patients had either heart failure or LVSD CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 21 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 into the natural history of asymptomatic LVSD. Overall, total mortality for patients receiving Stage B placebo was At high risk for heart failure; 25%, and structural heart disease but without clinical heart approximately failure 12% died within 1 year.16 Further, patients with a Have the following available Angiotensin-converting large left venPatient education enzyme-I or angiotensinmaterials/delivery receptor blocker (stages A tricle, measAdmitting order set and B) ured as a with criteria for use β-Blocker (stage B) Preprinted discharge baseline endImplantable cardioverter instructions defibrillator diastolic presAlgorithm for follow-up sure in the left care after discharge Reminder systems or ventricle checklists exceeding 30 Monitor quality mm Hg, had Advocate preventive therapies (flu shot) significantly higher rates of Figure 1 Asymptomatic left ventricular systolic dysfunction: guidelines for stage A and B heart failure: death or recommended therapies and nursing leadership to facilitate adherence with guidelines. severe heart Based on Hunt et al. failure at 4 years after acute myocardial infarction than did myocardial infarction, and death, within the first few days after a patients with a lower baseline left including sudden death.13-15 In the myocardial infarction.11 In populationventricular end-diastolic pressure.8 based community samples and regSAVE trial, the investigators specifiPatients with LVSD but no signs istries, the incidence of new-onset cally enrolled only patients with or symptoms of heart failure after heart failure after myocardial infarcacute myocardial infarction and myocardial infarction who seemed tion ranged from 22% to 48%, with a asymptomatic LVSD and followed 16 to be recovering well were also at mean of 37%, consistent with results up those cases for 3.5 years. Of high risk for sudden death. In the of the TRACE study.11 2231 patients with an ejection fracValsartan in Acute Myocardial tion of 40% or less, clinically signifiInfarction Trial (VALIANT), the incicant signs and symptoms of heart Prognosis dence and timing of sudden death in failure occurred in 16% of surviving Compared with patients without 14 609 patients with LVSD after patients receiving placebo, and 16% heart failure and LVSD after myocarmyocardial infarction were assessed.17 of all patients receiving placebo dial infarction, patients who have An increased early incidence of sudexperienced significant further deteheart failure and LVSD are at higher den death was most apparent rioration of left ventricular contracrisk for adverse outcomes, including among patients with low ejection tility, as indicated by a reduction of cardiac rupture, cardiac arrest, fraction. Of 156 sudden deaths or 9 units or more in ejection fraction. stroke, longer hospitalizations, vencardiac arrests with resuscitation These data provided some insight tricular arrhythmias, recurrent Stage A At high risk for heart failure but without structural heart disease or clinical (symptomatic) heart failure Therapy Treat/control medical conditions (hypertension, lipid abnormalities, metabolic syndrome or obesity, diabetes mellitus, vascular disease, coronary artery disease, or use of alcohol or illicit drugs) Nursing leadership Develop/implement algorithms or care pathways to optimize use of evidencebased therapies Be sure admission order sets include specialty consultation and treatment of medical conditions that place patients at high risk for heart failure Ensure that nurses understand education principles to teach patients about self-care 5 22 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org that occurred during the first 30 days, 85 cases, equating to 54% of all sudden deaths or cardiac arrests, occurred among patients with an ejection fraction of 30% or less,17 stressing the importance of early recognition of LVSD after myocardial infarction. necrotic tissue), or hypokinesis (decreased motion of left ventricular wall due to injured myocytes) after myocardial infarction cause sustained activation of the compensatory mechanisms, secondary damage of the left ventricle occurs, resulting in worsening remodeling of the left ventricle and cardiac decompensation.18 Norepinephrine, angiotensin II, endothelin, aldosterone, and tumor necrosis factor have been implicated as biologically active molecules that contribute to heart failure; however, adrenergic activation is thought to play the most powerful role via βadrenergic signaling responses. Adrenergic receptors have both beneficial and harmful biological Pathophysiology responses. They create a positive inotropic and chronotropic response and vasodilatation, but activation also leads to growth of cardiac myocytes, further muscle damage, vasoconstriction, and other harmful responses.18 In addition to activation of harmful signaling mechanisms, progression of disease in the left ventricle could be related to loss of beneficial effects of endogenous vasodilators such as nitric oxide, natriuretic peptides, and others if the vasodilators cannot counteract peripheral vasoconstrictor properties of norepinephrine and angiotensin II18 (Figure 2). The biological and physiological processes of heart failure are complex and beyond the scope of this article, but In asymptomatic LVSD after myocardial infarction, the myocardial infarction is the event that initiates a decline in pumping capacity, which leads to a reduction in ejection fraction. In order to compensate, mechanisms are activated in the adrenergic nervous system, renin-angiotensin aldosterone system, and cytokine system.18 The changes lead to restoration of cardiac Acute myocardial infarction function, and the patient Activation of remains Adrenergic nervous system Renin-angiotensin-aldosterone system asymptoCytokine system matic. If changes in left ventricular Negative prolonged adrenergic activation: Positive acute responses of adrenergic stimulation systolic and Cardiac myocyte growth Positive inotropy diastolic perCardiac muscle damage Positive chronotrophy Vasoconstriction and other harmful responses Vasodilatation formance from akinesis (lack of Left ventricular disease progression Maintain motion of left leading to remodeling asymptomatic left ventricular (dilatation and hypertrophy) ventricular dysfunction status wall due to tissue cell Hemodynamic effects death), dyski↑ Left ventricular end-diastolic stress nesis (abnor(afterload) ↑ Systolic left ventricular work mal motion of ↓ Cardiac output left ventricular ↓ Ejection fraction wall due to Figure 2 The complex pathophysiology of asymptomatic left ventricular systolic dysfunction after myocardial aneurysm forinfarction. mation at Based on Mann and Bristow and Philippides. injured or 18 http://ccn.aacnjournals.org 19 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 23 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 these processes lead to deterioration in left ventricular performance through progressive remodeling of the left ventricle, and such remodeling may independently lead to progression of heart failure.18 Similar to biological and physiological responses, the mechanical responses created by remodeling of the left ventricle are also complex and involve alterations in the biology of cardiac myocytes, the myocardium, and/or the left ventricle itself.18 As left ventricular size increases and geometry changes from an elliptical to a spherical shape, the end-diastolic wall stress (afterload) in the left ventricle tion, and functional deterioration. Alternatively, neurohormonal antagonism acts in asymptomatic LVSD by blocking the remodeling process responsible for the progressive dilatation of the left ventricle and declining systolic function that occurs after a myocardial infarction.19-21 Numerous clinical trials16,19,22,23 have drawn attention to the clinical importance of progressive remodeling of the left ventricle, and trial results suggest that clinical development of heart failure may be connected to the development of