Author
Wilson S Colucci, MD
Section Editor
Stephen S Gottlieb, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC

Last literature review for version 17.3: September 30, 2009  |  This topic last updated: February 1, 2009

INTRODUCTION — Left ventricular (LV) systolic dysfunction with symptoms of heart failure (HF) is a common clinical problem. Population-based studies suggest that asymptomatic LV dysfunction is at least as prevalent as symptomatic HF in the general population.

Patients with asymptomatic LV systolic dysfunction progress to overt HF over time. In the placebo arm of the SOLVD trial, patients with asymptomatic LV dysfunction not treated with an angiotensin converting enzyme (ACE) inhibitor progressed to symptomatic HF at a rate of 9.7 percent per year [1]. In addition, the mortality rate in patients with asymptomatic LV dysfunction is increased, although to a lesser degree than in symptomatic HF (graph 1). In the placebo arm of the SOLVD trial, the three-year mortality rate was 16 percent [1]. (See 'Chronic LV systolic dysfunction' below.)

The management of patients with asymptomatic LV systolic dysfunction will be reviewed here. Issues related to the prevalence of and possible screening for asymptomatic LV systolic dysfunction and the management of symptomatic systolic HF are presented separately. (See "Screening for asymptomatic left ventricular dysfunction" and "Overview of the therapy of heart failure due to systolic dysfunction".)

Asymptomatic LV diastolic dysfunction is also common and associated with an adverse prognosis [2]. However, there are no data on the efficacy of treating diastolic dysfunction before the onset of symptoms. (See "Treatment and prognosis of diastolic heart failure", section on Asymptomatic subjects.)

CLINICAL FEATURES — By definition, patients with asymptomatic LV dysfunction have no symptoms. The diagnosis is usually made by echocardiography performed because the patient might have underlying heart disease or cardiomegaly is detected on chest x-ray.

These patients also should have no clear physical findings of HF (pulmonary rales, mild lower extremity edema). However, more subtle abnormalities may be present. In a review of 4100 patients from the SOLVD prevention trial, 5.1 percent had an S3 gallop and 1.7 percent had an elevated jugular venous pressure [3]. After adjusting for other markers of disease severity, these two findings were each associated with an increased risk of progression to overt HF (relative risk 1.38 and 1.51 compared to those without an S3 gallop). One limitation to these observations is the operator-dependence for the detection of these physical findings.

Neurohumoral activation — In addition to a low LVEF, patients with asymptomatic left ventricular systolic dysfunction show signs of secondary neurohumoral activation that indicate decreased tissue perfusion. The serum concentrations of norepinephrine, renin, antidiuretic hormone, and atrial and brain natriuretic peptides are elevated (graph 2) [4-9], reaching levels intermediate between age-matched controls and patients with symptomatic heart failure [5]. (See "Pathophysiology of heart failure: Neurohumoral adaptations" and "Brain natriuretic peptide measurement in left ventricular dysfunction and other cardiac diseases".)

The degree of neurohumoral activation is predictive of outcome [5,6]. In the SOLVD trial, for example, elevated serum norepinephrine concentrations predicted mortality (all-cause and cardiovascular) and clinical events related to the subsequent onset of heart failure or acute ischemic syndromes (graph 3) [7]. (See "Predictors of survival in heart failure due to systolic dysfunction", section on Neurohumoral activation.)

EVALUATION — The diagnosis of asymptomatic LV systolic dysfunction is made from the history and from the demonstration of a reduced LVEF, most often by echocardiography. In some patients, echocardiography is performed to assess LV function because of known heart disease (eg, prior myocardial infarction). In other cases, echocardiography is performed for some other reason and a low LVEF is noted. In this setting, further evaluation is required to establish the cause of the LV dysfunction.

The evaluation is in many ways similar to that in patients with symptomatic heart failure, including the need to exclude underlying coronary artery disease. (See "Evaluation of the patient with suspected heart failure".)

