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Asymptomatic left ventricular diastolic dysfunction

Asymptomatic left ventricular diastolic dysfunction
Literature review current through: Jan 2024.
This topic last updated: Jan 10, 2023.

INTRODUCTION — Heart failure (HF) afflicts six million Americans and represents one of the leading causes of hospitalization among older adults [1]. Symptomatic HF (stage C and stage D) is commonly preceded by a stage in which cardiac dysfunction is present, but symptoms are absent (stage B) [2,3]. With the widespread utilization of echocardiography, asymptomatic cardiac dysfunction is commonly identified. This topic discusses identification, prognosis, and management of asymptomatic left ventricular (LV) diastolic dysfunction (ALVDD). (See "Determining the etiology and severity of heart failure or cardiomyopathy", section on 'Stages in the development of HF'.)

Other syndromes of LV dysfunction are discussed separately, including (see "Heart failure: Clinical manifestations and diagnosis in adults"):

HF with preserved ejection fraction and other causes of HF with normal or near normal ejection fraction. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Treatment and prognosis of heart failure with preserved ejection fraction" and "Pathophysiology of heart failure with preserved ejection fraction".)

HF with reduced ejection fraction. (See "Overview of the management of heart failure with reduced ejection fraction in adults".)

HF with mid-range ejection fraction. (See "Treatment and prognosis of heart failure with mildly reduced ejection fraction".)

Asymptomatic LV systolic dysfunction and asymptomatic valvular heart disease are discussed in separate topic reviews. (See "Approach to diagnosis of asymptomatic left ventricular systolic dysfunction" and "Management and prognosis of asymptomatic left ventricular systolic dysfunction".)

DEFINITIONS — LV diastolic dysfunction (LVDD) refers broadly to abnormalities in myocardial relaxation, compliance, and filling [4]. LVDD is most commonly identified by echocardiography (figure 1). LVDD can cause increased LV diastolic filling pressure, which in turn can increase pulmonary capillary pressure, resulting in lung congestion and dyspnea [5-7]. (See 'Echocardiographic criteria for LVDD' below.)

The American College of Cardiology/American Heart Association guidelines endorse a staging system for HF based upon the progressive nature of this syndrome [2]. Stage A refers to asymptomatic patients with HF risk factors but normal cardiac structure and function. Stage B includes asymptomatic patients with cardiac structural or functional abnormalities. Asymptomatic LVDD (ALVDD) is one of the clinical presentations for stage B HF [8-10]. Stage C refers to symptomatic HF, and stage D refers to refractory HF requiring specialized interventions. A later consensus document from the Heart Failure Society of America, the Heart Failure Association of the European Society of Cardiology, and the Japanese Heart Failure Society refers to stage A as "at risk" for HF and stage B as "pre-HF" [11]. (See "Determining the etiology and severity of heart failure or cardiomyopathy" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis".)

PREVALENCE — The prevalence of ALVDD varies depending upon the criteria used to identify ALVDD (see 'Echocardiographic criteria for LVDD' below):

Impact of stringency of criteria – The prevalence of ALVDD is lower when more stringent (more specific and less sensitive) criteria are applied to identify LVDD. The prevalence of ALVDD in adult populations (with mean ages 53 to 73) ranged from 25 to 35 percent using echocardiographic criteria included in the 2009 American Society of Echocardiography (ASE)/European Association of Echocardiography guidelines [12-16]. Application of the more stringent 2016 ASE/European Association of Cardiovascular Imaging guideline criteria for LVDD [17] resulted in a dramatic reduction in the prevalence of ALVDD, decreasing from 38.1 percent with the 2009 criteria to 1.4 percent with the 2016 criteria [18,19]. However, the greater specificity of the 2016 criteria may have compromised sensitivity, as the prevalence of ALVDD according to this definition is lower than the general population prevalence of symptomatic (ie, stage C) HF, estimated at 2.4 to 3.0 percent [1]. As such, many echocardiography laboratories continue to use the earlier, broader criteria for LVDD, as discussed below. (See 'Detection' below.)

