Heart failure

Definition

    • Condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure

    • It can result from any cardiac disease that compromises ventricular systolic or diastolic function or both

    • The term "congestive heart failure" is reserved for patients with breathlessness and abnormal sodium and water retention resulting in oedema

Risk Factors

    • Strong

      • MI

      • diabetes mellitus

      • dyslipidaemia

      • old age

      • male

      • hypertension

      • left ventricular dysfunction

      • cocaine abuse

      • exposure to cardiotoxic agents

      • history of left ventricular hypertrophy

      • renal insufficiency

      • valvular heart disease

      • sleep apnoea

      • elevated homocysteine

      • elevated tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)

      • elevated C-reactive protein (CRP)

      • decreased insulin-like growth factor-1 (IGF-1)

      • elevated natriuretic peptides

      • dilation of the left ventricle

      • increased left ventricular mass

      • abnormal left ventricular diastolic filling

      • family history of heart failure

    • Weak

      • low socio-economic status

      • tobacco consumption

      • excess alcohol consumption

      • excess sodium intake

      • excess coffee consumption

      • obesity

      • tachycardia

      • depression/stress

      • microalbuminuria

Differential diagnosis

    • Ageing/physical inactivity

Epidemiology

    • The prevalence of CHF in the western world has been estimated at 1% to 2%

    • The incidence is thought to approach 5 to 10 per 1000 people per year. [3]

    • In the UK, CHF is thought to account for a total of 1 million inpatient bed days and 5% of all emergency admissions

    • These figures are projected to rise by as much as 50% in the next 25 years. [4]

    • The number of deaths is increasing steadily despite advances in treatment

      • in part because of increasing numbers of patients with heart failure

      • due to better treatment and reduced mortality of patients with acute MIs earlier in life.

    • The incidence of heart failure approaches 10 per 1000 population after age 65 years

    • Approximately 80% of patients hospitalised are more than 65 years old. [1]

Aetiology

    • There are numerous and varied causes of heart failure:

      • Other cardiovascular disease:

        • coronary artery disease

        • cardiomyopathies

        • hypertension

        • myocarditis

        • valvular heart disease

        • congenital heart diseases

      • Pericardial disease

      • Toxin-induced

        • heroin

        • alcohol

        • cocaine

        • amfetamines

        • lead

        • arsenic

        • cobalt

        • phosphorus

      • Infection

        • bacterial

        • fungal

        • viral (HIV)

        • Borrelia burgdorferi (Lyme disease)

      • Infiltrative diseases

        • amyloidosis

        • haemochromatosis

        • sarcoid

      • Electrolyte imbalance

        • hypocalcaemia

        • hypophosphataemia

        • hypokalaemia

        • hyponatraemia

      • Endocrine disorders

        • diabetes mellitus

        • thyroid disease

        • hypoparathyroidism with hypocalcaemia

        • phaeochromocytoma

        • acromegaly

      • Systemic collagen vascular diseases

        • lupus

        • rheumatoid arthritis

        • systemic sclerosis

        • polyarteritis nodosa

        • hypersensitivity vasculitis

        • Takayasu syndrome

        • polymyositis

        • Reiter's syndrome

      • Drug-induced

        • adriamycin

        • cyclophosphamide

        • sulphonamides

        • some antiviral agents

      • Nutritional deficiencies

        • thiamine

        • protein

        • selenium

        • L-carnitine

      • Pregnancy

        • peripartum cardiomyopathy.

    • These conditions tend to increase metabolic demand

      • May or may not be matched by a sufficient increase in cardiac output by the failing heart

    • Tachyarrhythmias also decrease the diastolic ventricular filling time and increase myocardial oxygen demand

    • Uncontrolled hypertension depresses systolic function

      • Increases the afterload against which the failing ventricle must pump blood

      • May be the first clinical manifestation.

