Recognizing and Managing Asymptomatic Left Ventricular Dysfunction

Improve survival and quality of life in patients by promoting prompt use of evidence-based treatments.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.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.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.11Compared 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.8Patients 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.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.18Norepinephrine, 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 2). 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.18Similar 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 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 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.19–21Numerous 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 and contribute to the progression of systolic and diastolic myocardial dysfunction and the of signs or symptoms of heart failure after myocardial infarction may in LVSD, patients of that can the progression of heart failure and the risk of arrhythmias, and sudden death. of ejection fraction after myocardial infarction is because of the large increase in risk for LVSD associated with myocardial infarction. Asymptomatic LVSD should be in patient who had a myocardial infarction and not have symptoms of heart failure, especially patients with signs of heart failure such as elevated jugular venous pressure, positive and an S3 diagnosis of asymptomatic LVSD is as by clinical in which and other were neurohormonal was ventricular function should be measured by of or in all patients after myocardial infarction. Although not a for of left ventricular function, of the of natriuretic is in heart failure and only a In of the of natriuretic was in LVSD and remodeling after myocardial infarction. of natriuretic had an in the of asymptomatic LVSD in patients without symptomatic heart failure after myocardial some clinical features are associated with LVSD in acute myocardial infarction, and these features should suggest LVSD in asymptomatic 1). An that the of new infarction, clinical signs of heart failure, or or more myocardial infarctions an increase in of than in patients who had not had a and a for an ejection fraction of 40% or in patients with acute myocardial of early diagnosis of LVSD after myocardial infarction the patient is in the hospital should not be The hospital in and a coronary care provides a within an acute with care or care to and who work in and the capacity to of and cardiac and clinicians can create a between the acute myocardial infarction and the for by an is the of natriuretic and clinical features known to be associated with LVSD after myocardial with LVSD after myocardial infarction for a large proportion of patients in These patients are at a high risk for adverse outcomes, and in the hospital be in and as well as to increase the use of and promote have the care of patients who have had a myocardial from indicate that care of patients with LVSD after myocardial infarction is the of clinical trial data that of with data from the of Myocardial Infarction of patients with acute myocardial infarction found that patients who had heart failure at the of hospitalization or in whom heart failure developed were likely to be with evidence-based cardiac than were patients without heart failure after myocardial infarction. patients with heart failure were likely to be with and in the first than were patients without heart The of with of the of registry investigators discharge of patients with myocardial infarction and heart the of hospitalization, patients had signs of heart failure and had clinical heart and outcomes in both of patients were compared with those of patients without signs of heart The results indicated that patients with signs of heart failure were often with medications and cardiac in the first after studies suggest significant of cardiac for patients with signs of heart failure or clinical heart failure during the early of hospital care after myocardial infarction. Although no specifically measured in patients with asymptomatic LVSD after myocardial infarction, these patients likely also do not receive the best evidence-based are of recognition of LVSD symptoms are not present or of to patients with using a can associated with of cardiac work with other and use a approach with nurse to all patients who have had a myocardial infarction for the of asymptomatic develop processes and that promote use of evidence-based promote education of patients the hospital not and on process and of importance in this of patients (Figure 1). and nurse can education to increase the of nurse clinicians of changes after myocardial infarction that lead to heart failure, timing of and for of patients that care is and to patients’ should as a for patients and their about the importance of during hospitalization to ensure after who do not with a in the hospital are also likely to receive that after that used a care approach to promote of evidence-based during hospitalization were The Cardiac was a hospital that and after myocardial The in a increase in the of and in the year after its (Figure and a reduction in new myocardial infarction, heart failure, hospitalizations, and total mortality rates in patients after myocardial infarction were sustained for care approach can prompt early and use of from the for of in trial that patients with heart failure in whom with a was in the hospital were more likely to at days after discharge than were patients who were without a with a to in an days after hospital of patients who in the hospital were treatment, compared with of patients who after discharge from who followed up patients found that for acute coronary was in the patients were more likely to to hospital discharge education and disease management and disease management are disease care processes of education or and are on of care, developed performance and from randomized controlled Although in disease management patients are about receive related to the disease are for to and receive risk reduction and management is to the discharge Thus, care and discharge of patients after myocardial infarction may not about chronic heart for stage B heart failure and education of patients with asymptomatic LVSD after myocardial infarction be even because patients do not have clinical or stage heart and discharge education for patients with asymptomatic LVSD after myocardial infarction be into management on and education about and self-care are as as patients receive who to not and are at high risk for a secondary cardiac event, including a new myocardial infarction. patients are in the hospital is a class from the of for myocardial infarction with to to and evidence-based medications after the should early during hospitalization, be at discharge and at follow-up during with cardiac and with community by cardiac that can be to the of patients are nurse clinicians are in the between and secondary of patients should be as a process that is a of with a including each during clinicians in hospital management of patients who have had a myocardial infarction be to the timing for to promote care that decreases the risk for poor have on coronary as as because of a significant mortality from in patients with acute myocardial infarction. do not or the progression of left ventricular remodeling occurs after successful coronary sustained of the artery and of and function of the left In a of patients who had after acute myocardial infarction and with medications and experienced increases in left ventricular within 6 1 year after acute myocardial infarction of the wall in patients, had left ventricular remodeling, even though coronary of the and 54% if a patient had or not have signs or symptoms of heart failure, LVSD may be present and be and to progression of the by the for both heart