Familial disease — It has been estimated that as many as 20 to more than 50 percent of cases of idiopathic dilated cardiomyopathy are familial. It is therefore possible to detect evidence of early disease by screening asymptomatic family members, an approach that is recommended by the 2005 ACC/AHA guidelines and others [10-12]. (See "Genetics of dilated cardiomyopathy", section on 'Familial dilated cardiomyopathy'.)

This was illustrated in a prospective cohort study that evaluated (by echocardiography) 767 asymptomatic first- and second-degree relatives of 189 consecutive patients with idiopathic dilated cardiomyopathy [11]. There were two major findings:

* Dilated cardiomyopathy, left ventricular enlargement without systolic dysfunction, or systolic dysfunction without left ventricular enlargement was present in 23 percent of relatives.
* At a median follow-up of 53 months, 13 of the 124 relatives (10.4 percent) with left ventricular enlargement without systolic dysfunction or systolic dysfunction without left ventricular enlargement progressed to dilated cardiomyopathy.

Based upon observations such as these, some have suggested initiating therapy with an ACE inhibitor to slow progression in patients with left ventricular enlargement, even in the absence of a reduced LVEF [12]. This is in contrast to the usual LVEF threshold of ≤40 percent in other patients with asymptomatic left ventricular dysfunction. (See 'Threshold for therapy' below.)

We feel that such an approach is premature, since there is no evidence of benefit [11]. However, periodic echocardiographic monitoring for progression is warranted.

TREATMENT — Treatment of patients with asymptomatic LV systolic dysfunction with an ACE inhibitor (or, if not tolerated, an angiotensin II receptor blocker) and probably a beta blocker reduces the rate of progression of ventricular dysfunction, delays the onset of symptomatic HF, and decreases morbid events and mortality. In contrast, there is no evidence that other measures useful in the treatment of symptomatic heart failure, such as digoxin, or lifestyle modifications, including salt restriction, exercise, or nutritional supplements, are of benefit in these patients.

Several groups of patients with asymptomatic left ventricular systolic dysfunction have been identified in whom early pharmacologic intervention may be important:

* Postmyocardial infarction
* Postrevascularization
* Chronic LV systolic dysfunction

The management of asymptomatic left ventricular systolic dysfunction in these settings will be reviewed here. There are two other conditions, discussed elsewhere, in which medical therapy can improve or preserve left ventricular function: hypertension with left ventricular hypertrophy and aortic regurgitation.

* Untreated hypertension is an important risk factor for the development of left ventricular hypertrophy, left ventricular dysfunction, and heart failure. Although heart failure in these patients is most often the result of diastolic dysfunction, symptomatic systolic heart failure and asymptomatic left ventricular dysfunction resulting from left ventricular hypertrophy may also occur [13]. Among hypertensive patients who develop left ventricular hypertrophy, angiotensin II receptor blockers, calcium channel blockers, and ACE inhibitors appear to decrease left ventricular mass more rapidly and to a greater extent than beta blockers, thereby reducing diastolic dysfunction (graph 4) [14,15]. However, many of the commonly used agents eventually produce a similar effect. (See "Clinical implications and treatment of left ventricular hypertrophy in hypertension".)

* In aortic regurgitation, the regurgitant flow of blood produces a chronic increase in left ventricular end-diastolic volume and wall stress. If untreated, left ventricular hypertrophy and systolic dysfunction eventually ensue. By the time symptoms of heart failure occur, many patients have irreversible left ventricular dysfunction. This observation has provided the rationale for early therapy with vasodilators to reduce afterload in asymptomatic patients, although evidence of benefit is inconclusive. (See "Vasodilator therapy in asymptomatic severe chronic aortic regurgitation in adults".)

Post-MI — Myocardial infarction (MI) is the leading cause of heart failure in the United States. (See "Epidemiology and causes of heart failure".) Although a large MI may result in the early appearance of heart failure, symptoms of heart failure usually do not appear for several months to years after the MI. In the interval between infarction and the development of heart failure, there is progressive left ventricular remodeling, which results in cavity dilation and contractile dysfunction. This process begins with myocyte necrosis and formation of a fibrotic scar in the infarcted region, followed by changes in the shape and function of the noninfarcted region [16,17]. (See "Cardiac remodeling: Clinical assessment and therapy".)