Impact of adjustment for age – The frequency of ALVDD increases strikingly with age and with comorbidities such as obesity, coronary heart disease, atrial fibrillation, hypertension, and chronic kidney disease. Some clinical investigators have proposed age-specific cut-points for LVDD, resulting in a much less striking increase in the prevalence of LVDD with aging [20,21]. However, conditions associated with LVDD, particularly HF with preserved ejection fraction (HFpEF), also increase with age [1], and classification of age-related LVDD as "normal" could have the unintended consequence of undermining clinical detection of LVDD and HFpEF [22]. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Evaluation'.)

DETECTION — ALVDD is identified in individuals who have LVDD and lack symptoms of HF.

Identification of LVDD — Echocardiography is the key test for identification of LVDD, assessment of LV ejection fraction, and identification or exclusion of other cardiac abnormalities. LVDD is commonly detected as an incidental finding in patients undergoing transthoracic echocardiography for other indications. An evaluation of diastolic function is a standard component of a complete echocardiographic examination [3,4,17]. (See "Echocardiographic evaluation of left ventricular diastolic function in adults", section on 'When to evaluate diastolic function'.)

Echocardiographic criteria for LVDD — Echocardiographic findings associated with LVDD include alterations in the pattern of diastolic blood inflow across the mitral valve into the LV, abnormalities in the pulmonary venous inflow pattern, and reductions in diastolic tissue velocities. When sustained over time, worsening LVDD causes left atrial enlargement and increases in pulmonary artery pressure, which can also be detected using echocardiography. Details on the detection of LVDD by echocardiography are discussed separately. (See "Echocardiographic evaluation of left ventricular diastolic function in adults".)

The definition of LVDD has evolved over the past two decades. LVDD was initially defined by abnormalities in the transmitral and pulmonary venous inflow patterns along with tissue Doppler velocities, as described in the 2009 American Society of Echocardiography (ASE) recommendations for evaluation of diastolic function [12,13]. The 2018 updated ASE guidelines established a more stringent definition for diastolic dysfunction [17], which has affected the apparent prevalence of LVDD, as discussed above [18,19]. (See 'Prevalence' above and 'Detection' above.)

As noted above, echocardiographic criteria for LVDD included in the 2009 ASE guidelines [13] are more sensitive and less specific than the criteria for LVDD in the 2016 ASE guidelines [17]. Indeed, even among patients with symptomatic (stage C) HF with preserved ejection fraction (HFpEF), the 2016 ASE criteria are insufficiently sensitive to identify patients with abnormal hemodynamics. A study found that the 2016 criteria for LVDD had a sensitivity of 34 percent and specificity of 83 percent in 50 patients with invasively proven HFpEF and 24 patients with dyspnea but no cardiac abnormality [23].

Given the limited sensitivity of the 2016 criteria for LVDD and use of earlier broader criteria (included in the 2009 ASE guidelines) in most prior studies, our echocardiography laboratory and many others continue to utilize the earlier, broader criteria for LVDD based primarily on Doppler interrogation of the mitral inflow pattern (figure 1). (See "Echocardiographic evaluation of left ventricular diastolic function in adults".)

Concurrent findings — Echocardiography also enables identification of cardiac findings commonly associated with LVDD, including LV hypertrophy (common in patients with hypertension) and systolic dysfunction (including regional abnormalities caused by coronary heart disease). (See "Echocardiographic evaluation of left ventricular diastolic function in adults", section on 'Detection and evaluation' and "Left ventricular hypertrophy: Clinical findings and ECG diagnosis".)

Some patients with LVDD have regional or global systolic dysfunction. The evaluation and management of the asymptomatic and symptomatic patients with systolic dysfunction are discussed separately. (See "Approach to diagnosis of asymptomatic left ventricular systolic dysfunction" and "Management and prognosis of asymptomatic left ventricular systolic dysfunction" and "Heart failure: Clinical manifestations and diagnosis in adults".)

