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Clinical Review Evidence based cardiology

Prevention of congestive heart failure and management of asymptomatic left ventricular dysfunction

BMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7195.1400 (Published 22 May 1999) Cite this as: BMJ 1999;318:1400

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  1. R S McKelvie (mckelrob{at}hamcivhos.on.ca), career scientist, Ontario Ministry of Healtha,
  2. C R Benedict, director of heart failure programmeb,
  3. S Yusuf, career investigator, Medical Research Council of Canadaa
  1. a Department of Medicine, Division of Cardiology, McMaster University, Hamilton Health Sciences Corporation-General Division, 237 Barton Street East, Hamilton, ON, Canada L8L 2X2
  2. b Division of Cardiology, University of Texas, Health Sciences Centre, 6431 Fannin, Houston, TX 77030, USA
  1. Correspondence to: Dr R S McKelvie

    This is the second of four articles

    The epidemiology of heart failure has been studied largely among symptomatic individuals because identification of these patients is based on clinical criteria and does not require measuring left ventricular function.1 However, identifying people who are at high risk of heart failure could lead to the implementation of strategies that could potentially prevent heart failure and improve prognosis. This article reviews the prevalence of left ventricular dysfunction, the management of asymptomatic left ventricular dysfunction, and the prevention of heart failure.

    Summary points

    • Asymptomatic left ventricular dysfunction seems to be common

    • Risk factors for the development of heart failure exist and may be used to determine those patients at greatest risk of left ventricular dysfunction

    • Aggressive control of these risk factors is important

    • Although screening of people at high risk may be of value, at this time it cannot be justified

    Prevalence of left ventricular dysfunction

    The data on the prevalence of asymptomatic left ventricular dysfunction are limited, even though treatment of patients with this condition may be expected to improve their outcome.2–3 In 1992 McDonagh et al measured ejection fraction in 1467 people during a survey of coronary risk factors.3 The mean ejection fraction was 47% among people defined as not having cardiovascular disease, and 34% was two standard deviations below the mean. Of the 2.9% with an ejection fraction of 30%, half had no symptoms. The frequency of both left ventricular dysfunction and symptoms was greater in older age groups, increasing sharply up to the age of 45 and less sharply thereafter (table 1). Of the 7.7% with an ejection fraction of 35%, 77% were asymptomatic. Of those with definite left ventricular dysfunction (table 1), the proportion with symptoms increased with age. The group with left ventricular dysfunction had a greater prevalence of ischaemic heart disease and hypertension than did the group with normal ventricular function (table 2). Similar results have been found in other population based studies.4


    Embedded Image

    (Credit: SUE SHARPLES)

    Factors leading to development of heart failure

    Hypertension represents a continuous risk variable for heart failure, with no clear cut off point. Even moderate increases in blood pressure in patients with other risk factors increase risk.4

    Left ventricular hypertrophy predicts the development of heart failure independent of hypertension.4 Although the relative risk of heart failure associated with left ventricular hypertrophy is higher in the younger age group, the absolute excess in risk is higher in the older age group.

    Smoking is an independent and strong risk factor for the development of heart failure in men. The findings are less consistent in women, but there is a trend to an increase in risk in older women.4

    Hyperlipidaemia —Although the importance of lipid abnormalities has not been unequivocally shown for heart failure, data show an increased incidence of heart failure in association with raised triglyceride concentrations or a high ratio of total cholesterol to high density lipoprotein cholesterol.4 Furthermore, data from the 4S trial have shown that lipid lowering reduced the risk of developing heart failure.5

    Diabetes mellitus is an independent factor responsible for the development of heart failure. It is seen in about 20% of patients, with a similar number of patients having glucose intolerance, indicating that about 40% of heart failure patients have glucose abnormalities.6–11 In asymptomatic patients with ejection fraction of ≤35%, diabetes was an independent predictor for mortality, development of heart failure, and admission to hospital for heart failure.12 Furthermore, even when enalapril was given, diabetes remained an important predictor of outcome.12

    Microalbuminuria —The ongoing heart outcomes prevention evaluation trial13 found that microalbuminuria was an independent predictor of heart failure and other cardiovascular events in both diabetic and non-diabetic patients.14 After one year of follow up, 3.2% of patients (n=1987) with an albumin/creatinine ratio ≥2 mg/mmol were admitted to hospital for heart failure at one year compared with 1.0% (n=7292, P<0.0001) of normoalbuminuric patients.14

    Vital capacity —A low or decreased vital capacity over time is associated with an increased risk of developing heart failure.4 However, this has not been a consistent finding in all studies.

    Heart rate —The risk of developing heart failure increases with higher resting heart rate in a continuous graded fashion in hypertensive patients.4 This may indicate asymptomatic left ventricular dysfunction and subtle activation of the neuroendocrine system.

    Obesity is an independent risk factor for the development of heart failure.4 Weight loss would also help to correct lipid abnormalities.