The net effect of this remodeling process is an increase in ventricular cavity volume in excess of ventricular mass, leading to a fall in LVEF, which is typically identified and quantified by noninvasive testing (eg, echocardiography). (See "Noninvasive methods for measurement of left ventricular systolic function".)

Current therapeutic approaches to preserving myocardial function following an acute MI are aimed at increasing coronary artery patency and reducing the initial infarct size with the early use of aspirin and reperfusion therapy (see "Coronary artery patency and outcome after myocardial infarction", and at preventing or slowing remodeling and the late loss of myocardial function with ACE inhibitors and possibly beta blockers [18-21]. These therapies are also associated with improved survival [1,22-26].

ACE inhibitors — Two large clinical trials, SAVE and TRACE, showed that long-term treatment with ACE inhibitors in patients with asymptomatic left ventricular systolic dysfunction soon after MI delays the onset of symptomatic heart failure and may improve survival. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Clinical trials".)

In the SAVE trial of 2231 asymptomatic patients with an LVEF ≤40 percent after MI, captopril therapy (12.5 mg TID increasing to a final target dose of 50 mg TID), starting three to sixteen days after the MI, was associated with the following significant benefits compared to placebo after an average follow-up of 42 months [22]:

* A 19 percent (95 percent confidence interval [CI] 3 to 32 percent) reduction in total mortality (20 versus 25 percent) (graph 5)

* A 21 percent reduction in cardiovascular mortality
* A 37 percent (95% CI 20 to 50 percent) decrease in the risk of developing heart failure

These benefits were noted in all patient groups including those who received other adjunctive therapies such as thrombolysis, aspirin, and/or beta blockers.

The TRACE trial randomly assigned 1749 patients with an acute MI associated with an LVEF ≤35 percent to trandolapril (titrated to a dose of 4 mg/day) or placebo three to seven days after the event; 41 percent of the patients had no symptoms of heart failure [23]. After a two to four year follow-up, trandolapril significantly reduced total mortality (by 22 percent), sudden death (by 24 percent), and progression to severe heart failure (by 29 percent) compared to placebo. The mortality benefit was equivalent in subgroups of patients who were asymptomatic. At a minimum follow-up of six years, patients receiving trandolapril had a life expectancy of 6.2 years versus 4.6 years for placebo (graph 6) [27].

There are conflicting data as to whether ACE inhibitors reduce the incidence of recurrent MI in these patients. The SAVE trial noted a significant 25 percent reduction in recurrent MI [22], a finding that was not seen in TRACE [27].

Acute anterior MI — Several trials have evaluated the efficacy of early ACE inhibitor therapy (beginning on the first day) in all patients with an acute anterior MI who are generally at greatest risk for left ventricular dysfunction. The efficacy of this approach appears to depend upon whether reperfusion has been achieved.

Early ACE inhibitor therapy (begun within 24 hours of the infarction and continued for six weeks) in patients with anterior MI who were not eligible for thrombolysis was evaluated in the SMILE trial [28]. In this trial, 1556 asymptomatic patients were randomly assigned to zofenopril (7.5 mg initial dose and progressively doubled every 12 hours until the target dose of 30 mg twice daily was reached) or placebo. Criteria for exclusion included cardiogenic shock, systolic pressure below 100 mmHg, plasma creatinine concentration above 2.5 mg/dL (221 µmol/L), a history of heart failure, and current therapy with an ACE inhibitor.

The primary six week combined end point, mortality plus severe heart failure, was reduced with zofenopril (7 versus 10.6 percent for placebo; risk reduction 34 percent, 95% CI 8 to 54 percent); this benefit was mainly attributable to less heart failure. At one year, patients receiving zofenopril had a significantly lower mortality rate (10 versus 14 percent; risk reduction 29 percent, 95% CI 6 to 51 percent) (graph 7).