    • Many of these causes may be completely reversible given appropriate and timely treatment/intervention

    • Some causes, such as scarred myocardium or dilated cardiomyopathy, are currently considered irreversible

Clinical features

    • Key diagnostic factors

      • presence of risk factors (common)

      • dyspnoea (common)

      • neck vein distension (common)

      • S3 gallop (common)

      • cardiomegaly (common)

      • hepatojugular reflux (common)

      • rales (common)

      • orthopnoea and paroxysmal nocturnal dyspnoea (uncommon)

      • nocturia (uncommon)

    • Other diagnostic factors

      • tachycardia (HR >120 bpm) (common)

      • chest discomfort (common)

      • hepatomegaly (common)

      • ankle oedema (common)

      • night cough (common)

      • pleural effusion (common)

      • fatigue, muscle weakness or tiredness (common)

      • palpitations, pre-syncope, or syncope (uncommon)

      • lethargy/confusion (uncommon)

Pathophysiology

    • Heart failure represents a complex syndrome

    • An initial myocardial insult results in the over-expression of multiple peptides

      • With different short- and long-term effects on the cardiovascular system

    • Neurohormonal activation is recognised to play a pivotal role in the development as well as the progression of heart failure

      • In the acute phase, neurohormonal activation seems to be beneficial

        • Maintains adequate cardiac output and peripheral perfusion

      • Sustained neurohormonal activation, however, is deleterious

        • Results in increased wall stress, dilation, and ventricular remodelling

        • Contribute to disease progression in the failing myocardium

        • Eventually leads to further neurohormonal activation.

    • Remodelling occurs in several clinical conditions, including MI, cardiomyopathy, hypertension, and valvular heart disease

      • Hallmarks include hypertrophy, loss of myocytes, and increased interstitial fibrosis.

    • One potential deleterious outcome of remodelling is the development of mitral regurgitation

      • As the left ventricle dilates and the heart assumes a more globular shape

    • Mitral regurgitation results in an increasing volume overload on the overburdened left ventricle

      • Further contributes to remodelling and progression of disease and symptoms

Investigations

    • transthoracic echocardiogram

      • systolic heart failure

        • depressed and dilated left and/or right ventricle with low ejection fraction

      • diastolic heart failure

        • left ventricular ejection fraction (LVEF) normal

        • but left ventricular hypertrophy (LVH) and abnormal diastolic filling patterns

    • ECG

      • evidence of underlying CAD, LVH, or atrial enlargement

      • may be conduction abnormalities and abnormal QRS duration

    • CXR

      • abnormal

    • FBC

      • Anaemia and high lymphocyte percentage are strong risk factors and prognostic markers of poor survival

      • laboratory testing may reveal important heart failure aetiologies

        • presence of disorders or conditions that can lead to or exacerbate heart failure

      • laboratory testing could also reveal important modulators of therapy

    • serum electrolytes (including calcium and magnesium)

      • decreased sodium (usually <135 millimols/L)

      • altered potassium

      • Important to record baseline values

    • serum creatinine, blood urea nitrogen

      • Reflects tissue perfusion, fluid status, rules out renal disease

      • normal to elevated

    • blood glucose

      • elevated in diabetes

    • LFT

      • normal to elevated

    • TFTs (especially TSH)

      • hypothyroidism: elevated TSH, decreased FT3, decreased FT4

      • hyperthyroidism: decreased TSH, elevated FT3, elevated FT4

    • blood lipids

      • elevated in dyslipidaemia

      • decreased in end-stage heart failure, especially in the presence of cardiac cachexia

    • B-type natriuretic peptide (BNP)/N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels

      • elevated

    • standard exercise stress testing (bicycle or treadmill)

      • reduced exercise capacity in idiopathic dilated cardiomyopathy

      • reduced exercise capacity and signs of impaired myocardial perfusion in ischaemic cardiomyopathy

    • cardiopulmonary exercise testing (CPX) with VO2max

      • reduced VO2max

    • 6-minute walking test exercise

      • as an alternative to CPX it may provide an objective assessment of the patient's functional status

    • right heart catheterisation

      • provides objective haemodynamic assessment of left ventricular filling pressure

      • gives direct measures of cardiac output and pulmonary and systemic resistance

    • endomyocardial biopsy

      • rarely necessary to establish the aetiology of heart failure

      • provides definitive pathological evidence of cardiac and systemic disease

Management

a) conservative

    • Dietary sodium intake

      • Easily modifiable factor that complements pharmacological therapy for heart failure.

      • Patient and family are advised to follow a daily dietary sodium intake between 2 and 3 g.

