INTRODUCTION — Asymptomatic left ventricular systolic dysfunction (ALVSD) is defined as depressed LV systolic function in the absence of heart failure. Studies of asymptomatic LV systolic dysfunction have used heterogeneous criteria to identify this condition. For the discussion in this topic, ALVSD is defined as depressed LV systolic function with a subnormal LV ejection fraction, regional wall motion abnormality, or both. (See "Approach to diagnosis of asymptomatic left ventricular systolic dysfunction", section on 'Definition'.)
Population-based studies suggest that ALVSD is at least as common as heart failure with reduced ejection fraction (HFrEF). Structural heart disease (including LV systolic dysfunction) without symptoms or signs of HF is defined as "stage B HF" in the American College of Cardiology Foundation/American Heart Association guidelines [1]. Although asymptomatic, these patients are at increased risk for clinical (ie, stage C or D) HF and death, and therefore it is important that they be identified and treated.
The management and prognosis of patients with asymptomatic LV systolic dysfunction will be reviewed here. Issues related to the management of HFrEF are presented separately.
MANAGEMENT — The approach to management of asymptomatic left ventricular systolic dysfunction (ALVSD) includes treatment (management of contributing conditions, neurohormonal blockade, and arrhythmia management), avoidance of drugs that may precipitate heart failure (HF), and monitoring for progression.
Management of contributing conditions — Conditions that may lead or contribute to HF should be recognized and managed according to standard recommendations [1]. These conditions include hypertension, dyslipidemia, obesity, and diabetes mellitus. Patients should also be counseled regarding smoking cessation as well as avoidance of cocaine, amphetamines, and heavy alcohol use. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Choice of drug therapy in primary (essential) hypertension".)
Management of patients with stable ischemic heart disease (including assessment for revascularization and antianginal therapy) and lipid therapy in patients with known cardiovascular disease (including ischemic heart disease) is discussed separately. (See "Chronic coronary syndrome: Overview of care" and "Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease".)
Other therapies are appropriate in patient-specific conditions such as specific therapies for myocardial disease (eg, cardiac sarcoidosis) or severe valve disease (stenosis or regurgitation) [2,3].
Neurohormonal blockade — Pharmacologic intervention in the management of patients with asymptomatic LV systolic dysfunction may delay the onset of HF, reduce the cardiac event rate, and improve survival. Recommendations for therapy are based upon the severity of LV systolic dysfunction (ie, presence of LV ejection fraction [LVEF] ≤40 percent), as well as the cause of dysfunction (ie, post-myocardial infarction [MI] or other) (algorithm 1).
Evaluation prior to initiation of an ACE inhibitor (or ARB) includes assessment of LVEF, determining if there is a prior history of angioedema, and assessment of electrolytes and renal function (blood urea nitrogen and serum creatinine). ACE inhibitor therapy is contraindicated in patients with prior history of idiopathic or hereditary angioedema or drug-induced angioedema. Evaluation prior to initiation of a beta blocker includes assessing the heart rate and obtaining a baseline electrocardiogram.
Evaluation prior to MRA therapy includes assessing renal function and serum potassium level. In addition, MRA should be prescribed only to patients who can be carefully monitored for changes in serum potassium and renal function.
For patients with no prior myocardial infarction
Recommendations for therapy — For patients with ALVSD with no prior MI with LVEF ≤40 percent, we recommend the following therapy (algorithm 1):
●For asymptomatic patients with no prior MI with LVEF ≤40 percent, we recommend angiotensin converting enzyme (ACE) inhibitor therapy. (See 'ACE inhibitors' below.)
•An angiotensin II receptor antagonist (ARB) is recommended for patients who have indications for an ACE inhibitor but have a cough with ACE inhibitor or history of angioedema. (See 'ARB as an alternative to ACE inhibitor' below.)
●For asymptomatic patients with no prior MI with LVEF ≤40 percent, we suggest beta blocker therapy. (See 'Beta blockers' below.)
We initiate therapy in appropriate patients with no prior MI when the LVEF is ≤40 percent [1]. In randomized trials cited below, such as SOLVD, SAVE, TRACE, and CAPRICORN, the LVEF was ≤35 to 40 percent [4-7]. The above recommendations for beta blocker and ACE inhibitor are similar to those in the 2013 American College of Cardiology/American Heart Association HF guidelines [1]. (See 'Chronic LV systolic dysfunction' below.)
