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European Journal of Heart Failure 2009 11(2):130-139; doi:10.1093/eurjhf/hfn013
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology

Nathaniel Mark Hawkins1,*, Mark C. Petrie2, Pardeep S. Jhund3, George W. Chalmers2, Francis G. Dunn4 and John J.V. McMurray3

1 Aintree Cardiac Centre, University Hospital Aintree, Longmoor Lane, Liverpool L9 7AL, UK
2 Royal Infirmary, Glasgow, UK
3 Western Infirmary, Glasgow, UK
4 Stobhill Hospital, Glasgow, UK

* Corresponding author. Tel: +44 151 529 2717, Fax: +44 151 529 2724, Email: nathawkins{at}hotmail.com


   Abstract
Top
 Abstract
Introduction
 Problems diagnosing heart...
 Problems diagnosing heart...
 Problems diagnosing chronic...
 Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
 Conclusions
 Funding
 Appendix
 References
 
Heart failure (HF) and chronic obstructive pulmonary disease (COPD) are global epidemics incurring significant morbidity and mortality. The combination presents many diagnostic challenges. Clinical symptoms and signs frequently overlap. Evaluation of cardiac and pulmonary function is often problematic and occasionally misleading. Echocardiography and pulmonary function tests should be performed in every patient. Careful interpretation is required to avoid misdiagnosis and inappropriate treatment. Airflow obstruction, in particular, must be demonstrated when clinically euvolaemic. Very high and very low concentrations of natriuretic peptides have high positive and negative predictive values for diagnosing HF in those with both conditions. Intermediate values are less informative. Both conditions are systemic disorders with overlapping pathophysiological processes. In patients with HF, COPD is consistently an independent predictor of death and hospitalization. However, the impact on ischaemic and arrhythmic events is unknown. Greater collaboration is required between cardiologists and pulmonologists to better identify and manage concurrent HF and COPD. The resulting symptomatic and prognostic benefits outweigh those attainable by treating either condition alone.

Key Words: Heart failure • Chronic obstructive pulmonary disease

Received January 24, 2008; Revised August 31, 2008; Accepted November 3, 2008


   Introduction
Top
 Abstract
 Introduction
Problems diagnosing heart...
 Problems diagnosing heart...
 Problems diagnosing chronic...
 Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
 Conclusions
 Funding
 Appendix
 References
 
Heart failure (HF) and chronic obstructive pulmonary disease are global epidemics, each affecting in excess of 10 million patients.1,2 Both conditions incur significant morbidity and mortality, and present major challenges to healthcare providers.1 Few reports have addressed this often ignored combination, and fewer still the simple questions of interest to physicians. What are the pitfalls of diagnosing HF in patients with chronic obstructive pulmonary disease, and vice versa? How frequent a comorbidity is chronic obstructive pulmonary disease? What are the clinical consequences of both conditions co-existing? Here, we examine the diagnostic problems posed by the two conditions, before reviewing the prevalence and prognostic implications of chronic obstructive pulmonary disease in patients with HF.


   Problems diagnosing heart failure in patients with chronic obstructive pulmonary disease
Top
 Abstract
 Introduction
 Problems diagnosing heart...
Problems diagnosing heart...
 Problems diagnosing chronic...
 Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
 Conclusions
 Funding
 Appendix
 References
 
Clinical features
Heart failure is a complex syndrome without a simple objective definition. Diagnosis requires both typical clinical features and objective evidence of cardiac dysfunction.2 Pulmonary disease may produce or obscure every symptom and sign defined by Framingham criteria.3 Exertional breathlessness, nocturnal cough, and paroxysmal nocturnal dyspnoea are common to both conditions. No qualitative features of dyspnoea are unique to HF.4 Stigmata of right ventricular failure may also be misleading, including jugular venous distention, ankle oedema, and hepatomegaly. Lung hyperinflation with hepatic displacement mimics the latter, while hindering palpation of cardiomegaly and auscultation of rales or a third heart sound. The difficulty in differentiating between HF and chronic obstructive pulmonary disease symptoms and signs is illustrated in a single cohort study comparing the Framingham and Cardiovascular Health Study criteria for HF. The prevalence of concurrent chronic obstructive pulmonary disease was twice as great in patients fulfilling only Framingham as opposed to only Cardiovascular Health Study criteria (13% vs. 6%).5

