Identifying patients with heart failure in primary care

Heart failure can be defined as an abnormality of the structure or function of the heart that leads to a failure of the heart to deliver sufficient oxygen to the metabolising tissues (or when the heart can only do so with elevated diastolic filling pressures).¹ Compensatory mechanisms, e.g. an increase in heart rate, cardiac muscle mass, cardiac filling pressures and blood volume, work to maintain the ability of the heart to pump effectively, however, over time the heart progressively fails.

Heart failure can be regarded as a complex clinical syndrome with typical symptoms and signs that develops as a result of a large number of diverse cardiac and non-cardiac abnormalities.¹⁴ There are multiple risk factors for heart failure, which include:^{5, 14, 15}

• Coronary heart disease – ischaemic heart disease (IHD)leading primarily to left ventricular dysfunction; the most significant risk factor for heart failure in developed countries
• Hypertension – 75% of patients with heart failure have a history of hypertension16
• Valvular heart disease, including valvular damage from rheumatic fever
• Abnormalities of rhythm (e.g. atrial fibrillation) or conduction (e.g. left bundle branch block)
• Cardiomyopathy, e.g. idiopathic, viral, alcoholic, toxic, peripartum
• Diabetes – independent risk factor for coronary heart disease but also increases the risk of heart failure directly
• Male gender
• Excessive alcohol use – increasing cardiovascular risk and as a direct cardiotoxin
• Smoking – increasing cardiovascular risk and as a direct cardiotoxin
• Obesity – increasing cardiovascular risk and an independent risk factor
• Dyslipidaemia
• Respiratory conditions, e.g. COPD, obstructive sleep apnoea
• Thyroid disorders – both hypo- and hyperthyroidism
• Medicines e.g. NSAIDs, pioglitazone (see Box below)
• Cardiotoxins e.g. chemotherapy medicines, cocaine
• Infections or inflammation – leading to myocarditis or cardiomyopathy
• Congenital heart disease

Heart failure with reduced or preserved ejection fraction

Heart failure has, in the past, been predominately thought of in terms of systolic dysfunction of the left ventricle, i.e. a reduction in left ventricular ejection fraction. Clinical trials, however, have found that left ventricular failure can develop in patients who have an essentially normal ejection fraction and that this is a separate clinical syndrome.¹⁷ This has led to the adoption of the terms heart failure with reduced ejection fraction (HF-REF, previously referred to as systolic heart failure) and heart failure with preserved ejection fraction (HF-PEF, previously referred to as diastolic heart failure). Although, the terms systolic and diastolic heart failure remain in use in the literature there is now a preference for the terms HF-REF and HF-PEF.^1,17 Up to 50% of people with symptoms and signs of heart failure have been shown to have preserved or relatively preserved (≥45 – 50%) left ventricular ejection fraction.^{8, 17} The underlying causative conditions and the treatment of each type of heart failure differ.

Heart failure with reduced ejection fraction (HF-REF) – i.e. impaired left ventricular systolic function, is typically seen in patients with structural heart disease, e.g. ischaemic heart disease.¹⁷ Many other causative factors may contribute to HF-REF, including hypertension, diabetes and idiopathic dilated cardiomyopathy.¹

The majority of research into effective, evidence-based treatment strategies for heart failure has been based on patients who have HF-REF.

Heart failure with preserved ejection fraction (HF-PEF) – i.e. impaired diastolic function (such as impaired diastolic relaxation and filling due to stiffening of the ventricles) is more frequently seen in older people, females and people who are obese. People with HF-PEF are also more likely to have atrial fibrillation and to be more hypertensive.^{8, 17} In addition, other underlying causes include constrictive pericarditis or cardiomyopathy, hypertrophic cardiomyopathy and restrictive cardiomyopathy, e.g. from amyloidosis or sarcoidosis.

Symptoms and signs of heart failure

Patients with heart failure present with a variable combination of symptoms and signs (Table 1, over page), each of which influence the level of clinical suspicion and help guide the investigations and initial management. Patients may present (either as a first presentation or with a known history of heart failure) with a sudden onset of acute symptoms consistent with heart failure or have symptoms that have developed more gradually.

Symptoms typically include dyspnoea, orthopnoea, fatigue, reduced exercise tolerance and ankle oedema, however, many of the symptoms are not necessarily specific to heart failure and vary with the acuteness of the condition.³ The significance of symptoms and signs may be more difficult to interpret in people who are older, obese or those with co-morbidities such as chronic obstructive pulmonary disease (COPD).