Some experts favor initiating medical therapy at a higher LVEF threshold than 40 percent (ie, with less severely depressed LV function) in asymptomatic relatives of patients with familial dilated cardiomyopathy. (See "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment", section on 'Early treatment'.)
Administration of therapy — For patients with ALVSD without prior MI with LVEF ≤40 percent, we generally start ACE inhibitor therapy prior to beta blocker therapy, particularly since the evidence supporting ACE inhibitor therapy is stronger.
ACE inhibitor therapy is initiated at low doses (eg, 5 to 10 mg of lisinopril daily) to reduce the likelihood of complications such as hypotension and azotemia. The dose is doubled at regular intervals (eg, every two to three weeks in the outpatient setting) as tolerated until the target dose is reached. Target maintenance dose is 40 mg per day of lisinopril or quinapril unless side effects occur. These relatively high doses reflect those used in the SOLVD trial described below [8]. Although it is not known if these doses are more beneficial than lower doses, the maximum-tolerated dose is recommended. If the target doses cannot be administered or are poorly tolerated, lower doses should be used.
Beta blocker therapy is started after ACE inhibitor therapy has been started and titrated to at least a moderate dose. Beta blocker therapy should begin with low doses, with the dose doubled at regular intervals (eg, every two to three weeks in the outpatient setting) as tolerated until the target dose is reached. ACE inhibitor can be titrated to target dose before or after target beta blocker dose is reached. Initial and target doses are as follows:
●For carvedilol, 3.125 mg twice daily with target dose of 25 to 50 mg twice daily (the higher dose being used in subjects over 85 kg).
●For extended release metoprolol succinate, 25 mg daily with target dose of 200 mg/day.
●For bisoprolol, 1.25 mg once daily with target dose of 5 to 10 mg once daily.
If target doses are not tolerated, low doses may be of benefit and should be used.
For patients post-myocardial infarction
Recommendations post-myocardial infarction — Many patients with LV systolic dysfunction have had a prior ST elevation or non-ST elevation MI; standard indications for ACE inhibitor therapy and beta blocker therapy post-MI apply to these patients (algorithm 1). (See "Overview of the nonacute management of ST-elevation myocardial infarction" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction" and "Acute myocardial infarction: Role of beta blocker therapy" and "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use".)
●For patients with prior (recent or remote) MI, we recommend beta blocker therapy. (See 'Beta blockers' below and "Acute myocardial infarction: Role of beta blocker therapy", section on 'Indications'.)
●For patients with prior (recent or remote) MI with high-risk features (LVEF ≤40 percent, diabetes mellitus, or stable chronic kidney disease), we recommend ACE inhibitor therapy. (See 'ACE inhibitors' below and "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use", section on 'Summary and recommendations'.)
●For patients with prior MI who lack any high-risk features, major society guidelines suggest (weak recommendation) an ACE inhibitor. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use", section on 'Summary and recommendations' and 'ACE inhibitors' below.)
●For patients with prior MI who have an indication for ACE inhibitor but have cough or angioedema with ACE inhibitor, an ARB is suggested as an alternative. (See 'ARB as an alternative to ACE inhibitor' below.)
●Mineralocorticoid receptor antagonist (MRA) therapy is recommended in patients with prior MI without significant renal dysfunction (defined as eGFR≥30 mL/min per 1.73 m2) or hyperkalemia (K+ >5 mEq/L) who are receiving therapeutic doses of ACE inhibitor and beta blocker and have a LVEF ≤0.40, diabetes mellitus, or HF. (See "Overview of the nonacute management of ST-elevation myocardial infarction", section on 'Aldosterone antagonists' and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction", section on 'Mineralocorticoid receptor antagonists' and "Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults", section on 'Approach to secondary therapy' and "Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults", section on 'Mineralocorticoid receptor antagonist'.)