left ventricular dilatation and may occur years after the initial ischemic injury. Certain patient-specific factors patients of therapies that can prevent the progression of heart failure and reduce the risk of arrhythmias, reinfarction, and sudden death. Measurement of ejection fraction after myocardial infarction is extremely important because of the large increase in risk for LVSD associated with myocardial infarction. Asymptomatic LVSD should be suspected in any patient who has recently had a myocardial infarction and does not have symptoms of heart failure, especially patients with signs of heart failure such as elevated jugular venous pressure, positive hepatojugular reflux, and an S3 gallop. Early diagnosis of asymptomatic Compared with patients without heart failure and LVSD after myocardial infarction, patients who have heart failure and LVSD are at higher risk for adverse outcomes, including cardiac rupture, cardiac arrest, stroke, longer hospitalizations, ventricular arrhythmias, recurrent myocardial infarction, and death, including sudden death. increases, leading to an increase in left ventricular work during systole that contributes to a decrease in cardiac output18 (Figure 2). Higher filling pressures (higher end-diastolic pressure in the left ventricle) in patients with asymptomatic LVSD are associated with lower ejection fraction and are a significant predictor of death or clinical heart failure.8 Thus, neurohormonal activation leads to further loss of cardiomyocytes and worsening systolic dysfunction, promoting further remodeling, neurohormonal activa- contribute to progression from asymptomatic LVSD to symptomatic heart failure. Older age, diabetes, and hypertension contribute to the progression of underlying systolic and diastolic myocardial dysfunction and the atherosclerotic process.19 Importance of Diagnosis or Recognition The absence of signs or symptoms of heart failure after myocardial infarction may result in unrecognized LVSD, depriving LVSD is important, as suggested by clinical trials in which mortality, reinfarction, and other cardiovascular events were prevented when neurohormonal inhibitor therapy was implemented.16,24,25 Left ventricular function should be quantitatively measured by means of echocardiography, angiography, or radionuclide imaging in all patients after myocardial infarction. Although not a substitute for quantitative assessment of left ventricular function, measurement of the plasma level of brain natriuretic 24 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org peptide is useful in detecting heart failure and requires only a single, rapidly performed blood test. In 2 studies,26,27 measurement of the level of brain natriuretic peptide was helpful in predicting LVSD and remodeling after myocardial infarction. Plasma levels of brain natriuretic peptide had an 84% sensitivity in identifying the presence of asymptomatic LVSD in 75 patients without symptomatic heart failure after myocardial infarction.28 Further, some clinical features are associated with LVSD in acute myocardial infarction, and when present, these features should suggest LVSD in asymptomatic patients11,15,26,28-30 (Table 1). An algorithm that reflects the presence of new anterior Q-wave infarction, clinical signs of heart failure, or 2 or more previous myocardial infarctions plus an increase in level of cre- atine phosphokinase greater than 1000 U/L in patients who had not received thrombolytic agents had a 91% sensitivity and a 78% specificity for detecting an ejection fraction of 40% or less in patients with acute myocardial infarction.31 The value of early diagnosis of LVSD after myocardial infarction while the patient is still in the hospital should not be overlooked. The hospital in general, and a coronary care unit specifically, provides a structured setting within an acute environment with integrated care pathways or care plans; access to physicians, pharmacists, and specialty nurses who work in partnership; and the capacity to monitor serum levels of hormones and enzymes, cardiac hemodynamic parameters, and medication tolerance. Nurse clinicians can create a link between the acute myocardial Table 1 Diagnostic cues of left ventricular systolic dysfunction in the absence of symptomsa Type of cue Cue Definitive In hospital: echocardiography, ventriculography, or radionuclide imaging results of wall motion abnormality and left ventricular ejection fraction ≤40% After discharge: echocardiographic results of increased end-diastolic volume include increase in left ventricular mass and increased wall motion score index Adjunctive (but not definitive) Brain natriuretic peptide level >100 pg/dL Clinical features associated with left ventricular systolic dysfunction (does not imply causality; not definitive) Killip class II: rales, S3 gallop, and elevated jugular venous pressure Presence of hepatojugular reflux Early heart failure (shortly after admission for myocardial infarction): older age, history of symptomatic cardiac disease or diabetes mellitus Late heart failure (4 days or more after myocardial infarction): history of hypertension, male sex, tachycardia, higher peak level of creatine phosphokinase Early or late myocardial infarction: myocardial infarction of anterior wall a Based on Hellermann et al,11 Wu et al,15 Crilley and Farmer,26 Choy et al,28 Cowie et al,29 and Papadopoulos et al.30 infarction and the need for longterm treatment by ensuring an echocardiogram is obtained, assessing the level of brain natriuretic peptide (when obtained), and tracking clinical features known to be associated with LVSD after myocardial infarction. Underuse of Therapies for Myocardial Infarction Patients with LVSD after myocardial infarction account for a large proportion of patients treated in hospitals. These patients are at a high risk for adverse outcomes, and thus therapy initiated in the hospital must be optimized. Recent developments in pharmacological and device therapy, as well as initiatives to increase the use of standard orders and promote in-hospital communication, have improved the care of patients who have had a myocardial infarction. Data from registries indicate that care of patients with LVSD after myocardial infarction is surprisingly poor, despite the wealth of clinical trial data that show benefits of treatment with numerous agents. Researchers analyzing data from the National Registry of Myocardial Infarction (NRMI) of 606 500 patients with acute myocardial infarction found that patients who had heart failure at the time of hospitalization or in whom heart failure developed later, were less likely to be treated with evidence-based cardiac therapies than were patients without heart failure after myocardial infarction. Specifically, patients with heart failure were much less likely to be treated with aspirin and β-blockers in the first 24 hours than were patients without heart failure.33 The 26 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org Nurses must work collaboratively with other healthcare providers and use a team approach with nurse peers to test all patients who have had a myocardial infarction for the presence of asymptomatic LVSD; develop processes and systems that promote use of evidence-based practices; promote education of patients throughout the hospital stay, not just before discharge; and implement performance-improvement initiatives based on process and outcome measures of importance in this population of patients (Figure 1). Additionally, advance practice nurses and nurse educators can provide education to increase the understanding of nurse clinicians of pathophysiological changes after myocardial infarction that lead to heart failure, optimal treatment strategies, timing of treatment strategies, and expectations for teaching of patients so that care 1992-1993 1994-1995 1996-1997 2000-2001 2002-2003 80 70 60 50 40 30 20 10 0 β-Blocker Applying a Multidisciplinary Approach http://ccn.aacnjournals.org 1998-1999 90 Aspirin Nurse clinicians, using a multidisciplinary approach, can help overcome obstacles associated with underuse of cardiac therapies. delivery is