    Asymptomatic left ventricular dysfunction is an independent predictor of cardiovascular risk.15 Asymptomatic patients with a reduced ejection fraction are at increased risk for death, hospital admission for heart failure, and development of heart failure.4

    Table 1

    Prevalence of definite left ventricular systolic dysfunction (ejection fraction 30%) by age according to presence of symptoms. Values are numbers (percentages) of patients

    View this table:
    Table 2

    Risk factors for left ventricular systolic dysfunction in symptomatic and asymptomatic participants

    View this table:

    Pathophysiological abnormalities predicting heart failure

    Neuroendocrine activation

    Neurohormonal activation has been shown in patients with asymptomatic and symptomatic left ventricular dysfunction. 4 16 17 The degree of left ventricular dysfunction is also related to the degree of neurohormonal activation.18 Plasma noradrenaline (norepinephrine) concentration in asymptomatic left ventricular dysfunction is a strong and independent predictor of mortality, hospital admission for heart failure, development of heart failure, occurrence of ischaemic events, and myocardial infarction.19 In patients with symptomatic left ventricular dysfunction increased concentrations of natriuretic peptides are also associated with adverse clinical outcomes. 20 21 Natriuretic peptides may be useful in screening for left ventricular dysfunction, but more studies are required to confirm this potential role. 4 22–24

    Cardiac dilatation and remodelling

    Ventricular dilatation and remodelling start soon after the initial myocardial event. The process is progressive and does not cause symptoms for several years.4

    Using the Framingham study database, Vasan et al reported that in asymptomatic people increases in left ventricular end diastolic and systolic internal dimensions were important predictors for subsequent development of heart failure.25 It seems likely that patients with left ventricular dysfunction represent a continuum, with the rate of ventricular dilatation accelerating at later stages. 26 27 Though the exact stimuli effecting these changes in myocardial structure remain unknown, increased myocardial wall stress and activation of the renin-angiotensin-aldosterone system are potential mechanisms. 4 26 27

    Prevention of symptomatic heart failure

    Although several trials have shown that angiotensin converting enzyme inhibitors and β blockers reduce mortality in patients with symptomatic heart failure, the prognosis in this condition remains poor.4 These results suggest that the greatest opportunity for reducing the incidence and excess mortality of heart failure is through preventive strategies.

    Treatment of hypertension

    The treatment of hypertension substantially reduces the risk for the development of heart failure.4 A recent meta-analysis showed that heart failure was effectively prevented with low dose diuretics, high dose diuretics, or β blockers.28 Although current data do not definitively show that using angiotensin converting enzyme inhibitors to treat hypertension will reduce the incidence of heart failure, the results of ongoing trials should answer some of these questions. 13 29

    Treatment of hyperlipidaemia

    The 4S Study Group recently reported that lipid lowering treatment with simvastatin reduces the risk of heart failure.5 In this study 228 patients (10.3%) in the placebo group were diagnosed with heart failure during follow up compared with 184 (8.3%) in the simvastatin group, resulting in a 21% reduction in the incidence of heart failure for the simvastatin group (P<0.015). Further studies are required to determine if this reduction is related to the effect of lipid lowering on coronary artery disease or is exerted through another independent mechanism.

    Prevention of myocardial ischaemia

    In heart failure it has been shown that a new myocardial infarction increases the risk of subsequent death and that many deaths in these patients are preceded by a major ischaemic event. 30 31 The development of angina is also a predisposing factor for adverse clinical outcome.30 These data emphasise that prevention of ischaemic events should be an integral part of the management of patients with left ventricular dysfunction; part of the effect of simvastatin in the 4S trial could be due to this mechanism.5

    Treatment with angiotensin converting enzyme inhibitors

    To date angiotensin converting enzyme inhibitors have been the only group of drugs shown to consistently reduce mortality and morbidity in patients with asymptomatic or symptomatic left ventricular dysfunction.32 Therefore an angiotensin converting enzyme inhibitor should be routinely administered to any patient with left ventricular dysfunction (ejection fraction <40%) who does not have a contraindication to this form of treatment. Recent data indicate that the addition of an angiotensin II receptor antagonist or a β blocker to an angiotensin converting enzyme inhibitor reduces ventricular dilatation in patients with low ejection fraction and heart failure.4 Current studies are evaluating the clinical impact of these two classes of agents. These data emphasise the importance of the renin-angiotensin and adrenergic systems in contributing to the progression of left ventricular dysfunction. “Cardiovascular protection” could be attained by using agents that block these mechanisms.

    Conclusions

    Symptomatic heart failure has an incidence of 0.5-1.0% and a prevalence of 1.0-2.0%. Once heart failure has developed, mortality and morbidity are high and patients have poor quality of life. Recent evidence indicates that asymptomatic left ventricular dysfunction occurs in 1-5% of the adult population, depending on the prevalence of other cardiovascular risk factors. Although routine screening of the general population cannot be justified, screening people at high risk may be of value. Risk factors for the development of heart failure have been identified, and these could be used to determine who is at the greatest risk of developing left ventricular dysfunction and ultimately symptomatic heart failure. These people should receive appropriate counselling, lifestyle advice, aggressive control of blood pressure, and treatment to alter other risk factors for cardiovascular disease and heart failure. In patients with left ventricular dysfunction, treatment with an angiotensin converting enzyme delays the development of heart failure. Because the prognosis for patients with heart failure remains poor, the greatest opportunities for improving the prognosis of such patients may be through strategies directed towards preventing the development of heart failure.

    Acknowledgments

    Competing interests: None declared.

    This article is adapted from Evidence-Based Cardiology, edited by S Yusuf, J A Cairns, A J Camm, E L Fallen, and B J Gersh, which was published by BMJ Books in 1998.

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