      • Further restriction to 1 to 2 g/day may be necessary for patients with advanced symptoms refractory to therapy.

    • Fluid restriction

      • Mostly used as an in-hospital complimentary measure in cases of acute exacerbations

      • In addition, fluid restriction may be warranted in cases of severe hyponatraemia.

      • However, it would be of importance to advise the patient to keep a daily intake/output balance at home.

      • Patients are advised to monitor their weight daily

    • Heart failure patients need continuous and close monitoring of their health

      • A variety of programmes have been shown to decrease morbidity and rehospitalisation in this context

      • Home nursing, telephone advice/triage, telemedicine services, and specialised heart failure clinic-based care. [131]

    • Exercise training

b) medical

    • ACE inhibitors

      • Shown to decrease the morbidity and mortality associated with heart failure, [1] [88] [89] [A Evidence]

      • Should be given to all patients with left venticular (LV) dysfunction, symptomatic or otherwise

        • Unless there is a contra-indication or prior intolerance to therapy.

      • Should be used with caution in patients in cardiogenic shock, with marginal renal output or hyperkalaemia.

      • If patients have an idiosyncratic reaction, with angio-oedema, ACE inhibitors should not be rechallenged.

    • Beta-blockers

      • All patients with chronic heart failure receive a beta-blocker once established on an ACE inhibitor

        • Unless there is a contra-indication

      • Carvedilol seems superior to metoprolol, [132] although there is no evidence of superiority to other beta-blockers.

    • Aldosterone antagonists

      • Decrease the morbidity and mortality associated with symptomatic chronic heart failure

      • Should be used in early post-MI patients with LV dysfunction and/or moderate-to-severe heart failure (NYHA III or IV). [1]

      • Should be initiated after titration of standard medical therapy.

      • Spironolactone[B Evidence] and eplerenone[A Evidence] can both cause hyperkalaemia

        • Precautions should be taken to minimise the risk.

      • These agents should be used with caution in patients with renal dysfunction and hyperkalaemia.

    • Hydralazine + isosorbide dinitrate

      • Reasonable for patients with reduced left ventricular ejection fraction (LVEF) who are already taking an ACE inhibitor and beta-blocker for symptomatic heart failure and who have persistent symptoms (class IIa), [1]

      • Has demonstrated benefit in black patients with heart failure. [99] [100]

      • May decrease symptoms of dyspnoea at night and during exercise

      • May improve exercise tolerance in patients who have persistent limitations despite optimisation of other therapies. [133] [134]

      • Development of nitrate tolerance seems to be minimised by prescription of a nitrate-free interval of at least 10 hours. [1]

      • Carvedilol use has been shown to prevent nitrate tolerance in patients with CHF. [135] [136]

    • Diuretics

      • Produce symptomatic benefits more rapidly than any other drug for heart failure.

      • Can relieve pulmonary and peripheral oedema within hours or days.

      • Few patients with heart failure and fluid retention can maintain sodium balance without the use of diuretic drugs. [139]

      • Diuretics alone are unable to maintain the clinical stability of patients with heart failure for long periods of time, [139]

      • Risk of clinical decompensation can be reduced when they are combined with an ACE inhibitor and a beta-blocker. [140]

    • Digoxin

      • Can be beneficial in patients with current or prior symptoms of heart failure or reduced left ventricular ejection fraction (LVEF)

        • Especially those with atrial fibrillation.

c) surgical

    • Cardiac transplantation

Prognosis

    • All existing models to predict the risk of death or need for urgent transplantation have features that may limit their applicability.

    • Haemoglobin A1c was also found to be an independent progressive risk factor for cardiovascular death, hospitalisation, and mortality, even in non-diabetic patients. [187]

    • The most comprehensive prognostic model is the Seattle Heart Failure Model. [The Seattle Heart Failure Model] (external link)

      • Has been implemented as an interactive programme that employs the Seattle Heart Failure Score to estimate mean, 1-, 2-, and 5-year survival and the benefit of adding medicines and/or devices for an individual patient. [181]

    • Despite standard medical therapy, a patient with persistent NYHA class IV symptoms still has an annual mortality risk of 40% to 60%, compared with 5% to 10% for NYHA I or II patients. [1]