coordinated and synchronized to improve patients’ outcomes. Hospitalization should serve as a teaching opportunity for patients and their healthcare providers about the importance of delivering optimal therapy during hospitalization to ensure cardiovascular health after discharge. Patients who do not start treatment with a lifesaving cardiovascular agent in the hospital are also less likely to receive that therapy after discharge.35 Programs that used a multidisciplinary care approach to promote optimization of evidencebased therapies during hospitalization were tremendously successful.35,36 The Cardiac Hospitalization Atherosclerosis Management Program (CHAMP) was a multidisciplinary hospital initiative that involved nurses, physicians, medication advice, dietary advice, and exercise counseling after myocardial infarction.35 The multimodal intervention 100 % of patients CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines) registry investigators examined discharge therapy of 45 744 patients with non–ST-elevation myocardial infarction and heart failure. At the time of hospitalization, 10 398 patients (22.7%) had signs of heart failure and another 1664 (3.6%) had clinical (symptomatic) heart failure. Treatment patterns and in-hospital outcomes in both sets of patients were compared with those of patients without signs of heart failure.34 The results indicated that patients with signs of heart failure were treated less often with medications and invasive cardiac procedures in the first 24 hours after presentation. These studies suggest significant underuse of important cardiac therapies for patients with signs of heart failure or clinical heart failure during the early course of hospital care after myocardial infarction. Although no one has specifically measured treatment patterns in patients with asymptomatic LVSD after myocardial infarction, these patients likely also do not receive the best evidence-based care. Possible causes are lack of recognition of LVSD when symptoms are not present or unwarranted fear of prescribing vasoactive cardiovascular therapy to patients with LVSD. Angiotensinconverting enzyme inhibitor Drugs prescribed Statin Figure 3 Sustained impact of the Cardiac Hospitalization Atherosclerosis Management Program. Reprinted from Fonarow,37 with permission. CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 27 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 resulted in a dramatic increase in the prescription of angiotensin-converting enzyme (ACE) inhibitors, βblockers, statins, and aspirin in the year after its implementation37 (Figure 3) and a reduction in new myocardial infarction, heart failure, hospitalizations, and total mortality events.35 Increased predischarge prescription rates in patients hospitalized after myocardial infarction were sustained for 10 years.37 A hospital-based multidisciplinary care approach can prompt early and continued use of lifesaving agents. Researchers from the Initiation Management Predischarge: Process for Assessment of Carvedilol Therapy in Heart Failure (IMPACTHF) trial showed that patients with heart failure in whom treatment with a β-blocker was started in the hospital were more likely to maintain treatment at 60 days after discharge than were patients who were discharged without a β-blocker with a plan to start taking it in an outpatient setting. At 60 days after hospital discharge, 91% of patients who started treatment in the hospital were still taking treatment, compared with 73% of patients who started treatment after discharge (P < .001).38 Investigators from multidisciplinary programs who followed up many patients over time found that when therapy for acute coronary syndrome was started in the hospital, patients were more likely to adhere to therapies long term.39 Many hospital discharge education and disease management programs and postdischarge disease management programs are disease specific; care processes (documentation of education delivered or laboratory testing) and drug therapies Table 2 American College of Cardiology/American Heart Association guidelines for patients with ST-elevation myocardial infarction: class I recommendations for education at dischargea Time Education on and planning for adherence Before hospital discharge For patients Lifestyle changes Drug therapies important for secondary prevention of cardiovascular disease At discharge For patients and their families (to ensure early evaluation and treatment if signs or symptoms recur) Recognizing acute cardiac signs and symptoms Appropriate actions to take in response to signs or symptoms Calling 911 if symptoms are Unimproved or worsen after 5 minutes of onset Unimproved or worsen 5 minutes after 1 dose of sublingual nitroglycerin Automated external defibrillators Cardiopulmonary resuscitation, including referral to a training program (training programs with a social support component for high-risk patients preferred) Need for follow-up appointment to assess for left ventricular function and need for implantable cardioverter defibrillator (if ejection fraction <35% after optimal medical therapies) For patients’ families a Based on Antman et al.40 are based on disease-specific standards of care, nationally developed performance measures, and consensus guidelines derived from multicenter, randomized controlled studies. Although in disease management programs, patients generally are taught about self-care, receive treatment related to the disease process, are monitored for adherence to medical therapy, and receive risk reduction testing and therapies, management is usually specific to the primary discharge diagnosis. Thus, care and discharge instructions of patients after myocardial infarction may not include material about chronic heart failure. Principles for managing stage B heart failure and education of patients with asymptomatic LVSD after myocardial infarction might be even less likely, because patients do not have clinical (symptomatic or stage C) heart failure. Care and discharge education for patients with asymptomatic LVSD after myocardial infarction must be integrated into emerging multidisciplinary management programs. In-hospital emphasis on and predischarge education about preventive and self-care measures are as important as ensuring patients receive proper medications. Patients who continue to smoke, not exercise, and eat poorly are at high risk for a secondary cardiac event, including a new myocardial infarction. Educating patients while they are in the hospital is a class I recommendation from the American College of Cardiology/American Heart Association (ACC/AHA) guidelines40 for myocardial infarction with STsegment elevation to maximize adherence to treatments and evidence-based medications after the event. Education should begin early during hospitalization, be delivered intensively at discharge (Table 2), and continue at follow-up during visits with providers, cardiac rehabilitation, and interactions with 28 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org community support groups.40 Individualized teaching programs led by cardiac nurses that can be tailored to suit the needs of different patients are clearly needed.41 Cardiovascular nurse clinicians are invaluable in bridging the gap between primary and secondary care. Education of patients should be viewed as a continuous process that is a part of every encounter with a patient, including each encounter during hospitalization. Pharmacological and Device Therapies Nurse clinicians involved in hospital management of patients who have had a myocardial infarction must be able to accurately determine the timing for initiating treatment strategies to promote optimal care that decreases the risk for poor outcomes. Some studies42 have focused on reestablishing coronary blood flow as soon as possible because of a significant mortality benefit from thrombolytic therapy in patients with acute myocardial infarction. Reperfusion therapies do not halt or slow the progression of LVSD; left ventricular remodeling still occurs after successful percutaneous transluminal coronary angioplasty despite sustained