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Crit Care Nurse 2008 Apr; 28(2): 20-37
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Cover Article
CE Article

Recognizing and Managing Asymptomatic Left Ventricular Dysfunction

After Myocardial Infarction

Nancy M. Albert, PhD, CCNS, CCRN, CNA
 Connie Lewis, MSN, ACNP, ANP, CCRN

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.

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, reprints{at}aacn.org.

dot
To learn more about heart failure, read "Evidence-Based Practice for Acute Decompensated Heart Failure" by Nancy M. Albert, Cathy A. Eastwood, and Michelle L. Edwards in Critical Care Nurse 2004:24:14–29.[Free Full Text] Aavailable online at ccn.aacnjournals.org.

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.

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

Corresponding author: Nancy M. Albert, RN, PhD, Cleveland Clinic Foundation, 9500 Euclid Ave, Mail Code P32, Cleveland, OH 44195 (e-mail: albertn{at}ccf.org).

Approximately 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 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 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
Top
 Asymptomatic LVSD
Underuse of Therapies for...
 Applying a Multidisciplinary...
 Pharmacological and Device...
 Care Pathways
 Conclusions
 PRIME POINTS
 References
 
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 1Go). 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.


Figure 1
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  		Figure 1 Asymptomatic left ventricular systolic dysfunction: guidelines for stage A and B heart failure: recommended therapies and nursing leadership to facilitate adherence with guidelines.
Based on Hunt et al.5

 
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. 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 within the first few days after a myocardial infarction.11 In population-based community samples and registries, the incidence of new-onset heart failure after myocardial infarction ranged from 22% to 48%, with a mean of 37%, consistent with results of the TRACE study.11

Prognosis
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.13–15 In the SAVE trial, the investigators specifically enrolled only patients with acute myocardial infarction and asymptomatic LVSD and followed up those cases for 3.5 years.16 Of 2231 patients with an ejection fraction of 40% or less, clinically significant signs and symptoms of heart failure occurred in 16% of surviving patients receiving placebo, and 16% of all patients receiving placebo experienced significant further deterioration of left ventricular contractility, as indicated by a reduction of 9 units or more in ejection fraction. These data provided some insight into the natural history of asymptomatic LVSD. Overall, total mortality for patients receiving placebo was 25%, and approximately 12% died within 1 year.16 Further, patients with a large left ventricle, measured as a baseline end-diastolic pressure in the left ventricle exceeding 30 mm Hg, had significantly higher rates of death or severe heart failure at 4 years after acute myocardial infarction than did patients with a lower baseline left ventricular end-diastolic pressure.8

Patients with LVSD but no signs or symptoms of heart failure after myocardial infarction who seemed to be recovering well were also at high risk for sudden death. In the Valsartan in Acute Myocardial Infarction Trial (VALIANT), the incidence and timing of sudden death in 14 609 patients with LVSD after myocardial infarction were assessed.17 An increased early incidence of sudden death was most apparent among patients with low ejection fraction. Of 156 sudden deaths or cardiac arrests with resuscitation 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.

Pathophysiology
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 function, and the patient remains asymptomatic. If changes in left ventricular systolic and diastolic performance from akinesis (lack of motion of left ventricular wall due to tissue cell death), dyskinesis (abnormal motion of left ventricular wall due to aneurysm formation at injured or 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 β-adrenergic signaling responses. Adrenergic receptors have both beneficial and harmful biological 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 2Go). The biological and physiological processes of heart failure are complex and beyond the scope of this article, but 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


Figure 2
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  		Figure 2 The complex pathophysiology of asymptomatic left ventricular systolic dysfunction after myocardial infarction.
Based on Mann and Bristow18 and Philippides.19

 
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 increases, leading to an increase in left ventricular work during systole that contributes to a decrease in cardiac output18 (Figure 2Go). 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 activation, 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 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 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 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 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 1Go). 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 creatine 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


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  		Table 1 Diagnostic cues of left ventricular systolic dysfunction in the absence of symptomsa

 
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 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.


   Underuse of Therapies for Myocardial Infarction
Top
 Asymptomatic LVSD
 Underuse of Therapies for...
Applying a Multidisciplinary...
 Pharmacological and Device...
 Care Pathways
 Conclusions
 PRIME POINTS
 References
 
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 CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Out comes 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.