Other cardiac tests — Other cardiac tests can detect diastolic dysfunction but are not routinely used to detect ALVDD.

The gold standard method for assessment of diastolic function is cardiac catheterization, which enables simultaneous assessment of LV pressure and volume [24]. However, this procedure is generally not performed to screen asymptomatic individuals. Elevations in LV diastolic filling pressure are occasionally noted during cardiac catheterization performed for other reasons (eg, coronary angiography to assess for coronary artery disease). (See "Cardiac catheterization techniques: Normal hemodynamics".)

Cardiovascular magnetic resonance imaging (CMR) offers a variety of methods to detect abnormalities in LV structure and function, as well as myocardial fibrosis (via extracellular volume computation) associated with diastolic dysfunction, but these methods are not generally used to evaluate asymptomatic individuals [25,26]. Nuclear scintigraphic methods for assessment of diastolic function have been proposed but are not established [27,28].

Exclusion of symptoms of HF — A careful clinical evaluation is required to determine whether a patient has symptoms of HF; this includes taking a history to elicit symptoms and, for patients with uncertain activity tolerance, an exercise evaluation to delineate any functional limitations [29]. Many patients deny symptoms of dyspnea but may be highly sedentary, potentially obscuring activity intolerance. Evaluation with exercise testing or even a simple hall walk may reveal significant limitations in activity tolerance, thus revealing that the patient has occult HF with symptoms that may have been minimized or ignored [8].

Patients with activity intolerance and dyspnea merit further evaluation for HF and other causes, as discussed separately. (See "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Heart failure: Clinical manifestations and diagnosis in adults".)

MANAGEMENT PRINCIPLES — The management of patients with ALVDD includes therapeutic lifestyle changes, treatment of comorbid conditions, monitoring for symptoms and signs of progression to HF, and prompt evaluation and treatment of incident HF.

Therapeutic lifestyle changes — Therapeutic life-style changes may reduce the risk of progression to HF. An analysis from the ARIC cohort including 13,462 adults found that greater adherence to the American Heart Association's Life's Simple 7 guidelines on smoking, body mass, physical activity, diet, cholesterol, blood pressure, and glucose in middle age was associated with lower lifetime occurrence of HF and preservation of cardiac function [30]. The lifetime heart failure risk was 14.4 percent for those with an optimal middle-age Life's Simple 7 score, 26.8 percent for an intermediate score, and 48.6 percent for an inadequate score. This finding was confirmed in a prospective cohort study from Europe, in which optimal and intermediate Life’s Simple 7 scores were associated with reduced risk for HF compared with an inadequate score (hazard ratio [HR] 0.45, 95% CI 0.34-0.60 and HR 0.53, 95% CI 0.44-0.64, respectively) [31].

Greater physical activity may reduce the risk of HF. A randomized trial in 61 healthy, sedentary, middle-aged participants found that two years of exercise training improved maximal oxygen uptake and decreased cardiac stiffness [32]. An observational study following 13,810 participants for a median of 26 years found that recommended levels of physical activity were associated with lower HF risk among individuals with hypertension, obesity, diabetes, or metabolic syndrome, but not among those with prevalent atherosclerotic cardiovascular disease (coronary heart disease, stroke, or peripheral arterial disease) [33].

Management of comorbidities — As ALVDD is strongly associated with comorbid conditions such as hypertension, diabetes mellitus, coronary heart disease, and obesity, care of individuals with ALVDD involves management of these comorbidities [2]. Treatment of these conditions improves cardiovascular outcomes, and some of these measures reduce the risk of developing HF:

Treatment of hypertension. (See "Overview of hypertension in adults" and "Goal blood pressure in adults with hypertension".)

Standard recommendations for management of hypertension apply to patients with ALVDD. Antihypertensive therapy is central to reducing the risk of developing heart failure [34,35], as discussed separately. (See "Goal blood pressure in adults with hypertension" and "Treatment of hypertension in patients with heart failure".)