patency of the infarct-related artery and preservation of regional and global function of the left ventricle.43 In a study30 of 55 patients who had reperfusion after acute myocardial infarction and treatment with antiremodeling medications (ACE inhibitor and βblocker), 28% experienced increases in left ventricular volume within 6 months. Similarly, 1 year after acute myocardial infarction of the anterior wall in 266 patients, 31% had left Table 3 American College of Cardiology/American Heart Association guidelines for management of ST-elevation myocardial infarctiona Acute therapies Discharge and postdischarge therapies Aspirin Aspirin Clopidogrel (if percutaneous coronary intervention) Clopidogrel β-Blocker Angiotensin-converting enzyme inhibitor Heparin (low-molecularweight heaprin or unfractionated heparin) Glycoprotein IIb-IIIa inhibitor (if percutaneous coronary intervention) Percutaneous coronary intervention or primary thrombolysis β-Blocker Angiotensin-converting enzyme inhibitor Aldosterone antagonist Statin (preferred) or other lipid-lowering therapy Smoking cessation counseling Cardiac rehabilitation or aerobic exercise Weight control if obese; diet high in omega-3 fatty acids Control of blood pressure (resting systolic blood pressure <140 mm Hg; resting diastolic blood pressure <90 mm Hg) Control of diabetes (fasting blood glucose level 80-100 mg/dL) Anticoagulants, if indicated Placement of implantable cardioverter defibrillator (after 40 days after myocardial infarction) if ejection fraction remains <35% after optimal medical therapies a Based on Antman et al40 and Amin.45 ventricular remodeling, even though 87% underwent coronary stenting of the infarct-related lesion and 54% received thrombolysis therapy.44 Even if a patient has had revascularization or does not initially have signs or symptoms of heart failure, LVSD may still be present and must be appropriately and aggressively treated to halt progression of the disease. As recommended by the ACC/ AHA treatment guidelines for both heart failure and myocardial infarction, management of patients with asymptomatic LVSD after myocardial infarction should be directed at treating neurohormonal activation due to remodeling and progression of coronary artery disease.5,40 The guidelines recommend treatment of risk factors for coronary artery disease, including hypertension, cigarette smoking, and dyslipidemia, and the use of evidence-based therapies for left ventricular dysfunction including, ACE inhibitors and βblockers.5 Use of neurohormonal antagonists is strongly recommended for acute myocardial infarction.40 A number of other therapies are beneficial in patients with asymptomatic LVSD after myocardial infarction and are reviewed briefly in the following sections and in Table 3. Table 4 gives the major clinical outcomes from trials that included patients with asymptomatic LVSD.12,16,21,46-55 ACE Inhibitors/Angiotensin Receptor Blockers An ACE inhibitor should be administered orally within the first 24 hours after a myocardial infarction in patients with anterior myocardial infarction, heart failure, or an ejection fraction less than 40% 30 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org Table 4 Clinical trials in patients with asymptomatic left ventricular systolic dysfunction12,16,21,46-55 Risk reduction, % Study Average duration, months Relative mortality Sudden death Death due to worsening heart failure Population of patients (N) Treatment Acute myocardial infarction and asymptomatic LVSD (2231) Captopril vs placebo 42 19 (P = .02) No difference (P = NS) 36 (P = .032) Asymptomatic LVSD (4228) Enalapril vs placebo 37.4 8 (P = NS) No difference (P = NS) Trandolapril vs placebo 24-50 22 (P = .001) 24 (P = .03) 20a (P < .001) 29b ACE inhibitors SAVE SOLVD prevention TRACE Myocardial infarction and LVSD (6676; 1749 randomized); asymptomatic LVSD (542) (P = .003) β-Blockers Retrospective analysis of SOLVD prevention Asymptomatic LVSD (4228; 1015 patients taking β-blockers) β-Blockers vs no β-blockers plus enalapril 37.4 23 (P < .01) 28c (P < .05) 29 (P < .05) Post hoc analysis of SAVE Asymptomatic LVSD (2231; 789 patients taking β-blockers ) β-Blockers vs no β-blockers plus captopril 42 43 (P < .001) NR 32b (P < .001) Heart failure (415); asymptomatic LVSD (124) Carvedilol vs placebo 19 36a (P = .02) 10 (P = NS) 8 (P = NS) LVSD after acute myocardial infarction (1959); asymptomatic LVSD (1023) Carvedilol vs placebo (including ACE inhibitor) 15.6 23 (P = .03) 26 (P = .098) 40 (P = .08) Myocardial infarction and LVSD, heart failure, or both (14 703); asymptomatic LVSD (4099) Valsartan, captopril, or both 24.7 No difference (P = NS) NR No difference (P = NS) Acute myocardial infarction and symptomatic heart failure (5477); asymptomatic LVSD (1735) Losartan vs captopril 32.4 13% increase in risk with losartan (P = .07) 19% increase in risk with losartan (P = .07) NR ANZ CAPRICORN Angiotensin-receptor blockers VALIANT OPTIMAAL Implantable cardioverter defibrillators MADIT-II Myocardial infarction and LVEF ≤30% (1232); Asymptomatic LVSD (461) ICD vs CMT 20 31 (P = .02) NR NR DEFINITE Nonischemic dilated cardiomyopathy, LVEF <36% (458); Asymptomatic LVSD (99) ICD vs CMT 29 35 (P = NS) 80d (P = .006) NR Abbreviations: ACE, angiotensin-converting enzyme; CMT, conventional medical therapy; ICD, implantable cardioverter defibrillator; LVEF, left ventricular ejection fraction; LVSD, left ventricular systolic dysfunction; NR, not reported; NS, not significant. a Death or hospitalization for heart failure. b Severe heart failure. c Arrhythmic death. d Sudden death from arrhythmia. Reprinted from Goldberg and Jessup,55 with permission. reflecting asymptomatic LVSD. If tolerated, the ACE inhibitor should http://ccn.aacnjournals.org be administered during convalescence and continued indefinitely after discharge.40 Researchers in a pivotal randomized clinical trial CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 31 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 (SAVE),16 specifically addressed patients with asymptomatic LVSD after myocardial infarction. Compared with placebo, use of captopril was associated with a 19% risk reduction in all-cause mortality (P = .02).16 Captopril also decreased progression to clinical heart failure by 37% (P < .001), hospitalization for heart failure by 22% (P = .02), and recurrent myocardial infarction by 25% (P = .02).16 An echocardiographic substudy56 of SAVE indicated that left ventricular remodeling can be attenuated by ACE inhibitors. In 420 patients, 2dimensional echocardiography was performed soon after infarction and repeated after 1 year. The size of the left ventricle increased both in patients who received placebo and in patients who received captopril; however, the increases were significantly greater in the placebo-treated group (P = .02 for diastolic and for systolic).56 In VALIANT, patients with left ventricular dysfunction after myocardial infarction were randomized to treatment with captopril alone (target dose: 50 mg 3 times daily), valsartan alone (target dose: 160 mg twice daily), and combination therapy (target doses: captopril 50 mg 3 times daily, valsartan 80 mg TIMELY DIAGNOSIS AND A MULTIDISCIPLINARY APPROACH TO PATIENT CARE IS CRUCIAL twice daily).51 After median followup of 24.7 months, no significant differences in the risk of death among the 3 groups were apparent, although the combination group had more drug-related adverse events (hypotension, hyperkalemia, renal dysfunction). VALIANT provided evidence that the angiotensinreceptor blocker valsartan was just as effective as an ACE inhibitor in patients with asymptomatic LVSD after myocardial infarction. However, the addition of an angiotensinreceptor blocker to an ACE inhibitor did not provide an incremental benefit and therefore is not recommended as an addition to therapy.51 Angiotensin-receptor blockers may be used as an alternative for patients who are intolerant of ACE inhibitors because of cough, symptomatic hypotension, or angioedema. β-Adrenergic Blockers Although the benefits of βblocker therapy in patients who have had a myocardial