Administration post-myocardial infarction — Administration of a beta blocker, ACE inhibitor (or ARB), and mineralocorticoid receptor blocker post-MI is discussed separately. A beta blocker is started within 24 hours of presentation with an acute MI (or later if there are early contraindications). An ACE inhibitor (or ARB) is generally started prior to discharge (particularly in patients with high-risk features). For patients with criteria for MRA therapy, initiation prior to discharge is generally preferred. (See "Overview of the nonacute management of ST-elevation myocardial infarction", section on 'Aldosterone antagonists' and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction", section on 'Mineralocorticoid receptor antagonists'.)
Arrhythmia management — Among patients with asymptomatic LV systolic dysfunction, arrhythmia should be managed according to standard evidence-based guidelines. This section will address two issues that should be considered in these patients: tachycardia-mediated cardiomyopathy as a potential cause of LV systolic dysfunction and the role of implantable cardioverter-defibrillator ICD implantation for primary prevention of sudden cardiac death.
Patients with long-standing tachycardia (eg, atrial fibrillation and atrial flutter) can develop a tachycardia-mediated cardiomyopathy, in which the tachycardia results in the development of LV systolic dysfunction. In patients with pre-existing ALVSD, prolonged tachycardia can precipitate HF. In some cases, it may be difficult to determine whether the tachycardia caused the cardiomyopathy or whether the tachycardia is a consequence of the cardiomyopathy. When tachycardia-mediated cardiomyopathy is present, reversion to sinus rhythm or slowing the ventricular rate results in an improvement in LV function. (See "Arrhythmia-induced cardiomyopathy".)
Some patients with asymptomatic LV systolic dysfunction are candidates for ICD implantation for primary prevention of sudden cardiac death (algorithm 1):
●ICD therapy is indicated in asymptomatic patients with LV dysfunction due to prior MI who are at least 40 days post-MI (and more than three months post-revascularization) and have an LVEF ≤30 percent. (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF", section on 'Summary and recommendations'.)
●ICD therapy is indicated in patients with nonsustained ventricular tachycardia (VT) due to prior MI, LVEF ≤40 percent, and inducible ventricular fibrillation or sustained VT at electrophysiological study. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management", section on 'Summary and recommendations'.)
Drugs to avoid — Drugs that may precipitate HF should be avoided in patients with asymptomatic LV systolic dysfunction such as calcium channel blockers (except amlodipine and felodipine) and antiarrhythmics with negative inotropic effects [1]. In addition, some antiarrhythmic drugs pose proarrhythmic risk, particularly class I agents and the class III agents ibutilide and sotalol. (See "Major side effects of class I antiarrhythmic drugs" and "Clinical uses of sotalol" and "Therapeutic use of ibutilide".)
Other drugs that should be avoided or used with caution in patients with HF should generally also be avoided or used with caution in patients with asymptomatic LV systolic function. (See "Drugs that should be avoided or used with caution in patients with heart failure".)
Monitoring — Periodic monitoring is indicated to assess for possible worsening LV function and progression to HF. We recommend echocardiographic assessment when symptoms of HF appear in patients with prior ALVSD. In addition, some experts suggest follow-up echocardiographic evaluation at approximately one year in patients with newly diagnosed ALVSD who remain asymptomatic. The frequency of subsequent monitoring is determined by the stability of LVEF in the past, and the likelihood that a change in LVEF will lead to a change in therapy.
EFFICACY OF NEUROHORMONAL BLOCKADE
Chronic LV systolic dysfunction — Angiotensin converting enzyme (ACE) inhibitors and possibly beta blockers appear to be beneficial in patients with asymptomatic chronic left ventricular systolic dysfunction (ASLVD). Treatment recommendations for ACE inhibitor therapy in patients with chronic LV systolic dysfunction due to coronary disease or cardiomyopathy are largely based upon the SOLVD prevention trial [4]. Evidence of benefit from beta blockers is more limited [9].
ACE inhibitors — A benefit from ACE inhibitors has been noted in both the SOLVD prevention trial and the much smaller Munich Mild Heart Failure trial [4,10,11]. The SOLVD prevention trial consisted of 4228 asymptomatic patients (83 percent had had a myocardial infarction [MI] more than 30 days from entry) with an LV ejection fraction (LVEF) ≤35 percent; the patients were randomly assigned to enalapril (20 mg once per day) or placebo [4]. At a mean follow-up of just over three years, enalapril therapy was associated with a nonsignificant reduction in cardiovascular mortality compared with placebo (14 versus 16 percent) and a 29 percent reduction (95% CI 21-36) in the combined incidence of symptomatic heart failure (HF) or cardiovascular death (figure 1). Mortality rates were not significantly different in the two treatment groups (14.8 and 15.8 percent).