Management of diabetes mellitus and treatment of diabetic kidney disease. (See "Overview of general medical care in nonpregnant adults with diabetes mellitus" and "Initial management of hyperglycemia in adults with type 2 diabetes mellitus" and "Management of persistent hyperglycemia in type 2 diabetes mellitus" and "Treatment of diabetic kidney disease".)

As noted below, patients with diabetes are at high risk for development HF in the setting of ALVDD [36] (see 'Prognosis' below). Management of hyperglycemia in patients with type 2 diabetes and ALVDD is generally the same as for other patients at risk for developing HF, including use of metformin (the initial agent for most patients; use associated with lower cardiovascular risk compared with other initial agents) and sodium-glucose cotransporter 2 [SGLT2] inhibitors (which reduce the risk of HF and the risk of kidney failure). The use and effects of metformin and SGLT2 inhibitors are discussed separately. (See "Initial management of hyperglycemia in adults with type 2 diabetes mellitus", section on 'Initial pharmacologic therapy' and "Management of persistent hyperglycemia in type 2 diabetes mellitus", section on 'Established cardiovascular or kidney disease' and "Metformin in the treatment of adults with type 2 diabetes mellitus" and "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus" and "Treatment of diabetic kidney disease".)

Assessment of atherosclerotic cardiovascular risk to guide primary (or secondary) prevention including lipid therapy and use of aspirin. (See "Atherosclerotic cardiovascular disease risk assessment for primary prevention in adults: Our approach" and "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Overview of atherosclerotic cardiovascular risk factors in females".)

The presence of ALVDD does not modify the approach to statin therapy. While there are theoretical mechanisms whereby statins may exert benefits, their role in reducing the risk of HF has not been established. Studies evaluating the effects of statin therapy on the risk of HF are discussed separately. (See "Statin therapy in patients with heart failure".)

The presence of ALVDD does not modify the approach to antiplatelet therapy. The effects of antithrombotic therapy in patients with HF are discussed separately. (See "Aspirin in the primary prevention of cardiovascular disease and cancer" and "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease" and "Antithrombotic therapy in patients with heart failure".)

Management of coronary heart disease. (See "Chronic coronary syndrome: Overview of care" and "Management of coronary heart disease in women".)

Management of obesity. Studies in people with obesity suggest that weight loss has beneficial hemodynamic effects and may reduce the risk of HF [37-40]. (See "Obesity in adults: Overview of management".)

Management of LV systolic dysfunction. Some patients with ALVDD have regional or global systolic dysfunction. The evaluation and management of asymptomatic LV systolic dysfunction are discussed separately. (See "Approach to diagnosis of asymptomatic left ventricular systolic dysfunction" and "Management and prognosis of asymptomatic left ventricular systolic dysfunction".)

Monitoring — Patients with ALVDD should be monitored clinically for symptoms and signs of progression to symptomatic HF in concert with follow-up and management of any associated comorbidities. Patients should receive counseling on the risk of HF and the importance of seeking medical care for HF symptoms. As noted above, careful evaluation of symptoms is required to identify patients with occult HF. (See 'Exclusion of symptoms of HF' above.)

The recommended frequency of monitoring varies depending upon the presence and severity of concurrent conditions, ranging from annual visits (eg, for adults ≥50 years old with no chronic conditions), to two or more times per year (eg, for those on a stable antihypertensive regimen), to at least monthly (eg, for titration of antihypertensive therapy to reach goal blood pressure). (See "Overview of preventive care in adults" and "Overview of hypertension in adults", section on 'Blood pressure goals (targets)'.)

Follow-up echocardiography is performed only as clinically indicated to evaluate changes in clinical status (eg, new symptoms of HF). (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Diagnosis' and 'Progression to HF' below.)

Progression to HF — Patients who develop symptoms and/or signs of HF require evaluation to determine whether HF is present, the cause of HF, and the appropriate treatment, as discussed separately. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults" and "Determining the etiology and severity of heart failure or cardiomyopathy".)