infarction are established, relative risks and benefits in patients with LVSD after myocardial infarction are not as well understood. Many early trials of βblocker therapy excluded patients with heart failure or known LVSD. • Survivors of myocardial infarction should be assessed for asymptomatic left ventricular systolic dysfunction (LVSD). Investigators in the Carvedilol PostInfarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) trial specifically enrolled 1959 patients who had LVSD after myocardial infarction (ejection fraction ≤40%), with or without signs or symptoms of heart failure, and compared the effect of carvedilol with that of placebo on mortality and morbidity.21 In the CAPRICORN study, 34% of participants had no signs or symptoms of heart failure. Patients received an ACE inhibitor (97%) and aspirin (86%), and many had thrombolysis or primary angioplasty (46%) for acute myocardial infarction before enrollment. Carvedilol-treated patients experienced a 23% relative risk reduction in all-cause mortality (P = .03) and a 41% relative risk reduction in recurrent nonfatal myocardial infarction (P = .01) during 1.3 years of followup.21 Subgroup analysis indicated that all-cause mortality was reduced similarly in patients treated with carvedilol regardless of their status relative to signs and symptoms of heart failure.55 The improvement in clinical outcomes in the CAPRICORN trial is consistent with a retrospective analysis49 of patients enrolled in • Patients who have asymptomatic LVSD after myocardial infarction have worse outcomes than do patients without LVSD. 32 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 • Cardiac nurses are uniquely positioned to help improve patients’ survival and quality of life by facilitating recognition of LVSD and promoting use of evidence-based therapies early in the course of treatment. http://ccn.aacnjournals.org SAVE who concomitantly received βblockers (approximately 35% of study participants). β-Blocker use was associated with a 30% risk reduction in cardiovascular death and a 21% risk reduction in progression to severe heart failure that were independent of concomitant use of an ACE inhibitor or a placebo.49 In the SOLVD Prevention trial,48 the combination of a β-blocker and an ACE inhibitor was associated with a synergistic reduction in the risk of death in patients with asymptomatic LVSD. An echocardiographic substudy57 of 127 patients from the CAPRICORN trial indicated that β-blocker treatment was associated with reversal of left ventricular remodeling at 6 months. Although carvedilol treatment did not significantly alter enddiastolic volume, end-systolic volume decreased 4.8 mL with carvedilol and increased 4.5 mL with placebo (P = .02). Left ventricular ejection fraction also increased in the carvedilol group by 5% after 6 months of treatment; no change was observed with placebo.57 blocker) reduced the risk of mortality in patients with LVSD after myocardial infarction and symptomatic heart failure in the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS).20 Aldosterone antagonists have not been investigated in patients with asymptomatic LVSD. In EPHESUS, 6642 patients with LVSD after myocardial infarction were randomized to treatment with eplerenone or placebo. Eplerenone treatment was associated with a relative risk reduction in all-cause mortality (15%; P = .008), sudden death (21%; P = .03), and hospitalization for heart failure (15%; P = .03).20 Aldosterone blockade with eplerenone also had early benefits. In an analysis58 of all-cause mortality and sudden cardiac death in the EPHESUS trial after 30 days of treatment, researchers found a 31% risk reduction in all-cause mortality and a 37% risk reduction in sudden cardiac death compared with placebo. Statins Statins (hydroxymethylglutarylCoA reductase inhibitors) are indicated in the management of patients after myocardial infarction and Use of an aldosterone antagonist should be considered in patients (added to an ACE inhibitor and a βwith asymptomatic • A multidisciplinary • Cardiac nurses can LVSD after approach to care of reduce risks and enhance myocarpatients with asymptopatients’ adherence to dial matic LVSD after myocarmedical therapies by infarcdial infarction prompts ensuring that each tion. Repatient understands what evidence-based treatment searchers he or she is taught before and may help patients in 2 lipidcontinue with therapies. hospital discharge. lowering studies59,60 Aldosterone Receptor Antagonists http://ccn.aacnjournals.org specifically enrolled survivors of myocardial infarction without heart failure. Researchers of the Scandinavian Simvastatin Survival Study59 found that simvastatin reduced the relative risk of new nonfatal myocardial infarction by 38% and the overall risk of heart failure by 21% in 4444 randomized patients with a history of myocardial infarction. In the Cholesterol and Recurrent Events (CARE) trial60 4159 survivors of myocardial infarction without evidence of heart failure were randomized to treatment with pravastatin or placebo.60 Compared with placebo, pravastatin reduced the relative risk of myocardial infarction by 25%. In a CARE trial subgroup of patients with LVSD (706 with ejection fraction between 25% and 40%), pravastatin provided a significant 28% reduction in risk for myocardial infarction.60 Implantable Cardioverter Defibrillators Although the ACC/AHA guidelines stress the importance of preventing the progression of LVSD from an asymptomatic state to symptomatic heart failure, patients who have had a myocardial infarction, especially those with LVSD, die suddenly and unexpectedly of lethal arrhythmias.16,21,61 The role of treatment with an implantable cardioverter defibrillator (ICD) was compared with drug therapy for patients with LVSD after myocardial infarction in several trials. Investigators in the Multicenter Unsustained Tachycardia Trial (MUSTT) enrolled 2202 patients with unsustained ventricular tachycardia, left ventricular ejection fraction less than 40%, and coronary artery disease.62 Rates of CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 33 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 arrhythmic death and overall mortality were lower in the patients who had an ICD.62 In the second Multicenter Automatic Defibrillator Implantation Trial (MADIT II), 1232 patients with a left ventricular ejection fraction of 30% or less and a history of prior myocardial infarction were randomized to receive preventive placement of an ICD or conventional medical therapy after myocardial infarction. Patients who received an ICD had a myocardial infarction include implantation of an ICD if ejection fraction criteria are met 40 days after myocardial infarction. Care Pathways Risk-stratification tools are available for patients with acute coronary syndromes.65-70 These clinical prediction models can facilitate optimization of patients’ management and were integrated into national guidelines to help enhance patients’ out- vide resources and processes that match pathway actions. A number of tools, including preprinted orders,45,73 care maps,73,74 discharge forms,45,73,74 physician/nursing education plans,45,73,74 and treatment utilization reports,73,74 have been developed to encourage the initiation of as many lifesaving therapies as possible before patients are discharged. Tools are designed to specify guideline-recommended treatments and encourage proper Nurse clinicians can create a link between the acute myocardial infarction and the need for long-term treatment by ensuring an echocardiogram is obtained, assessing the level of brain natriuretic peptide (when obtained), and tracking clinical features known to be associated with LVSD after myocardial infarction. significantly better survival after 20 months.53 In the Defibrillator in Acute Myocardial Infarction Trial (DINAMIT), patients with a left ventricular ejection fraction of 35% or less and decreased heart rate variability were randomized to receive an ICD between 6 and 40 days after myocardial infarction.63,64 Overall mortality was not improved by early implantation of an ICD because the