Approach

Heart failure is primarily a condition of older people and has a higher prevalence in men at all ages.[4][8][79]

Identification of the condition responsible for the cardiac structural and/or functional abnormalities may be important, because some conditions that lead to left ventricular dysfunction are potentially treatable and/or reversible.[2] Efforts to identify a cause frequently allow the detection of co-existent conditions that may contribute to or exacerbate the severity of symptoms. However, it may not be possible to discern the cause of heart failure in many patients presenting with this syndrome, and in others, the underlying condition may not be amenable to treatment.

A number of precipitating factors may lead to impaired cardiac function, potentially leading to an episode of acute heart failure. Detection and treatment of precipitating factors plays an important role in patient management. Precipitating factors include excessive salt intake, lack of adherence (with respect to medication and diet), myocardial infarction, pulmonary embolism, uncontrolled hypertension, cardiac arrhythmias, infection, hypothyroidism, hyperthyroidism, renal dysfunction, and alcohol and drug abuse.[1]

Patient history

The complexity and variety of potential causative factors means that a multitude of patient historical factors may be relevant. A history of hypertension; diabetes mellitus; dyslipidaemia; tobacco use; coronary, valvular, or peripheral vascular disease; rheumatic fever; heart murmur or congenital heart disease; personal or family history of myopathy; mediastinal irradiation; and sleep-disturbed breathing should be enquired about. The drug history should record the past or current use of illicit drugs; alcohol; ephedra; or antineoplastic agents such as anthracyclines, trastuzumab, or high-dose cyclophosphamide, because heart failure may occur years after exposure to doxorubicin or cyclophosphamide. The history and physical evaluation should include specific consideration of non-cardiac diseases such as collagen vascular disease, bacterial or parasitic infection, obesity, thyroid excess or deficiency, amyloidosis, and phaeochromocytoma.

A detailed family history should be obtained, not only to determine whether there is a familial pre-disposition to atherosclerotic disease but also to identify relatives with cardiomyopathy, sudden unexplained death, conduction system disease, and skeletal myopathies.

Dyspnoea on exertion or at rest is the most common symptom of left-sided heart failure. With increasing failure patient may develop leg oedema and abdominal distension due to ascites.

Physical examination

Particular attention should be paid to the cardinal signs of heart failure. Their presence (and degree) may depend on severity of heart failure and associated comorbid disease.

General examination may reveal tachycardia and cyanosis. A focused cardiovascular examination may reveal elevated jugular venous pressure, ankle oedema, and a displaced apex beat, which suggests cardiomegaly. On auscultation, besides presence of pulmonary rales or crepitation, an S3 gallop may be present, which has prognostic significance.

Clinical manifestations of the underlying aetiology of heart failure may be present, for example, macroglossia and neuropathy may point to infiltrative cardiomyopathy like amyloidosis; pallor (which may reflect anaemia); irregularly irregular pulse (reflecting atrial fibrillation); systolic murmur of aortic stenosis and mid diastolic murmur of mitral stenosis; or overt signs of thyrotoxicosis. In patients on dialysis, a large arteriovenous fistula may occasionally be the precipitating factor. However, further discussion of the clinical features of aetiologic(al) pathways is beyond the scope of this topic.

Investigations

For all patients, initial investigations should include ECG, chest x-ray, transthoracic echocardiogram, and baseline haematology and blood chemistry, including full blood count, serum electrolytes (including calcium and magnesium), serum urea and creatinine, liver function tests, and B-type natriuretic peptide/N-terminal pro-brain natriuretic peptide levels. Anaemia and high lymphocyte percentage are strong risk factors and prognostic markers of poor survival. In patients presenting with dyspnoea, measurement of natriuretic peptide biomarkers is useful to support a diagnosis or exclude heart failure. However, elevated plasma levels of natriuretic peptides can occur with a wide variety of cardiac and non-cardiac causes; therefore, clinical judgement is necessary.[80]

Blood glucose, thyroid function tests and blood lipids are useful to assess for commonly associated comorbid disease.

Subsequent investigations that help in assessing severity of heart failure and functional status include non-invasive stress imaging (cardiovascular MRI, stress echocardiogram, SPECT, PET), standard exercise stress testing (bicycle or treadmill), coronary angiogram, cardiac CT angiography, cardiopulmonary exercise testing with VO₂ max, 6-minute walking test exercise, left and right heart catheterisation, and endomyocardial biopsy. Troponin measurement is helpful in further risk stratification in chronic heart failure, as an elevated level is associated with progressive left ventricular dysfunction and increased mortality.[2][81] Soluble ST2 and galectin-3 (biomarkers for myocardial fibrosis) are predictive of death and hospitalisation in patients with heart failure and are additive to natriuretic peptide in their prognostic value.[2]

Based on clinical history, HIV screening and measurement of iron levels and fasting transferrin saturation to screen for haemochromatosis may also be performed. A cardiac MRI scan is particularly useful in the investigation of myocarditis and infiltrative cardiomyopathy. Multi-slice CT (MSCT) can be used for left ventricular ejection fraction (LVEF) estimation. There appears to be no significant difference in LVEF estimation between MSCT and MRI, and also between MSCT and transthoracic echocardiogram.[82]

MSCT may offer additional benefit as it provides a combined evaluation of LVEF and coronary artery disease.


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