failure and myocardial infarction, management of patients with asymptomatic LVSD after myocardial infarction should be at neurohormonal activation due to remodeling and progression of coronary artery The of risk factors for coronary artery disease, including and and the use of evidence-based for left ventricular dysfunction and of neurohormonal is strongly for acute myocardial of other are beneficial in patients with asymptomatic LVSD after myocardial infarction and are in the and in 4 the major clinical outcomes from that patients with asymptomatic should be within the first after a myocardial infarction in patients with myocardial infarction, heart failure, or an ejection fraction than 40% reflecting asymptomatic LVSD. If the should be during and after in a randomized clinical trial specifically patients with asymptomatic LVSD after myocardial infarction. with placebo, use of was associated with a risk reduction in mortality also progression to clinical heart failure by hospitalization for heart failure by 22% and recurrent myocardial infarction by of SAVE indicated that left ventricular remodeling can be by In patients, was after infarction and after 1 The size of the left ventricle increased both in patients who placebo and in patients who however, the increases were significantly in the for diastolic and for patients with left ventricular dysfunction after myocardial infarction were randomized to with and follow-up of no significant in the risk of death among the were the had more adverse provided that the was as as an in patients with asymptomatic LVSD after myocardial infarction. the addition of an to an did not an and is not as an addition to may be used as an for patients who are of because of symptomatic or the of in patients who have had a myocardial infarction are and in patients with LVSD after myocardial infarction are not as well early of patients with heart failure or known LVSD. in the Survival in Ventricular trial specifically enrolled patients who had LVSD after myocardial infarction fraction with or without signs or symptoms of heart failure, and compared the of with that of placebo on mortality and In the of had no signs or symptoms of heart an and and had or for acute myocardial infarction patients experienced a risk reduction in mortality and a risk reduction in recurrent myocardial infarction during years of indicated that mortality was reduced in patients with of their to signs and symptoms of heart in clinical outcomes in the trial is consistent with a of patients enrolled in SAVE who of use was associated with a 30% risk reduction in death and a risk reduction in progression to severe heart failure that were of use of an or a In the the of a and an was associated with a reduction in the risk of death in patients with asymptomatic of patients from the trial indicated that was associated with of left ventricular remodeling at 6 Although did not significantly end-diastolic with and increased with placebo ventricular ejection fraction also increased in the by after 6 of no was with of an aldosterone to an and a reduced the risk of mortality in patients with LVSD after myocardial infarction and symptomatic heart failure in the Myocardial Infarction and Survival have not been in patients with asymptomatic LVSD. In patients with LVSD after myocardial infarction were randomized to with or was associated with a risk reduction in mortality sudden death and hospitalization for heart failure with also had early In an of mortality and sudden cardiac death in the trial after 30 days of treatment, researchers found a risk reduction in mortality and a risk reduction in sudden cardiac death compared with are indicated in the management of patients after myocardial infarction and should be in patients with asymptomatic LVSD after myocardial infarction. in specifically enrolled survivors of myocardial infarction without heart of the Survival found that reduced the risk of new myocardial infarction by and the risk of heart failure by in randomized patients with a history of myocardial infarction. In the and survivors of myocardial infarction without of heart failure were randomized to with or with placebo, reduced the risk of myocardial infarction by In a trial of patients with LVSD with ejection fraction between and provided a significant reduction in risk for myocardial the stress the importance of the progression of LVSD from an asymptomatic to symptomatic heart failure, patients who have had a myocardial infarction, especially those with LVSD, and of The role of with an was compared with for patients with LVSD after myocardial infarction in in the Trial enrolled patients with ventricular left ventricular ejection fraction than and coronary artery of death and mortality were lower in the patients who had an the Trial patients with a left ventricular ejection fraction of 30% or and a history of myocardial infarction were randomized to receive of an or after myocardial infarction. who an had significantly survival after In the in Acute Myocardial Infarction Trial patients with a left ventricular ejection fraction of or and heart were randomized to receive an between 6 and days after myocardial mortality was not by early of an because the reduction in death was by the use of an days after myocardial infarction is not studies a proportion of patients with asymptomatic LVSD, current for patients who have had a myocardial infarction of an if ejection fraction criteria are days after myocardial are for patients with acute coronary These clinical models can of patients’ management and were into to patients’ In the clinicians used significantly more after more patients and of care the hospital for myocardial infarction can as the for and management of patients after myocardial infarction by to for LVSD and of patients, of and discharge and can also be through that and processes that of including care discharge education and have been developed to the of as as patients are are to and in The results of an of hospital care in patients with acute coronary who were enrolled in the were to use of the In of cases, care were consistent with the The for to was significantly associated with mortality rates from for the to for the increase in in a hospital was associated with a decrease in its patients’ of mortality The significant between care process and outcomes the use of performance as a of and hospital that and other quality be used by and to the of evidence-based for patients with myocardial In the the can be used to an patient management provides of performance and also is the of patient education and used to or among care of data from the patient management can be used to factors related to patients and hospital that can be to patients’ outcomes or of clinicians play a role in for patients after myocardial infarction. of patients have LVSD after myocardial infarction, and about of patients with LVSD are asymptomatic. The risk of death or heart failure on the of injury of the left in asymptomatic LVSD can be from progressive heart failure, recurrent myocardial infarction, or The of signs or symptoms of heart failure after myocardial infarction may create a of and patients of diagnosis of asymptomatic LVSD by or is management of asymptomatic LVSD in patients who have had a myocardial infarction on early and neurohormonal antagonism of the and nervous with an or and because these risk of mortality and the of heart failure Although clinical do not specifically and have the most of in patients with asymptomatic LVSD after myocardial infarction. Of major importance is of risk factors for progression of heart failure and coronary artery disease, including and and of an as indicated for or secondary of sudden cardiac nurse and nurse should develop and use to recognition and of LVSD after myocardial infarction and to The of disease progression in patients with asymptomatic LVSD after myocardial infarction is on early and education.