reduction in arrhythmic death was offset by nonarrhythmic events; therefore, the use of an ICD before 40 days after myocardial infarction is not currently recommended.59 Both studies included a sizable proportion of patients with asymptomatic LVSD, thus current ACC/AHA guidelines for patients who have had comes.71 In the Duke Heart Failure Program, clinicians used significantly more β-blocker therapy after pathway implementation, more patients reached target β-blocker doses, and cost of care decreased throughout the hospital system.72 Management pathways for myocardial infarction can serve as the framework for developing and instituting optimal in-hospital management of patients after myocardial infarction by reminding caregivers to assess for LVSD and noting recommended treatments. Education of patients, assessment of social support and depression, discharge planning, follow-up, and outpatient monitoring can also be improved through critical pathways that pro- administration in appropriate patients. The results of an observational analysis of hospital care in 64 775 patients with acute coronary syndrome who were enrolled in the CRUSADE National Quality Improvement Initiative were assessed to evaluate use of the ACC/AHA guideline recommendations.75 In 74% of cases, care decisions were consistent with the ACC/AHA guidelines. The overall rate for adherence to guidelines was significantly associated with inhospital mortality: mortality rates decreased from 6.31% for the lowest adherence quartile to 4.15% for the highest adherence quartile (P < .001). Every 10% (risk-adjusted) increase in composite adherence in a hospital 34 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org was associated with a 10% decrease in its patients’ likelihood of inhospital mortality (P < .001).75 The significant association between care process and outcomes supports the use of broad, guideline-based performance metrics as a means of assessing and helping improve hospital quality. The ACC/AHA guidelines recommend that critical pathways, protocols, and other quality improvement tools be used by caregivers and institutions to improve the application of evidence-based treatments for patients with STsegment elevation myocardial infarction.40 In the AHA Get With the Guidelines program, many tools can be used to improve care. For example, an online patient management tool provides source documentation of performance measures and also is the source of patient education materials and treatment plan summaries used to educate or facilitate communication among health care providers.76 Analyses of data from the patient management tool can be used to identify factors related to patients and hospital systems that can be altered to improve patients’ outcomes or delivery of cardiovascular care. third of patients have LVSD after myocardial infarction, and about one-half of patients with LVSD are asymptomatic. The risk of death or heart failure depends on the extent of injury of the left ventricle. Mortality in asymptomatic LVSD can be from progressive heart failure, recurrent myocardial infarction, or lethal arrhythmias. The lack of signs or symptoms of heart failure after myocardial infarction may create a false sense of health and deprive patients of proven lifesaving therapies. Timely diagnosis of asymptomatic LVSD by echocardiography, ventriculography, or radionuclide imaging is crucial. Evidence-based management of asymptomatic LVSD in patients who have had a myocardial infarction centers on early and continued neurohormonal antagonism of the renin-angiotensin-aldosterone and sympathetic nervous systems with an ACE inhibitor or angiotensinreceptor blocker and β-blocker therapy because these agents reduce risk of mortality and the likelihood of heart failure developing. Although recent clinical guidelines do not specifically recommend any particular agent, captopril, enalapril, and carvedilol have the most evidence of effectiveness in patients with asympConclusions tomatic LVSD after myocardial Nurse clinicians play a critical infarction. Of major importance is role in caring for patients after treatment of risk factors for progresmyocardial infarction. About onesion of heart failure and coronary artery disease, including hypertension, diabetes, and dyslipidemia, and placement of an ICD as indicated for primary or secondary prevention of To learn more about heart failure, read sudden cardiac arrest. Hospital nurse “Evidence-Based Practice for Acute Decompensated Heart Failure” by Nancy M. Albert, clinicians, advanced practice nurses, Cathy A. Eastwood, and Michelle L. Edwards and nurse educators should develop in Critical Care Nurse 2004:24:14-29. Aavailable online at ccn.aacnjournals.org. and use critical pathways to improve • d t http://ccn.aacnjournals.org recognition and treatment of LVSD after myocardial infarction and to educate patients. The prevention of disease progression in patients with asymptomatic LVSD after myocardial infarction is based on early intervention and education. CCN Financial Disclosures Nancy Albert is on the speaker’s bureau and is a consultant for GlaxoSmithKline and is a consultant for Medtronic Inc. eLetters Now that you’ve read the article, create or contribute to an online discussion about this topic using eLetters. Just visit http://ccn.aacnjournals .org and click “Respond to This Article” in either the full-text or PDF view of the article. References 1. American Heart Association. Heart Disease and Stroke Statistics: 2007 Update. Dallas, TX: American Heart Association; 2007. 2. American Heart Association. Heart Disease and Stroke Statistics: 2006 Update. Dallas, TX: American Heart Association; 2006. 3. Kober L, Torp-Pedersen C, Jorgensen S, Eliasen P, Camm AJ. Changes in absolute and relative importance in the prognostic value of left ventricular systolic function and congestive heart failure after acute myocardial infarction. TRACE Study Group. Trandolapril Cardiac Evaluation. Am J Cardiol. 1998;81(11):1292-1297. 4. Fonarow GC, Abraham WT, Albert NM, et al. Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF): rationale and design. Am Heart J. 2004;148(1):43-51. 5. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). American College of Cardiology Web site. http://www .acc.org/qualityandscience/clinical /guidelines/failure/update/index.pdf. Accessed January 8, 2008. 6. Gheorghiade M, Bonow RO. Chronic heart failure in the United States: a manifestation of coronary artery disease. Circulation. 1998;97(3):282-289. 7. Frazier CG, Alexander KP, Newby LK, et al. Associations of gender and etiology with outcomes in heart failure with systolic dysfunction. J Am Coll Cardiol. 2007;49(13): 1450-1458. 8. Mielniczuk LM, Lamas GA, Flaker GC, et al. Left ventricular end-diastolic pressure and risk of subsequent heart failure in patients following an acute myocardial infarction. Congest Heart Fail. 2007;13(4):209-214. 9. Hasdai D, Behar S, Wallentin L, et al. A prospective survey of the characteristics, CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 35 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. treatments and outcomes of patients with acute coronary syndromes in Europe and the Mediterranean basin; the Euro Heart Survey of Acute Coronary Syndromes (Euro Heart Survey ACS). Eur Heart J. 2002;23(15):1190-1201. Cleland JG, Torabi A, Khan NK. Epidemiology and management of heart failure and left ventricular systolic dysfunction in the aftermath of a myocardial infarction. Heart. 2005;91(suppl 2):ii7-ii13. Hellermann JP, Jacobsen SJ, Gersh BJ, Rodeheffer RJ, Reeder GS, Roger VL. Heart failure after myocardial infarction: a review. Am J Med. 2002;113(4):324-330. Kober L, Torp-Pedersen C, Carlsen JE, et al. A clinical trial of the angiotensin-convertingenzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group. N Engl J Med. 1995;333(25):1670-1676. Hasdai D, Topol EJ, Kilaru R, et al. Frequency, patient characteristics, and outcomes of mild-to-moderate heart failure complicating ST-segment elevation acute myocardial infarction: lessons from 4 international fibrinolytic therapy trials. Am Heart J. 2003;145(1):73-79. Steg PG, Dabbous OH, Feldman LJ, et al. Determinants and prognostic impact of heart failure complicating acute coronary syndromes: observations from the Global Registry of Acute Coronary Events (GRACE). Circulation. 