Radiology
Radiological evidence of HF is likewise influenced by the presence of chronic obstructive pulmonary disease.6,7 Chest hyperinflation spuriously reduces the cardiothoracic ratio. Pulmonary vascular remodelling and radiolucent lung fields mask the typical alveolar shadowing of pulmonary oedema.7,8 Asymmetric, regional, and reticular patterns of pulmonary oedema are commonplace in those with concurrent chronic obstructive pulmonary disease.6,7,9 Emphysematous vascular bed loss causes upper lobe venous diversion, mimicking HF.9 Isolated right HF is also said to cause pleural effusions through impaired pleural lymphatic drainage secondary to elevated systemic venous pressure.10 However, in clinical practice pleural effusions are rarely due to right HF alone.11,12

Echocardiography
Transthoracic echocardiography may be impeded by poor acoustic windows caused by the pathological changes associated with chronic obstructive pulmonary disease.13 Inadequate visualization may relate to air trapping. In a recent primary care study, echocardiographic images were unsatisfactory in 10.4% of patients with chronic obstructive pulmonary disease.14 This proportion increases to 35% in patients with severe chronic obstructive pulmonary disease,15 and 50% in those with very severe airflow obstruction.16 Although studies have assessed contrast echocardiography in patients with poor endocardial definition, those with pulmonary disease were often excluded.17,18 In lung transplant candidates, Doppler estimation of pulmonary artery pressure was less frequently possible in patients with a residual volume exceeding 150% predicted (40% vs. 56%, P = 0.007).19 Studies would be welcome comparing the accuracy of left ventricular ejection fraction (LVEF) measured by contrast echocardiography against cardiac magnetic resonance imaging (CMR) in patients with chronic obstructive pulmonary disease.

Cardiac magnetic resonance imaging
Cardiac magnetic resonance imaging is the accepted reference standard for measuring LV volumes and ejection fraction.20 Results are accurate, reproducible, and extensively validated.20,21 The CMR allows precise quantification of RV volumes, function, and transvalvular flow, while avoiding ionizing radiation.22 Tissue characterization additionally identifies myocardial fibrosis that may predict risk of arrhythmias.23 Professional imaging societies recommend CMR to evaluate LV function in HF patients with technically limited echocardiogram images.24

Natriuretic peptides
Both B-type natriuretic peptide (BNP) and N-terminal pro-BNP are useful for excluding HF in subjects with acute dyspnoea.25–27 The diagnostic accuracy of BNP in patients with concurrent chronic obstructive pulmonary disease is less certain. Subgroup analysis of 417 patients with chronic obstructive pulmonary disease or asthma in the Breathing Not Properly study reported a mean BNP for those with and without HF of 587 ± 426 and 109 ± 221 pg/mL, respectively (P < 0.0001).28 In a Californian study of 321 patients presenting with acute dyspnoea, mean BNP was significantly higher in patients with HF compared with those with chronic obstructive pulmonary disease (759 ± 798 vs. 54 ± 71 pg/mL, P < 0.001).29 Both studies have two major limitations. First, the diagnosis of HF was adjudicated retrospectively by two cardiologists based on clinical criteria and subsequent investigations; in the Breathing Not Properly subgroup only 29% of patients had echocardiography.28 Secondly, right HF from cor pulmonale was possibly misdiagnosed or even specifically classified as HF.29 This falsely magnifies the apparent accuracy of BNP while neglecting the question of interest to clinicians, for whom diagnosing HF due to left ventricular dysfunction is paramount in guiding future therapy.