Management of HF is discussed separately. (See "Treatment and prognosis of heart failure with preserved ejection fraction" and "Overview of the management of heart failure with reduced ejection fraction in adults" and "Treatment and prognosis of heart failure with mildly reduced ejection fraction" and "Treatment of acute decompensated heart failure: General considerations" and "Treatment of acute decompensated heart failure: Specific therapies".)

PROGNOSIS — Individuals with ALVDD have poorer exercise capacity compared with those with normal diastolic function indices [8,26] and are at increased risk for progression to symptomatic HF [36,41-44] and for death [12,45]. In a community-based sample, the presence of mild LVDD was associated with an 8.3-fold increased risk for death (hazard ratio [HR] 8.31, 95% CI 3.00-23.1), while moderate to severe LVDD was associated with a 10.2-fold greater risk of death (HR 10.17, 95% CI 3.28-31.0) [12].

LVDD typically worsens with age, particularly among patients with obesity and weight gain [46,47], and progression in LVDD over time is associated with substantially increased risk of death [45]. In the community-based sample described above [12], worsening LVDD was associated with age ≥65 years (odds ratio 2.85, 95% CI 1.77-4.72) as well as the presence of hypertension, diabetes, and coronary heart disease [41]. ALVDD was independently associated with an 81 percent greater risk for developing incident HF (HR 1.81, 95% CI 1.01-3.48) after adjustment for other factors. Other studies have confirmed these findings, showing high risk for progression to HF among patients with ALVDD, particularly when associated with kidney disease, higher pulmonary artery pressures, respiratory limitations, and anemia [42-44].

Risk of progression to HF from ALVDD is particularly high among individuals with diabetes mellitus. A study of 1760 individuals with diabetes without HF found that 36.9 percent of those with ALVDD developed symptomatic HF within five years, compared with 16.8 percent for patients without LVDD [36]. In a large meta-analysis incorporating data from 11 studies of 25,369 patients, ALVDD was associated with a 70 percent increased risk for developing symptomatic HF during an average follow-up of 7.9 years [48]. The risk of progression from ALVDD to symptomatic HF with preserved ejection fraction is greatest among patients in whom other cardiac abnormalities subsequently develop, such as reduced LV contractility or contractile reserve, chronotropic incompetence, abnormal vascular function, or cardiac structural remodeling [49-51]. (See "Pathophysiology of heart failure with preserved ejection fraction".)

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: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

Left ventricular diastolic dysfunction (LVDD) refers broadly to abnormalities in myocardial relaxation, compliance, and filling. LVDD is most commonly identified by echocardiography (figure 1). LVDD can cause increased LV diastolic filling pressure, which in turn increases pulmonary capillary pressure, resulting in lung congestion and dyspnea. However, LVDD can also be asymptomatic (ALVDD). (See 'Definitions' above.)

The prevalence of ALVDD varies widely depending upon the echocardiographic criteria used. More stringent criteria and adjustment of criteria for age both reduce the measured prevalence of ALVDD. (See 'Prevalence' above.)

ALVDD is identified in individuals who have LVDD and no symptoms of HF. (See 'Detection' above.)

Echocardiography is the key test for identification of LVDD, assessment of LV ejection fraction, and identification or exclusion of other cardiac abnormalities. LVDD is commonly detected as an incidental finding in patients undergoing transthoracic echocardiography for other indications. An evaluation of diastolic function is a standard component of a complete echocardiographic examination.

Careful clinical evaluation is required to exclude symptoms of HF. (See 'Exclusion of symptoms of HF' above.)

The management of patients with LVDD involves therapeutic lifestyle changes, treatment of comorbid conditions (including hypertension, diabetes mellitus, coronary heart disease, and obesity), monitoring for symptoms and signs of progression to HF, and prompt evaluation and treatment of incident HF. (See 'Management principles' above.)

Individuals with ALVDD have worse exercise capacity, increased risk of progression to symptomatic HF, and greater mortality compared with those with normal diastolic function. (See 'Prognosis' above.)

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Topic 131241 Version 3.0

References

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