2004;109(4):494-499. Wu AH, Parsons L, Every NR, Bates ER. Hospital outcomes in patients presenting with congestive heart failure complicating acute myocardial infarction: a report from the Second National Registry of Myocardial Infarction (NRMI-2). J Am Coll Cardiol. 2002;40(8):1389-1394. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: results of the Survival and Ventricular Enlargement trial. The SAVE Investigators. N Engl J Med. 1992;327(10):669-677. Solomon SD, Zelenkofske S, McMurray JJ, et al. Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. N Engl J Med. 2005;352(25):2581-2588. Mann DL, Bristow MR. Mechanisms and models in heart failure: the biomechanical model and beyond. Circulation. 2005; 111(21):2837-2849. Philippides GJ. Managing the post-myocardial infarction patient with asymptomatic left ventricular dysfunction. Cardiology. 2005;105(2):95-107. Pitt B, Remme W, Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 2003;348(14):1309-1321. Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial. Lancet. 2001;357(9266):1385-1390. Wang TJ, Evans JC, Benjamin EJ, Levy D, LeRoy EC, Vasan RS. Natural history of asymptomatic left ventricular systolic dysfunction in the community. Circulation. 2003;108(8):977-982. 23. McDonald KM, Chu C, Francis GS, et al. Effect of delayed intervention with ACEinhibitor therapy on myocyte hypertrophy and growth of the cardiac interstitium in the rat model of myocardial infarction. J Mol Cell Cardiol. 1997;29(12):3203-3210. 24. GISSI-3 Investigators. GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute myocardial infarction. Gruppo Italiano per lo Studio della Sopravvivenza nell’infarto Miocardico. Lancet. 1994;343(8906):11151122. 25. ISIS-4 Collaborative Group. ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58 050 patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. Lancet. 1995;345(8951):669-685. 26. Crilley JG, Farrer M. Left ventricular remodelling and brain natriuretic peptide after first myocardial infarction. Heart. 2001;86(6):638-642. 27. Bettencourt P, Ferreira A, Pardal-Oliveira N, et al. Clinical significance of brain natriuretic peptide in patients with postmyocardial infarction. Clin Cardiol. 2000;23(12): 921-927. 28. Choy AM, Darbar D, Lang CC, et al. Detection of left ventricular dysfunction after acute myocardial infarction: comparison of clinical, echocardiographic, and neurohormonal methods. Br Heart J. 1994;72(1):16-22. 29. Cowie MR, Lacey L, Tabberer M. Heart failure after myocardial infarction: a neglected problem? Br J Cardiol. 2005;12(3):205-208. 30. Papadopoulos CE, Karvounis HI, Giannakoulas G, et al. Predictors of left ventricular remodeling after reperfused acute myocardial infarction. Am J Cardiol. 2007;99(7):1024-1025. 31. Darbar D, Gillespie N, Choy AM, et al. Diagnosing left ventricular dysfunction after myocardial infarction: the Dundee algorithm. QJM. 1997;90(11):677-683. 32. McDonagh TA. Lessons from the management of chronic heart failure. Heart. 2005;91(suppl 2):ii24-ii27. 33. Spencer FA, Meyer TE, Gore JM, Goldberg RJ. Heterogeneity in the management and outcomes of patients with acute myocardial infarction complicated by heart failure: the National Registry of Myocardial Infarction. Circulation. 2002;105(22):2605-2510. 34. Roe MT, Chen AY, Riba AL, et al. Impact of congestive heart failure in patients with non-ST-segment elevation acute coronary syndromes. Am J Cardiol. 2006;97(12):17071712. 35. Fonarow GC, Gawlinski A, Moughrabi S, Tillisch JH. Improved treatment of coronary heart disease by implementation of a Cardiac Hospitalization Atherosclerosis Management Program (CHAMP). Am J Cardiol. 2001;87(7):819-822. 36. Albert NM, Fonarow GC, Abraham WT, et al. Predictors of delivery of hospital-based heart failure patient education: a report from OPTIMIZE-HF. J Card Fail. 2007;13(3):189-198. 37. Fonarow GC. In-hospital initiation of statin therapy in acute coronary syndromes: maximizing the early and long-term benefits. Chest. 2005;128(5):3641-3651. 38. Gattis WA, O’Connor CM, Gallup DS, Hasselblad V, Gheorghiade M. Predischarge initiation of carvedilol in patients hospitalized for decompensated heart failure: results of the Initiation Management Predischarge: Process for Assessment of Carvedilol Therapy in Heart Failure (IMPACT-HF) trial. J Am Coll Cardiol. 2004;43(9):1534-1541. 39. Eagle KA, Kline-Rogers E, Goodman SG, et al. Adherence to evidence-based therapies after discharge for acute coronary syndromes: an ongoing prospective, observational study. Am J Med. 2004;117(2):73-81. 40. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol. 2004;44(3): 671-719. 41. Timmins F, Kaliszer M. Information needs of myocardial infarction patients. Eur J Cardiovasc Nurs. 2003;2(1):57-65. 42. GISSI Investigators. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico (GISSI). Lancet. 1986;1(8478): 397-402. 43. Bolognese L, Neskovic AN, Parodi G, et al. Left ventricular remodeling after primary coronary angioplasty: patterns of left ventricular dilation and long-term prognostic implications. Circulation. 2002;106(18): 2351-2357. 44. Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage Ventriculaire [REVE] study group). Am J Cardiol. 2006;98(9):1144-1149. 45. Amin A. Improving the management of patients after myocardial infarction, from admission to discharge. Clin Ther. 2006;28(10):1509-1539. 46. SOLVD Investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. The SOLVD Investigators. N Engl J Med. 1992; 327(10):685-691. 47. Kober L, Torp-Pedersen C. Clinical characteristics and mortality of patients screened for entry into the Trandolapril Cardiac Evaluation (TRACE) study. Am J Cardiol. 1995; 76(1):1-5. 48. Exner DV, Dries DL, Waclawiw MA, Shelton B, Domanski MJ. Beta-adrenergic blocking agent use and mortality in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a post hoc analysis of the Studies of Left Ventricular Dysfunction. J Am Coll Cardiol. 1999;33(4): 916-923. 49. Vantrimpont P, Rouleau JL, Wun CC, et al. Additive beneficial effects of beta-blockers to angiotensin-converting enzyme inhibitors in the Survival and Ventricular Enlargement (SAVE) Study. SAVE Investigators. J Am Coll Cardiol. 1997;29(2):229-236. 50. Australia/New Zealand Heart Failure Research Collaborative Group. Randomised, placebo-controlled trial of 36 CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 http://ccn.aacnjournals.org 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63. carvedilol in patients with congestive heart failure due to ischaemic heart disease. Australia/New Zealand Heart Failure Research Collaborative Group. Lancet. 1997;349(9049):375-380. Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003;349(20):1893-1906. Dickstein K, Kjekshus J. Effects of losartan and captopril on mortality and morbidity in high-risk patients after acute myocardial infarction: the OPTIMAAL randomised trial. Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan. Lancet. 2002;360(9335):752-760. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346(12):877-883. Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med. 2004;350(21):2151-2158. Goldberg LR, Jessup M. Stage B heart failure: management of asymptomatic left ventricular systolic dysfunction. Circulation. 2006;113(24):2851-2860. St John Sutton M, Pfeffer MA, Plappert T, et al. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction: the protective effects of captopril. Circulation. 1994;89(1):68-75. Doughty RN, Whalley GA, Walsh HA, Gamble GD, Lopez-Sendon J, Sharpe N. Effects of carvedilol on left ventricular remodeling after acute myocardial infarction: the CAPRICORN Echo Substudy. Circulation. 2004;109(2):201-206. Pitt B, White H, Nicolau J, et al. Eplerenone reduces mortality 30 days after randomization following acute myocardial infarction in patients with left ventricular systolic dysfunction and heart failure. J Am Coll Cardiol. 