   Applying a Multidisciplinary Approach
Top
 Asymptomatic LVSD
 Underuse of Therapies for...
 Applying a Multidisciplinary...
Pharmacological and Device...
 Care Pathways
 Conclusions
 PRIME POINTS
 References
 
Nurse clinicians, using a multi-disciplinary approach, can help overcome obstacles associated with underuse of cardiac therapies. 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 1Go). 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 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 evidence-based 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 resulted in a dramatic increase in the prescription of angiotensin-converting enzyme (ACE) inhibitors, β-blockers, statins, and aspirin in the year after its implementation37 (Figure 3Go) 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


Figure 3
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  		Figure 3 Sustained impact of the Cardiac Hospitalization Atherosclerosis Management Program.

 
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 (IMPACT-HF) 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 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 pre-discharge 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 ST-segment 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 2Go), and continue at follow-up during visits with providers, cardiac rehabilitation, and interactions with 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.


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  		Table 2 American College of Cardiology/American Heart Association guidelines for patients with ST-elevation myocardial infarction: class I recommendations for education at dischargea

 

   Pharmacological and Device Therapies
Top
 Asymptomatic LVSD
 Underuse of Therapies for...
 Applying a Multidisciplinary...
 Pharmacological and Device...
Care Pathways
 Conclusions
 PRIME POINTS
 References
 
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 trans-luminal 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 β-blocker), 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 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 β-blockers.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 3Go. Table 4Go gives the major clinical outcomes from trials that included patients with asymptomatic LVSD.12,16,21,46–55


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  		Table 3 American College of Cardiology/American Heart Association guidelines for management of ST-elevation myocardial infarctiona

 

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  		Table 4 Clinical trials in patients with asymptomatic left ventricular systolic dysfunction12,16,21,46–55

 
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% reflecting asymptomatic LVSD. If tolerated, the ACE inhibitor should be administered during convalescence and continued indefinitely after discharge.40 Researchers in a pivotal randomized clinical trial (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, 2-dimensional 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 twice daily).51 After median follow-up 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 angiotensin-receptor blocker valsartan was just as effective as an ACE inhibitor in patients with asymptomatic LVSD after myocardial infarction. However, the addition of an angiotensin-receptor 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 β-blocker 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 β-blocker therapy excluded patients with heart failure or known LVSD. Investigators in the Carvedilol Post-Infarct 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 follow-up.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


TIMELY DIAGNOSIS AND A MULTI-DISCIPLINARY APPROACH TO PATIENT CARE IS CRUCIAL

  • Survivors of myocardial infarction should be assessed for asymptomatic left ventricular systolic dysfunction (LVSD).
  • Patients who have asymptomatic LVSD after myocardial infarction have worse outcomes than do patients without LVSD.
  • 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.
  • Cardiac nurses can reduce risks and enhance patients’ adherence to medical therapies by ensuring that each patient understands what he or she is taught before hospital discharge.
  • A multidisciplinary approach to care of patients with asymptomatic LVSD after myocardial infarction prompts evidence-based treatment and may help patients continue with therapies.

 

The improvement in clinical outcomes in the CAPRICORN trial is consistent with a retrospective analysis49 of patients enrolled in SAVE who concomitantly received β-blockers (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 end-diastolic 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

Aldosterone Receptor Antagonists
Use of an aldosterone antagonist (added to an ACE inhibitor and a β-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 (hydroxymethylglutaryl-CoA reductase inhibitors) are indicated in the management of patients after myocardial infarction and should be considered in patients with asymptomatic LVSD after myocardial infarction. Researchers in 2 lipid-lowering studies59,60 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 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 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 a myocardial infarction include implantation of an ICD if ejection fraction criteria are met 40 days after myocardial infarction.


   Care Pathways
Top
 Asymptomatic LVSD
 Underuse of Therapies for...
 Applying a Multidisciplinary...
 Pharmacological and Device...
 Care Pathways
Conclusions
 PRIME POINTS
 References
 
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’ outcomes.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 provide 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 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 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 care-givers and institutions to improve the application of evidence-based treatments for patients with ST-segment 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.


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 Asymptomatic LVSD
 Underuse of Therapies for...
 Applying a Multidisciplinary...
 Pharmacological and Device...
 Care Pathways
 Conclusions
PRIME POINTS
 References
 
Nurse clinicians play a critical role in caring for patients after myocardial infarction. About one-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 angiotensin-receptor 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 asymptomatic LVSD after myocardial infarction. Of major importance is treatment of risk factors for progression 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 sudden cardiac arrest. Hospital nurse clinicians, advanced practice nurses, and nurse educators should develop and use critical pathways to improve 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.


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 Asymptomatic LVSD
 Underuse of Therapies for...
 Applying a Multidisciplinary...
 Pharmacological and Device...
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   References
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 Asymptomatic LVSD
 Underuse of Therapies for...
 Applying a Multidisciplinary...
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 References
 

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