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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
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
    • 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]
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