A subsequent analysis, called XSOLVD, evaluated virtually all of the original participants in the SOLVD prevention trial at a median of 11 years [10]. The enalapril group had significant reductions in all-cause mortality (51 versus 56 percent for placebo) and cardiovascular mortality (37 versus 42 percent). No data were available on post-trial drug use.
There are no large-scale trials that have specifically evaluated ACE inhibitors in patients with ASLVD due to idiopathic dilated cardiomyopathy. The SOLVD prevention and Munich trials included a small number of such patients. Sufficient benefits were observed in the SOLVD prevention trial to be able to justify the use of ACE inhibitors in these patients [4].
A rationale for early treatment is that outcomes are worse if effective therapy is initiated after patients develop overt HF (figure 2). The SOLVD treatment trial showed that ACE inhibitors were beneficial in patients with New York Heart Association (NYHA) functional class II to III HF with reduced ejection fraction (HFrEF) (table 1). However, in contrast to the mortality rates of 14.8 percent with enalapril and 15. 8 percent with placebo at just over three years in the SOLVD prevention trial [4], the mortality rate in the SOLVD treatment trial was 20 percent with enalapril compared with 25 percent with placebo at two years (figure 3) [8]. (See "Prognosis of heart failure", section on 'Effect of treatment'.)
ARB as an alternative to ACE inhibitor — An angiotensin II receptor blocker (ARB) is an option in patients with intolerance to ACE inhibitor given the evidence for a beneficial effect on outcomes in patients with hypertension with LV hypertrophy [12], as well as the evidence for similar benefits of ARB therapy and ACE inhibitor therapy in HFrEF.
Beta blockers — There are no randomized trials that have specifically evaluated the effect of beta blockers on clinical outcomes in patients with ASLVD who are not post-MI. In the REVERT trial of 149 asymptomatic patients with an LVEF <40 percent who were randomly assigned to treatment with either 200 or 50 mg of extended release metoprolol or placebo, an increase in LVEF was observed in both beta blocker groups as compared with placebo (6 and 4 versus 0 percent at 12 months) [13]. However, clinical outcomes were not evaluated.
A post-hoc analysis of the SOLVD prevention trial provided indirect evidence of clinical benefit from beta blocker therapy, similar to that described in post-MI patients [9]. Among the asymptomatic patients treated with enalapril, the 24 percent who also received a beta blocker had a significant independent reduction in the risk of death (relative risk 0.70, 95% CI 0.52-0.95) and in death or hospitalization for symptomatic HF (relative risk 0.64, 95% CI 0.49-0.83) compared with those using enalapril alone. The mortality benefit with beta blocker therapy was due to a reduction in arrhythmic and pump failure deaths and was not seen in patients assigned to placebo rather than enalapril.
Post-myocardial infarction — Post-MI therapies for preserving myocardial function and improving clinical outcomes include ACE inhibitors and beta blockers. In addition, mineralocorticoid receptor antagonists also improve outcomes in selected patients post-MI with HF or diabetes mellitus. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the nonacute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction".)
ACE inhibitors — Randomized trials (including SAVE [5]and TRACE [14]) of ACE inhibitor therapy initiated soon after MI have demonstrated improved outcomes including reduction in mortality. Patients with LVEF ≤40 percent are particularly likely to benefit from such therapy. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Clinical trials".)
ARB as an alternative to ACE inhibitor — An ARB is an option in patients with intolerance to ACE inhibitor (due to cough or angioedema) since efficacy of these agents appears to be similar in a post-MI setting. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use", section on 'ACE inhibitor versus ARB'.)
Beta blockers — Beta blockers are recommended for post-MI patients, independent of LV function, because they improve survival and reduce the rate of both sudden death and recurrent MI. (See "Acute myocardial infarction: Role of beta blocker therapy".) Fewer data are available on the efficacy of beta blocker therapy, when combined with ACE inhibitors, in patients with ASLVD post-MI. Efficacy has been suggested by one prospective randomized trial, CAPRICORN, and by a retrospective analysis of the SAVE trial.