The mechanism of early benefit is not clear. Both the cardioprotective effects of ACE inhibition and/or prompt blockade of the deleterious effects of neurohumoral activation may contribute. Early administration of ACE inhibitors should be performed only in a carefully monitored setting to permit rapid detection of drug-induced hypotension. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use".)

In contrast to the above data, there does not appear to be a protective effect of early ACE inhibition in patients with an acute anterior MI who are treated with thrombolytic therapy. In a meta-analysis of three trials involving 845 patients for whom echocardiographic data had been collected, early treatment with an ACE inhibitor did not significantly affect the diastolic or systolic volume index compared to placebo [29]. Subset analysis suggested that left ventricular dilation was significantly attenuated in patients who failed to achieve reperfusion; this group is similar to the patients enrolled in the SMILE trial who were not eligible for thrombolysis [28].

Beta blockers — Beta blockers are given to most post-MI patients, independent of left ventricular function, because they improve survival and reduce the rate of both sudden death and recurrent MI. (See "Beta blockers in the management of acute coronary syndrome".) Their specific role, when used alone, for asymptomatic left ventricular dysfunction post-MI, is less clear as controlled trials are lacking. However, possible benefit with beta blockers, when combined with ACE inhibitors, 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 [24]. 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 heart failure (17 versus 23 percent) [25].

Elderly — Beta blockers combined with ACE inhibitors are likely to be beneficial in elderly patients with asymptomatic left ventricular dysfunction, yet they are more likely not to receive either drug than younger patients. Although there are no controlled data addressing this issue, a retrospective analysis of almost 21,000 elderly patients with left ventricular dysfunction after an MI suggested a benefit from combined therapy compared to either drug alone [30].

Other medications — There are no studies that directly address the efficacy of digoxin, diuretics, nitrates, or calcium channel blockers in the management of patients with asymptomatic left ventricular dysfunction due to ischemic cardiomyopathy.

Although digoxin improves symptoms in many patients with overt heart failure, there is no evidence that it enhances survival in symptomatic or asymptomatic left ventricular dysfunction. This was best illustrated in the DIG trial in which there was no effect of digoxin on total mortality (graph 8) [31]. Although there was an insignificant trend for a reduction in death from worsening heart failure, this was counterbalanced by an apparent increase in arrhythmic death. (See "Use of digoxin in heart failure due to systolic dysfunction".)

There is no evidence of benefit from calcium channel blockers in patients with asymptomatic heart failure. (See "Calcium channel blockers in heart failure due to systolic dysfunction".)

Postrevascularization — Although the prognosis of patients with coronary artery disease and reduced left ventricular function is improved with revascularization, their outcome is worse than in patients who have normal left ventricular function. This suggests a potential benefit from ACE inhibitors in this setting.

This issue was examined in the APRES trial of 159 patients with chronic stable angina, an LVEF between 30 and 50 percent, and no clinical heart failure who underwent bypass surgery or angioplasty and were then randomly assigned to ramipril or placebo [32]. After a 33 month follow-up, ramipril significantly reduced the composite end point of cardiac death, acute MI, or clinical heart failure (10 versus 23 percent, risk reduction 58 percent, 95% CI 7 to 80 percent) (graph 9). The benefit of ramipril was independent of the LVEF and whether bypass surgery or angioplasty was performed but was related, in part, to a reduction in left ventricular end-diastolic and end-systolic volume indices [33].

Chronic LV systolic dysfunction — ACE inhibitors and possibly beta blockers also appear to be beneficial in patients with asymptomatic chronic left ventricular systolic dysfunction who are not post-MI.

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 [1,34,35]. The SOLVD prevention trial consisted of 4228 asymptomatic patients (83 percent had had an MI more than 30 days from entry) with an LVEF ≤35 percent; the patients were randomly assigned to enalapril (20 mg once per day) or placebo [1]. At a mean follow-up of just over three years, enalapril therapy was associated with a nonsignificant reduction in cardiovascular mortality compared to placebo (14 versus 16 percent) and a significant 29 percent reduction (95% CI 21 to 36 percent) in the combined incidence of symptomatic heart failure or cardiovascular death (graph 10).