Plasma BNP is elevated in both primary pulmonary hypertension and right HF secondary to chronic respiratory disease.31,32 Levels of BNP correlate with pulmonary artery pressure and independently predict mortality.31,32 However, few studies have assessed BNP specifically in patients with chronic obstructive pulmonary disease.32,34 Only one has examined the ability to identify HF in these patients.35 Four natriuretic peptide assays produced comparable results in 200 stable elderly patients with a clinical diagnosis of chronic obstructive pulmonary disease. Each test excluded HF with reasonable accuracy (all negative predictive values above 0.85). However, the positive predictive value and overall diagnostic accuracy were lower than observed in patients with acute dyspnoea.26,27 The explanation is two-fold. Stable patients exhibit lower BNP levels than those with acute volume overload and raised intracardiac pressures. Secondly, BNP levels are increased in patients with chronic obstructive pulmonary disease.32,35 Both factors lessen the diagnostic accuracy in these patients. The BNP Consensus Panel guidelines state that cor pulmonale is associated with an intermediate elevation of BNP, typically ranging from 100 to 500 pg/mL.25 Levels <100 and >500 pg/mL have high negative and positive predictive values, respectively, for HF. Between these thresholds a Bayesian approach is warranted, using BNP to corroborate the clinical evaluation.


   Problems diagnosing heart failure with preserved ejection fraction in patients with chronic obstructive pulmonary disease
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 Introduction
 Problems diagnosing heart...
 Problems diagnosing heart...
Problems diagnosing chronic...
 Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
 Conclusions
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 Appendix
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Defining and identifying HF with preserved ejection fraction (HF-PEF) is controversial and problematic in any population. These difficulties are magnified in patients with chronic obstructive pulmonary disease. BNP levels are moderately elevated in both HF-PEF and cor pulmonale.36–38 One small study compared 17 patients with chronic obstructive pulmonary disease against 9 patients with HF-PEF, defined by clinical and radiological pulmonary oedema responding to treatment, sinus rhythm, and preserved LV ejection fraction. BNP levels were significantly higher in those with HF-PEF (224 vs. 14 pg/mL, P < 0.0001).34 However, BNP was <100 pg/ml in four of the nine patients with HF-PEF, while few patients with chronic obstructive pulmonary disease had significant pulmonary hypertension (mean systolic pulmonary artery pressure was 36 mmHg). More robust studies are required to determine the diagnostic accuracy of BNP for HF in patients with chronic obstructive pulmonary disease and varying levels of pulmonary hypertension.


   Problems diagnosing chronic obstructive pulmonary disease in patients with heart failure
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 Problems diagnosing heart...
 Problems diagnosing heart...
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Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
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Patients with HF exhibit both obstructive and restrictive ventilatory defects, which may compound or conceal the characteristic airflow limitation of chronic obstructive pulmonary disease. Spirometry defines three standard indices: forced expiratory volume in 1 s (FEV1); forced vital capacity (FVC), the total volume delivered during forced expiration from a maximum inspiration; FEV1/FVC ratio, the proportion of the total volume expired in the first second.39 Obstruction is defined by a reduced FEV1/FVC ratio of <70% in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) and American Thoracic Society/European Respiratory Society guidelines.1,40 Restriction is characterized by reduced lung volumes. Both FEV1 and FVC are decreased with a normal or raised FEV1/FVC ratio. Since this pattern also occurs in severe obstruction with air trapping, the diagnosis of restriction additionally requires detection of reduced total lung capacity by plethysmography.39

Obstructive pulmonary function tests
Airflow obstruction is common in patients with decompensated HF,41,42 contrasting with restrictive defects when HF is stable. Interstitial and alveolar oedema cause compression and obstruction of the airways, compounded by bronchial hyperresponsiveness.43,44 Both misdiagnosis and overestimation of chronic obstructive pulmonary disease severity may result. With diuresis, mean FEV1 improves by up to 35% and often returns to normal.41,42 Pulmonary function tests are therefore most informative when patients are clinically euvolaemic.