●In the CAPRICORN trial, almost 2000 patients with an LVEF ≤40 percent after an acute MI (the majority of whom were asymptomatic) were treated with an ACE inhibitor and then randomly assigned to carvedilol (6.25 mg/day initially and then progressively increased during the next four to six weeks to a maximum of 25 mg twice daily) or placebo [7]. After a mean follow-up of 1.3 years, carvedilol did not reduce the primary end point of combined all-cause mortality and hospitalization for cardiovascular problems (35 versus 37 percent); however, there were significant reductions in all-cause mortality alone (12 versus 15 percent, hazard ratio 0.77, 95% CI 0.60-0.98) and the secondary end point of cardiovascular mortality and nonfatal MI (3 versus 6 percent).
●In the SAVE trial, 35 percent of patients were treated with a beta blocker at the time of randomization to captopril or placebo. After adjustment for baseline difference, beta blocker therapy was associated with a significant 30 percent reduction in the risk of cardiovascular death at one year (13 versus 22 percent for those not on a beta blocker) and a significant 21 percent decrease in the development of HF (17 versus 23 percent) [15].
Mineralocorticoid receptor antagonist — Evidence on the clinical use of mineralocorticoid receptor antagonist post-MI in patients with HF and/or diabetes mellitus is discussed separately. (See "Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults", section on 'Approach to secondary therapy' and "Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults", section on 'Mineralocorticoid receptor antagonist'.)
Efficacy in subgroups
Older patients — Beta blockers combined with ACE inhibitors are likely to be beneficial in older patients with ASLVD, yet they are more likely not to receive either drug than younger patients. Although there are no controlled data directly addressing this issue, a retrospective analysis of almost 21,000 older patients with LV dysfunction after an MI suggested a benefit from combined therapy compared with either drug alone [16].
Influence of sex — A meta-analysis of ACE inhibitor trials suggested that the mortality benefit from ACE inhibitors in patients with ASLVD may not apply to females [17]. Among trials of ACE inhibitor therapy in ASLVD, the relative mortality risk with ACE inhibitor therapy was significantly reduced in males at 0.83 (95% CI 0.71-0.96) but not females at 0.96 (95% CI 0.75-1.22).
However, until more definitive data are provided, ACE inhibitors should continue to be used in females with ASLVD.
Influence of race — The SOLVD trials provided information, some of it conflicting, on differences in response to ACE inhibitors between Black people and White people:
●In the prevention trial, Black people had higher rates of both progression to HF and overall mortality [18].
●In a matched-cohort study that included patients from both the prevention and treatment trials, enalapril therapy produced a significant 44 percent reduction in hospitalization for HF compared with placebo; there was no significant reduction among Black people (figure 4) [19].
●Other analyses of the SOLVD prevention trial (4054 patients, 403 of whom were Black people) found that the relative risks of death and progression to symptomatic HF were reduced to the same degree in both Black people and White people [17,20]. As in the matched-cohort study, a significant reduction in first hospitalization for HF was seen only in White people (relative risk 0.64 versus 0.85 in Black people) [20]. However, this end point was much less frequent than progression to symptomatic HF and it is therefore uncertain if the difference in response was real.
In summary, the role of ACE inhibitors in the treatment of ASLVD is the same in Black people as in White people.
PROGNOSIS — Individuals with asymptomatic left ventricular systolic dysfunction (ALVSD) with reduced LV ejection fraction (LVEF) have American College of Cardiology/American Heart Association stage B heart failure (HF), meaning they are at increased risk for clinical (ie, stage C or D) HF and death (figure 2). This risk was demonstrated by a meta-analysis including 10 reports with a total of 24,206 individuals with ASLVD followed for an average of approximately eight years [21]. The absolute risk of progression to HF was 8.4 per 100 person-years for those with ALVSD, as compared with 1 per 100 person-years in individuals without any ventricular dysfunction. The combined maximally adjusted relative risk of HF for ALVSD was 4.6. Based upon data from four studies that reported risk of HF per unit change in LVEF, the combined maximally adjusted relative risk of HF per 1 standard deviation lower EF was 1.4.