A subsequent analysis, called XSOLVD, evaluated virtually all of the original participants in the SOLVD prevention trial at a median of 11 years [34]. 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 asymptomatic left ventricular dysfunction due to idiopathic dilated cardiomyopathy (IDC). 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 [1].

Beta blockers — There are no randomized trials that have specifically evaluated the effect of beta blockers on cardiovascular outcomes in patients with asymptomatic LV dysfunction 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 to placebo (6 and 4 versus 0 percent at 12 months) [36]. However, clinical outcomes were not evaluated. (See "Cardiac remodeling: Clinical assessment and therapy", section on 'Beta blockers'.)

The SOLVD prevention trial provided indirect evidence of clinical benefit from beta blocker therapy, similar to that described above in post-MI patients [26]. Among the 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 heart failure (relative risk 0.64, 95% CI 0.49-0.83) compared to 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.

Influence of gender — A meta-analysis of ACE inhibitor trials suggested that the mortality benefit from ACE inhibitors in patients with asymptomatic left ventricular dysfunction may not apply to women [37]. Among trials of ACE inhibitor therapy in asymptomatic LV dysfunction, the relative mortality risk with ACE inhibitor therapy was significantly reduced in men at 0.83 (95% CI 0.71-0.96) but not women at 0.96 (95% CI 0.75-1.22). However, until more definitive data are provided, ACE inhibitors should continue to be used in women with asymptomatic LV dysfunction.

Influence of race — The SOLVD trials provided information, some of it conflicting, on differences in response to ACE inhibitors between blacks and whites. (See "ACE inhibitors in heart failure due to systolic dysfunction: Therapeutic use", section on 'Influence of race'.)

* In the prevention trial, blacks had higher rates of both progression to heart failure and overall mortality [38].
* 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 heart failure compared to placebo; there was no significant reduction among blacks (graph 11) [39].
* Other analyses of the SOLVD prevention trial (4054 patients, 403 of whom were black) found that the relative risks of death and of progression to symptomatic heart failure were reduced to the same degree in both blacks and whites [37,40]. As in the matched-cohort study, a significant reduction in first hospitalization for HF was seen only in whites (relative risk 0.64 versus 0.85 in blacks) [40]. 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 asymptomatic LV dysfunction is the same in blacks as in whites.

ARRHYTHMIA MANAGEMENT — Patients with certain arrhythmias can develop a tachycardia-mediated cardiomyopathy, in which the tachycardia results in the development of left ventricular dysfunction or the precipitation of heart failure in those with preexisting asymptomatic left ventricular dysfunction. (See "Tachycardia-mediated cardiomyopathy".)

A number of tachyarrhythmias have been associated with tachycardia-mediated cardiomyopathy; among patients with an IDC, the most common are atrial fibrillation and atrial flutter. (See "Pathogenesis of ventricular arrhythmias in heart failure and cardiomyopathy".) Regardless of the type of arrhythmia, reversion to sinus rhythm or slowing the ventricular rate results in an improvement in left ventricular function.

RECOMMENDATIONS — Pharmacologic intervention in the management of patients with asymptomatic left ventricular dysfunction may delay the onset of symptomatic disease, reduce the cardiac event rate, and improve survival. We agree with the recommendations of the 2005 ACC/AHA task force on the management of heart failure that patients with asymptomatic left ventricular systolic dysfunction should treated with an ACE inhibitor and beta blocker (table 1) [10]. The 2008 European Society of Cardiology (ESC) guidelines also recommended ACE inhibitors, but recommended beta blockers only in patients who have had a myocardial infarction [41].

In contrast, the administration of digoxin, salt restriction beyond that which is prudent for healthy individuals, exercise conditioning, and routine administration of nutritional supplements were NOT recommended.