A mild obstructive ventilatory pattern may be observed even when not fluid overloaded. A comparison dichotomising patients around a peak oxygen consumption of 14 mL/min/kg noted a lower FEV1/FVC ratio in severe HF (70% vs. 75%, P = 0.008).45 The ratio also declines with age in the general population, reaching 70% in those over 75 years of age.46 Chronic obstructive pulmonary disease may thus be over diagnosed in elderly patients with HF.47

Restrictive pulmonary function tests
Restrictive ventilatory defects predominate in patients with stable HF.48 FEV1 and FVC were normal or proportionately reduced in a multicentre study of 130 patients.49 Contributory factors include interstitial fibrosis,50 respiratory muscle weakness,45,51,52 cardiomegaly, and pulmonary congestion.53 FEV1 and FVC may also be proportionately reduced with a normal ratio in patients with severe chronic obstructive pulmonary disease and gas trapping. Usually in such cases increased total lung capacity and residual volume help diagnose obstruction.39 However, restricted lung volumes mask hyperinflation and thus the diagnosis of chronic obstructive pulmonary disease in patients with concurrent HF.6

Performing spirometry
Objective evidence of airflow obstruction is mandatory for diagnosing chronic obstructive pulmonary disease.1 Approximately one-third of patients labelled with chronic obstructive pulmonary disease do not fulfil the GOLD criteria (Table 1).35,54 Despite this, many physicians fail to confirm or refute the clinical diagnosis using spirometry. A recent US study revealed significant disparities in confirmatory testing practices.54 Among 219 patients discharged from a tertiary centre with both HF and chronic obstructive pulmonary disease, 82% received echocardiography as opposed to 36% pulmonary function testing. This lack of adherence to guidelines must be addressed, as both inhaled therapy and beta-blockade are dictated by the degree of airflow obstruction.


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  		Table 1 GOLD classification of chronic obstructive pulmonary disease severity based on post-bronchodilator FEV1

 

   Prevalence of chronic obstructive pulmonary disease in patients with heart failure
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 Introduction
 Problems diagnosing heart...
 Problems diagnosing heart...
 Problems diagnosing chronic...
 Prevalence of chronic...
Prevalence of heart failure...
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 Relationship between chronic...
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Estimates of chronic obstructive pulmonary disease prevalence vary according to the population studied, diagnostic criteria applied, measurement tools, and surveillance systems.55 Geographical variations largely relate to differences in population age structure and risk factor exposure, most notably smoking.1,55 The prevalence of chronic obstructive pulmonary disease was greater in patients with HF than the general population in the Cardiovascular Health Study (20% vs. 13%, P = 0.001).56 This may reflect both clustering of aetiological factors and misdiagnosis. No study has systematically examined pulmonary function in patients with stable HF.57 How many have severe, reversible, or misdiagnosed airflow obstruction is unknown.

The reported prevalence of chronic obstructive pulmonary disease ranges from 11 to 52% in North American patients with HF, and from 9 to 41% in European cohorts (Table 2). Half of the studies originate in the USA. The prevalence of chronic obstructive pulmonary disease is greater in more recent studies (Table 2). Four studies examining trends in HF epidemiology confirm the increasing prevalence.58–61 This may represent greater awareness of chronic obstructive pulmonary disease, an ageing population or increasing age at onset of HF. A consistent non-linear relationship is apparent between age and frequency of concurrent chronic obstructive pulmonary disease in patients with HF.62–65 The prevalence increases until around 75 years of age, and declines thereafter. Possibly the presence of chronic obstructive pulmonary disease reduces survival beyond this age. Alternatively, less intensive investigations in the elderly may under-diagnose comorbidity.


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  		Table 2 Prevalence of chronic obstructive pulmonary disease in patients with heart failure

 
Chronic obstructive pulmonary disease is more common in male compared with female HF patients,65–70 and in urban compared with rural areas.71 The prevalence is notably lower (by 6–11%) in those managed by cardiologists as opposed to general physicians.72–75 Non-cardiac comorbidity is a well recognized barrier to specialty referral.76 Alternatively, cardiologists perhaps fail to recognize airways disease. In patients with preserved ejection fraction the reported prevalence is generally higher (Table 3).77–87 A degree of misdiagnosis undoubtedly exists.88 Finally, remarkably few clinical trials report the presence of chronic obstructive pulmonary disease (Table 4). In these, the lower prevalence of 7–13% in stable outpatients suggests significant recruitment bias.