The following two studies were among those included in the meta-analysis:
●In the SOLVD trial, individuals with asymptomatic LV dysfunction treated with placebo progressed to symptomatic HF at a rate of 9.7 percent per year and the three-year mortality rate was 15.8 percent [4]. In the enalapril arm, symptomatic HF developed at a significantly lower rate of 6.7 percent per year but the mortality rate of 14.8 was not significantly lower than that in the placebo arm. (See 'Chronic LV systolic dysfunction' above.)
●Among 5004 participants in the Multi-Ethnic Study of Atherosclerosis (MESA), 112 individuals (1.7 percent) with asymptomatic LV systolic dysfunction and no prior history of cardiovascular disease were identified [22]. During nine-year follow-up, these individuals were at increased risk for incident HF (adjusted hazard ratio [HR] 8.69; 4.89 to 15.45), cardiovascular disease (adjusted HR 2.21; 1.13 to 3.73), and mortality (adjusted HR 2; 1.13 to 3.54).
Similarly, asymptomatic individuals with regional wall motion abnormalities are at increased risk of cardiovascular morbidity and mortality as illustrated by an analysis from the Strong Heart Study [23]. During eight-year follow-up, presence of baseline regional wall motion abnormalities was associated with 2.5-fold higher risk of cardiovascular events and 2.6-fold higher risk of cardiovascular death, after adjustment for other risk factors. Global wall motion abnormalities were associated with a 2.4-fold higher risk of cardiovascular events and 3.4-fold higher risk of cardiovascular death in similar multivariable models.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline links: Heart failure in adults".)
SUMMARY AND RECOMMENDATIONS
●The approach to management of ALVSD includes treatment (management of contributing conditions, neurohormonal blockade, and arrhythmia management), avoidance of drugs that may precipitate HF, and monitoring for progression. (See 'Management' above.)
●Pharmacologic intervention in the management of patients with ASLVD may delay the onset of HF, reduce the cardiac event rate, and improve survival. Recommendations for therapy are based upon the severity of LV systolic dysfunction (ie, presence of LVEF ≤40 percent) as well as the cause of dysfunction (ie, post-myocardial infarction [MI] or other) (algorithm 1). (See 'Neurohormonal blockade' above.)
•For patients with ALVSD with LVEF ≤40 percent without prior MI, we recommend the following therapy:
-For asymptomatic patients with LVEF ≤40 percent, we recommend angiotensin converting enzyme (ACE) inhibitor therapy (Grade 1B). An angiotensin II receptor blocker is suggested as an alternative for patients who have indications for an ACE inhibitor but have cough or angioedema with ACE inhibitor. (See 'ACE inhibitors' above and 'ARB as an alternative to ACE inhibitor' above.)
-For asymptomatic patients with LVEF ≤40 percent, we suggest beta blocker therapy (Grade 2C). (See 'Beta blockers' above.)
•Many patients with LV systolic dysfunction have had a prior ST elevation or non-ST elevation MI; standard indications for ACE inhibitor therapy and beta blocker therapy post-MI apply to these patients. (See "Overview of the nonacute management of ST-elevation myocardial infarction" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction" and 'Recommendations post-myocardial infarction' above and 'Post-myocardial infarction' above.)
●Among patients with ASLVD, arrhythmias should be managed according to standard evidence-based guidelines. Among the issues that may require consideration is the possibility of tachycardia-mediated cardiomyopathy as a potential cause of LV systolic dysfunction and the role of implantable cardioverter-defibrillator for primary prevention of sudden cardiac death (algorithm 1). (See 'Arrhythmia management' above.)
●Drugs that may precipitate HF should be avoided in patients with ASLVD such as nondihydropyridine calcium channel blockers and antiarrhythmics with negative inotropic effects. (See 'Drugs to avoid' above and "Drugs that should be avoided or used with caution in patients with heart failure".)
●Individuals with asymptomatic left ventricular systolic dysfunction (ASLVD) are at increased risk for heart failure (HF) and death (figure 2). A meta–analysis found that the absolute risk of progression to HF was 8.4 per 100 person-years for those with ALVSD, as compared with 1 per 100 person-years in individuals without any ventricular dysfunction. (See 'Prognosis' above.)