Threshold for therapy — The ACC/AHA task force did not specify a threshold for "reduced ejection fraction" [10]. In randomized trials cited above, such as SOLVD, SAVE, TRACE, and CAPRICORN, the LVEF was ≤35 to 40 percent [1,22-24]. The 2008 guidelines from the ESC defined an LVEF ≤40 as the threshold for therapy [41]. We initiate therapy in appropriate patients when the LVEF is ≤40 percent. Some a suggested a higher threshold in asymptomatic relatives of patients with idiopathic dilated cardiomyopathy. (See 'Familial disease' above.)

Post-MI or revascularization — Patients at high risk for the development of symptomatic heart failure after myocardial infarction or revascularization should receive an ACE inhibitor and beta blocker. As described above, two such groups have been identified: those with asymptomatic left ventricular dysfunction (as defined by an LVEF ≤40 percent); and those with an acute anterior wall infarction.

ACE inhibitors — The greatest number of lives saved per number treated with an ACE inhibitor has been demonstrated in high-risk patients with impaired left ventricular function and/or an anterior MI [1,22,28,32]. However, demonstration of asymptomatic left ventricular dysfunction requires bedside imaging studies, and selection of patients by infarct location alone may not result in early identification of all patients with significant left ventricular dysfunction.

Thus, unless the infarct is known to be small, it may be most reasonable to consider initial administration of ACE inhibitors in a nonselective fashion (ie, in all patients with an acute MI) and then withdraw therapy later based upon the absence of high-risk features.

The safe use of ACE inhibitors soon after acute MI requires oral administration at low doses with careful monitoring of the blood pressure; doses are titrated upward as long as the systolic blood pressure is above 90 to 100 mmHg. (See "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use".) Recommended regimens include:

* Captopril — initial dose of 6.25 mg, which is increased to a maximum of 50 mg TID
* Enalapril — initial dose 2.5 mg/day increased up to 20 mg BID
* Lisinopril — initial dose 2.5 mg/day increased to a maximum of 40 mg/day
* Ramipril — initial dose 2.5 mg/day increased up to a maximum of 20 mg/day

Despite the observations of benefit with ACE inhibitors in patients with asymptomatic left ventricular dysfunction, they are underutilized. In one report, only 48 percent of such patients were discharged on an ACE inhibitor and, when prescribed, the dose was inadequate in 67 percent [42].

Beta blockers — In the absence of a contraindication, all post-MI patients are treated with beta blockers because of the demonstrated survival benefit. Among patients with asymptomatic left ventricular dysfunction treated with ACE inhibitors, beta blockers appear to reduce mortality and the rate of progression to symptomatic heart failure [24,25]. Any of the agents without intrinsic sympathomimetic activity can be used, beginning with very low doses. Metoprolol or carvedilol is preferred. (See 'Beta blockers' above and "Use of beta blockers in heart failure due to systolic dysfunction".)

Chronic LV systolic dysfunction — Patients with dilated cardiomyopathy due to coronary disease or idiopathic dilated cardiomyopathy should be treated with an ACE inhibitor [10], largely based upon the SOLVD prevention trial [1]. Although there is not definitive evidence of benefit [26], it is recommended that such patients should also be treated with a beta blocker (table 1) [10].

Issues related to screening for familial disease are discussed above. (See 'Familial disease' above.)

Risk factor modification — As with other patients with heart disease, risk factor modification is important in patients with asymptomatic left ventricular dysfunction, regardless of etiology, in an attempt to reduce the risk of further injury and/or slowing the progression of left ventricular dysfunction. This includes control of hyperlipidemia, diabetes, and hypertension; cessation of smoking; and elimination of alcohol or illicit drugs. (See "Secondary prevention of cardiovascular disease: Risk factor reduction".)

Other therapies — Other recommendations from the ACC/AHA task force included valve replacement or repair for patients with hemodynamically significant regurgitation or stenosis and regular evaluation for the development of the signs or symptoms of heart failure [10].

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