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  		Table 3 Prevalence of chronic obstructive pulmonary disease in patients with HF and reduced or preserved left ventricular ejection fraction

 


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  		Table 4 Prevalence of chronic obstructive pulmonary disease in heart failure trials

 
Measurement of ejection fraction inherently changes the estimated prevalence. In the Olmsted County study,89 23% of patients with HF had ‘restrictive/chronic obstructive pulmonary disease’. However, the prevalence was lower (15%) among those undergoing echocardiographic assessment. An incorrect diagnosis of chronic obstructive pulmonary disease may be removed once left ventricular systolic dysfunction (LVSD) is confirmed. Additionally, fewer patients with chronic obstructive pulmonary disease are referred for echocardiography. Across 417 Italian centres, chronic obstructive pulmonary disease independently predicted failure to assess LV function during hospitalization (OR 1.25; 95% CI 1.02–1.53).90


   Prevalence of heart failure in patients with chronic obstructive pulmonary disease
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 Introduction
 Problems diagnosing heart...
 Problems diagnosing heart...
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 Prevalence of chronic...
 Prevalence of heart failure...
Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
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Cigarette smoking, the commonest cause of chronic obstructive pulmonary disease, is associated with a 50% increased risk of HF.80,91,92 Two studies have diagnosed HF using standardized criteria in patients with chronic obstructive pulmonary disease.28,93 Both examined the prevalence of unrecognized HF, excluding patients with an existing diagnosis. The prevalence of HF was 20.9% in a highly selected cohort with chronic obstructive pulmonary disease or asthma presenting to the emergency department with acute dyspnoea.28 However, the diagnosis was adjudicated retrospectively by two cardiologists, with echocardiography performed in only 29% of participants. The prevalence of unrecognized HF was the same (20.5%) in a comprehensive community study of 405 elderly patients with stable chronic obstructive pulmonary disease.93 Heart failure was diagnosed by an expert panel following chest radiography, electrocardiography, echocardiography, and pulmonary function tests. Not one patient had echocardiographic evidence of isolated right HF. This corroborates reports estimating the prevalence of cor pulmonale in chronic obstructive pulmonary disease to be ~0.2%.94 There is a simple clinical message. Patients with chronic obstructive pulmonary disease and suspected HF must be considered to have left ventricular dysfunction until proven otherwise.


   Prevalence of left ventricular systolic dysfunction in patients with chronic obstructive pulmonary disease
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A recent systematic review identified 18 reports quantifying LVEF among chronic obstructive pulmonary disease patients, most with small numbers of participants (n = 10–120).57 The prevalence of LVSD varied considerably, ranging from 10 to 46% in unselected patients with stable chronic obstructive pulmonary disease. Studies excluding patients with coronary disease observed a lower prevalence of 0–32%.


   Relationship between chronic obstructive pulmonary disease and heart failure
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Chronic obstructive pulmonary disease is characterized by low-grade systemic inflammation, which may contribute to the progression of atherosclerosis and adverse cardiovascular events.95–97 Myocardial dysfunction may ensue. In the NHANES III survey, moderate to severe airflow obstruction was associated with elevated inflammatory markers and electrocardiographic ischaemia.95 Reduced FEV1 independently predicts cardiovascular mortality in population studies after adjusting for age, cigarette smoking, hypertension, cholesterol, and obesity.98 A meta-analysis demonstrated an increased relative risk of 1.75 (1.54–2.01) when comparing worst and best FEV1 quintiles.99 However, the multivariable models were often limited, notably lacking adjustment for co-existing diabetes and cardiovascular disease.

Inflammation is itself implicated in the pathogenesis of HF. Incidence of HF was greater in Framingham subjects with elevated C-reactive protein and cytokine levels, independent of established risk factors [hazard ratio (HR) 4.07; 95% CI 1.34–12.37; P = 0.01].100 However, two population studies found no evidence of a relationship between chronic obstructive pulmonary disease and incidence of HF. The Cardiovascular Health Study prospectively examined 5888 elderly subjects over a mean of 5.5 years. Elevated C-reactive protein and reduced FEV1, but not a history of chronic obstructive pulmonary disease, were significant factors during stepwise selection of variables in this study.101 Likewise, chronic obstructive pulmonary disease was not an independent predictor of LVSD in the Copenhagen study.102 Both studies relied upon self-reported medical history. Such methods are particularly limited when examining conditions with diagnostic difficulties and overlapping symptoms.