2005;46(3):425-431. Kjekshus J, Pedersen TR, Olsson AG, Faergeman O, Pyorala K. The effects of simvastatin on the incidence of heart failure in patients with coronary heart disease. J Card Fail. 1997;3(4):249-254. Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med. 1996;335(14):1001-1009. Julian DG, Camm AJ, Frangin G, et al. Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. European Myocardial Infarct Amiodarone Trial Investigators. Lancet. 1997;349(9053):667-674. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341(25):1882-1890. Gruberg L. DINAMIT: the Defibrillator in Acute Myocardial Infarction Trial. Medscape/ACC Annual Scientific Session 2004. http://ccn.aacnjournals.org 64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. Medscape Web site. http://www .medscape.com/viewarticle/472003. Accessed January 8, 2008. Hohnloser SH, Connolly SJ, Kuck KH, et al. The defibrillator in acute myocardial infarction trial (DINAMIT): study protocol. Am Heart J. 2000;140(5):735-739. Boersma E, Pieper KS, Steyerberg EW, et al. Predictors of outcome in patients with acute coronary syndromes without persistent STsegment elevation: results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation. 2000;101:25572567. Califf RM, Pieper KS, Lee KL et al. Prediction of 1-year survival after thrombolysis for acute myocardial infarction in the global utilization of streptokinase and TPA for occluded coronary arteries trial. Circulation. 2000;101(22):2231-2238. Jacobs DR Jr, Kroenke C, Crow R, et al. PREDICT, a simple risk score for clinical severity and long-term prognosis after hospitalization for acute myocardial infarction or unstable angina: the Minnesota Heart Survey. Circulation. 1999;100(6):599607. Krumholz HM, Chen J, Chen YT, Wang Y, Radford MJ. Predicting one-year mortality among elderly survivors of hospitalization for an acute myocardial infarction: results from the Cooperative Cardiovascular Project. J Am Coll Cardiol. 2001;38(2):453-459. Morrow DA, Antman EM, Charlesworth A, et al. TIMI risk score for ST-elevation myocardial infarction: a convenient, bedside, clinical score for risk assessment at presentation. An Intravenous nPA for Treatment of Infarcting Myocardium Early II trial substudy. Circulation. 2000;102(17):20312037. Morrow DA, Antman EM, Giugliano RP, et al. A simple risk index for rapid initial triage of patients with ST-elevation myocardial infarction: an InTIME II substudy. Lancet. 2001;358(9293):1571-1575. 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. Whellan DJ, Gaulden L, Gattis WA, et al. The benefit of implementing a heart failure disease management program. Arch Intern Med. 2001;161(18):2223-2228. Hoekstra JW, Pollack CV Jr, Roe MT, et al. Improving the care of patients with non-STelevation acute coronary syndromes in the emergency department: the CRUSADE initiative. Acad Emerg Med. 2002;9(11):11461155. Cannon CP, Braunwald E; on behalf of the STRIVE Scientific Council. Strategies and Therapies for Reducing Ischemic and Vascular Events (STRIVE) acute coronary syndromes critical pathway toolkit. Crit Pathw Cardiol. 2003;2(3):153-177. 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. Get with the guidelines. American Heart Association Web site. http://www .americanheart.org/presenter.jhtml?identifier =1165. Accessed January 8, 2008. CRITICALCARENURSE Vol 28, No. 2, APRIL 2008 37 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 CE Test Test ID C082: Recognizing and Managing Asymptomatic Left Ventricular Dysfunction After Myocardial Infarction Learning objectives: 1. Identify the definitive measurement for the diagnosis of asymptomatic left ventricular systolic dysfunction (LVSD) after myocardial infarction 2. Describe the pathophysiology of asymptomatic LVSD after myocardial infarction 3. Discuss the pharmacologic management of asymptomatic LVSD after myocardial infarction 1. Which percentage of myocardial infarctions is accompanied by left ventricular systolic dysfunction (LVSD)? a. 20% b. 40% c. 60% d. 80% 7. Which of the following medication classes decreased progression from asymptomatic LVSD to clinical heart failure by 37% in the SAVE trial? a. Calcium-channel blocker b. Antiplatelet c. β-Blocker d. ACE inhibitor 2. Which of the following left ventricular end-diastolic pressures were associated with higher rates of death or severe heart failure in the SAVE trial? a. 15 mm Hg b. 20 mm Hg c. 25 mm Hg d. 30 mm Hg 8. Which of the following medication classes was just as effective as an ACE inhibitor in patients with asymptomatic LVSD in the VALIANT trial? a. Aldosterone receptor antagonist b. Angiotensin receptor blocker c. Adrenergic agonist d. Antiplatelet 3. Which of the following was most apparent among patients with low ejection fractions in the VALIANT trial? a. Cardiac rupture b. Recurrent myocardial infarction c. Sudden cardiac death d. Cardioembolic stroke 9. Which of the following medication classes increased left ventricular ejection fraction by 5% after 6 months of treatment in the CAPRICORN trial? a. Statin b. Aldosterone receptor antagonist c. β-Blocker d. ACE inhibitor 4. In asymptomatic LVSD after myocardial infarction, which of the following leads to loss of cardiomyocytes, left ventricular remodeling, and functional deterioration? a. Neurohormonal activation b. Normalized end-systolic wall stress c. Endogenous vasodilation d. Increased cardiac output 10. Which of the following medication classes added to an ACE inhibitor and beta-blocker reduced the risk of mortality in patients with LVSD in the EPHESUS trial? a. Statin b. Aldosterone receptor antagonist c. Loop diuretic d. Calcium-channel blocker 5. Which of the following measurements is a definitive diagnostic cue of asymptomatic LVSD after myocardial infarction? a. Creatine phosphokinase b. Brain natriuretic peptide c. Ejection fraction d. Left ventricular end-diastolic pressure 11. Which of the following medication classes reduced the risk of new nonfatal myocardial infarction and heart failure in asymptomatic LVSD after myocardial infarction in the Scandinavian Survival Study? a. ACE inhibitor b. Heparin c. Antiplatelet d. Statin 6. Which of the following pharmacologic regimens should be considered for patients with asymptomatic LVSD after myocardial infarction? a. Angiotensin-converting enzyme (ACE) inhibitor, β-blocker, aldosterone receptor antagonist, statin b. β-Blocker, statin, ACE inhibitor, loop diuretic c. Aldosterone receptor antagonist, calcium-channel blocker, β-blocker, ACE inhibitor d. Calcium-channel blocker, ACE inhibitor, statin, β-blocker 12. Which of the following ejection fractions was a criterion for an implantable cardioverter defibrillator in the MADIT II trial? a. 30% b. 35% c. 40% d. 45% Test answers: Mark only one box for your answer to each question. You may photocopy this form. 1. K a Kb Kc Kd 2. K a Kb Kc Kd 3. K a Kb Kc Kd 4. K a Kb Kc Kd 5. K a Kb Kc Kd 6. K a Kb Kc Kd 7. K a Kb Kc Kd 8. K a Kb Kc Kd 9. K a Kb Kc Kd 11. K a Kb Kc Kd 10. K a Kb Kc Kd 12. K a Kb Kc Kd Test ID: C082 Form expires: April 1, 2010 Contact hours: 1.5 Fee: AACN members, $0; nonmembers, $11 Passing score: 9 correct (75%) Category: A, Synergy CERP B Test writer: John P. Harper, RN-BC, MSN Program evaluation Name Yes K K K Mail this entire page to: AACN 101 Columbia Aliso Viejo, CA 92656 (800) 899-2226 Objective 1 was met Objective 2 was met Objective 3 was met Content was relevant to my nursing practice K My expectations were met K This method of CE is effective for this content K The level of difficulty of this test was: K easy K medium K difficult To complete this program, it took me hours/minutes. No K K K K K K Member # Address City State Country ZIP Phone E-mail RN Lic. 1/St Payment by: RN Lic. 2/St K Visa K M/C Card # K AMEX K Discover K Check Expiration Date Signature The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN programming meets the standards for most other states requiring mandatory continuing education credit for relicensure. Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014 Downloaded from http://ccn.aacnjournals.org/ by guest on June 9, 2014
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