Peripheral oedema is a non-specific symptom that may be seen frequently but can be due to other reasons such as varicose veins, medicines (e.g. calcium channel blockers) or decreased mobility. Crepitations in the chest on auscultation are also a non-specific sign and may confound the presentation, especially if the patient has an existing respiratory condition. The presence of orthopnoea and paroxysmal nocturnal dyspnoea are more specific symptoms of heart failure but are less often reported at presentation and tend to be associated with more severe heart failure.¹ Clinical signs that are more specific to heart failure, e.g. increased jugular venous pressure and displacement of the apex beat, can be difficult signs to detect accurately.¹ These factors, therefore, can make a clinical diagnosis of heart failure difficult, particularly in a primary care setting.

Echocardiography is the gold standard investigation

Depending on the findings from history and examination, a number of investigations may be required in a patient with suspected heart failure (Table 2). Some tests may support or rule out a clinical suspicion, other investigations are required for identification of a reversible cause, e.g. thyroid dysfunction, and for ongoing monitoring of the patient’s progress and medicine use.

Ideally all patients with suspected heart failure require echocardiography for an accurate diagnosis to be made. Referring every patient with suspected heart failure, however, is likely to be impractical, given resource limitations. To help identify which symptomatic patients require echocardiography, use the results from an ECG and brain natriuretic peptide (BNP) test – patients with either an abnormal ECG or an increased BNP level are likely to have heart failure and require referral for echocardiography.¹ Guidance from NICE suggests that the timeframe required for further assessment with echocardiogram is within two weeks if the patient has a history of a previous myocardial infarction (MI) and an elevated BNP, and within six weeks if there is no history of MI and a moderately raised BNP.⁷

The role of BNP in the diagnosis of heart failure

Laboratory assessment of BNP or N-terminal pro-BNP (NT-proBNP), depending on the laboratory, may provide additional information for some patients, where the diagnosis is uncertain. If BNP is normal (< 30 pmol/L), a diagnosis of heart failure is unlikely.²⁰ The cut-off values in patients presenting with a more gradual onset of symptoms may be lower.¹ Laboratories around New Zealand differ in their recommendations for cut-off values for using BNP or NT ProBNP for diagnosing heart failure, therefore it is best to check with your local laboratory or discuss the results with a clinical biochemist. (Table 3) gives an example of cut-off values.

Table 2: Investigations for diagnosis and monitoring of patients with heart failure¹

* Depending on the laboratory, BNP or N-terminal pro-BNP (NT-proBNP) may be measured. The normal ranges for each test are different (although provide similar information) and may also vary between laboratories. BNP can be affected by factors such as age, gender, obesity and renal impairment.

Table 3: Suggested cut-off values for BNP in the diagnosis of heart failure²⁰

Notes:
For indeterminate values, e.g. BNP > 30 pmol/L but < 145 pmol/L, clinical assessment is the key factor for interpretation
To covert BNP from pmol/L to pg/mL, multiply by 3.47
To convert NT-ProBNP from pmol/L to pg/mL, multiply by 8.46

Differential diagnosis of heart failure

• Non-cardiac causes of dyspnoea such as respiratory infections, COPD, pulmonary embolism, adult respiratory distress syndrome
• Other cardiac causes such as myocardial ischaemia, atrial fibrillation, pericardial disease

People with heart failure can be classified into functional groups depending on the amount of exertion needed to bring on symptoms such as dyspnoea, fatigue and palpitations (Table 4).

A functional assessment can be useful in people with an established diagnosis of heart failure but it is not disease-specific and does not help make a formal diagnosis. Although this type of functional classification is often used to select patients for clinical trials, it does not group patients in terms of the cause of the heart failure or take into account any underlying abnormalities of the heart that may contribute to heart failure. Its value in primary care is that the classes (as they increase) are associated with a worsening prognosis. Patients, however, may move between classes, e.g. they may present acutely unwell (Class IV) but after treatment become asymptomatic (Class I), or a stable patient with mild symptoms (Class II) may have a sudden onset of dyspnoea at rest due to arrhythmia (Class IV).^{1, 2, 21}

This form of classification for heart failure is also subject to other limitations such as variability between clinicians in detecting clinical signs and interpretation of terms such as “ordinary”, “slight” and “marked”.

Table 4: New York Heart Association functional classification of heart failure^{1, 3}