   Prognostic implications of chronic obstructive pulmonary disease in patients with heart failure
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Few studies focused on the prognosis of patients with HF and concomitant chronic obstructive pulmonary disease.70,103 However, chronic obstructive pulmonary disease was consistently an independent predictor of death and HF hospitalization when reported in multivariable models (Table 5). In many models the prognostic significance approached or exceeded that of traditional factors including male gender, diabetes, hypertension, NYHA class, and anaemia. As in all multivariable analyses, the risk relates in part to the number and type of variables adjusted for in the model. Only one study has explored the causes of increased mortality.103 The outcomes of patients with chronic obstructive pulmonary disease enrolled in the Val-HeFT trial were examined using multivariate models including demographic, clinical, biohumoral, and treatment variables. Chronic obstructive pulmonary disease strongly predicted non-cardiovascular mortality (HR 2.50 [1.58–3.96], P < 0.0001) and hospitalizations (HR 1.71 [1.43–2.06], P < 0.0001), but not cardiovascular death or hospitalizations. The relationship between chronic obstructive pulmonary disease and ischaemic or arrhythmic events has never been reported in patients with HF.


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  		Table 5 Prognostic implications of chronic obstructive pulmonary disease in patients with HF

 
The increased risk of HF hospitalization is unsurprising. Respiratory infections are associated with decompensation in 10–16% of admissions.104–109 Concomitant chronic obstructive pulmonary disease prolongs inpatient stay,110,111 increases risk of readmission,112–114 and independently predicts greater financial costs.115 Respiratory disease, and in particular chronic obstructive pulmonary disease, is a more frequently recorded comorbidity in winter.116 The ACC/AHA guidelines advocate influenza and pneumococcal immunization to reduce this risk.117 Administering influenza A vaccine to elderly patients with HF during the 1991–1992 influenza epidemic reduced the rate of HF hospitalization by 37%, and associated costs by 43%.118


   Conclusions
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 Introduction
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 Problems diagnosing heart...
 Problems diagnosing chronic...
 Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
 Conclusions
Funding
 Appendix
 References
 
The combination of HF and chronic obstructive pulmonary disease presents many diagnostic challenges. Clinical symptoms and signs require careful interpretation, in conjunction with objective evidence of each condition. Both are chronic progressive diseases complicated by exacerbations. Physicians must consider the timing of investigations within the disease trajectory. Over time, LVSD may develop, or the severity of airflow obstruction increase. Treatment will alter accordingly. Transthoracic echocardiography is adequate in many patients, while magnetic resonance imaging is the modality of choice in those with limited acoustic windows. Airflow obstruction must be demonstrated when clinically euvolaemic. Inadequate assessment risks both misdiagnosis and inappropriate treatment.

Greater collaboration is required between cardiologists, pulmonologists, and general practitioners. Both conditions are systemic disorders with potentially overlapping pathophysiological processes. The ‘fit’ of even complex multivariable HF models remains imperfect. Part of this undefined risk may arise in the lungs. The impact of chronic obstructive pulmonary disease on cardiovascular outcomes is yet to be fully defined. In the meantime cardiologists and pulmonologists, respectively, must better identify and manage concurrent chronic obstructive pulmonary disease and HF. The resulting symptomatic and prognostic benefits far outweigh those attainable by treating either condition alone.


   Funding
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Appendix
 References
 
Dr Hawkins thanks Heart Research UK for funding clinical research in Stobhill Hospital.

Conflict of interest: none declared.


   Appendix
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 Introduction
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 Problems diagnosing heart...
 Problems diagnosing chronic...
 Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
 Conclusions
 Funding
 Appendix
References
 
The full list of references is available in the online version of this paper.


   References
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 Introduction
 Problems diagnosing heart...
 Problems diagnosing heart...
 Problems diagnosing chronic...
 Prevalence of chronic...
 Prevalence of heart failure...
 Prevalence of left ventricular...
 Relationship between chronic...
 Prognostic implications of...
 Conclusions
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 Appendix
 References
 

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