Heart Failure Flashcards
HF DEFINITION - ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2021
Heart failure is not a single pathological diagnosis, but a clinical syndrome consisting of cardinal symptoms (e.g. breathlessness, ankle swelling, and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles, and peripheral oedema). It is due to a structural and/or functional abnormality of the heart that results in elevated intracardiac pressures and/or inadequate cardiac output at rest and/or during exercise.
What is Heart Failure?
Collection of signs and symptoms
Inability of the heart to pump blood to meet metabolic demand (rather than the heart no longer working).
Body depends on the heart’s pumping action to deliver oxygen- and nutrient-rich blood to the body’s cells.
Normal body function: when the cells are nourished properly.
With heart failure, compromised cardiac function can’t supply the metabolising tissues with enough blood.
This results in signs and symptoms of HF.
Heart failure is a chronic, progressive condition, and usually there’s no cure.
But with changes, people with heart failure can lead normal lives.
Changes:
– Heart failure medications
– Lifestyle changes
– Implantable cardiac devices
Causes of HF
Ischaemic heart disease and MI - COMMON
Hypertension - COMMON
Valvular heart disease
Familial cardiomyopathy or genetic heart disease (Dilated/hypertrophic/obstructive/restrictive/obliterative)
Endocrine or metabolic (thyroid, diabetes, obesity)
Chemotherapy and other cardiotoxic drugs
Rheumatic/autoimmune
Heart rhythm related (tachy-mediated, PVCs, RV pacing)
Myocarditis (infectious, toxin/medication, immunological)
Peripartum cardiomyopathy
Substance abuse
Alcohol
Left-sided heart failure
Categorised into the following:
Systolic Failure - Heart failure with reduced ejection fraction (HFrEF) – 50% of patients
– LV unable to contract normally.
– The heart can’t pump with enough force to push enough blood into circulation.
Diastolic Failure - Heart failure with preserved ejection fraction (HFpEF)
– LV loses its ability to relax normally (because the muscle has become stiff).
– The heart can’t properly fill with blood during diastole.
Right-sided heart failure
Usually occurs as a result of left-sided failure.
When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart’s right side.
When the right side loses pumping power, blood backs up in the body’s veins, causing swelling/congestion in the legs, ankles and abdomen such as the GI tract and liver.
The heart tries to compensate by:
Enlarging. The heart stretches to contract more strongly and keep up with the demand to pump more blood. Over time this causes the heart to become enlarged.
Developing more muscle mass – due to contracting myocardial cells increasing in size. This enables the heart to pump more strongly, at least initially.
Pumping faster. This helps to increase cardiac output.
The body also tries to compensate in other ways:
Blood vessels narrow to keep BP up, trying to make up for the heart’s loss of power.
The body diverts blood away from less important tissues and organs (e.g. kidneys), and towards the heart and brain.
Mortality is significantly better for those who have access to specialist care i.e. those seen by cardiologists or specialist heart failure services (23 per cent).
Incidence and cost
Global pandemic - 26 million worldwide.
Around 920,600 people in the UK today have been diagnosed with heart failure (1.6% population; Bellanca et al., 2023).
Symptomatic and non-symptomatic HF evident in 4% of population.
The incidence of heart failure increases steeply with age, and the average age at diagnosis is 77.
Prevalence in 70-80 yr olds between 10 and 20%.
Overall prevalence increasing due to ageing population.
Average length of hospital stay for HF: 13 days
1 in 7 heart failure patients die in hospital or in the month following discharge.
Within a year of admission, 32% of patients die.
Cost per hospital admission: £3,796.
Heart Failure accounts for:
2% of the total NHS budget (70% of these costs due to hospitalisation, 10% due to medications)
1 million patient bed days per annum.
5% of all emergency admissions (commonest cause of admission in people > 65yrs).
Stages of HF
Stages Definition and Criteria - AHA, 2022 guidelines
Stage A: At Risk for HF At risk for HF but without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury (eg, patients with hypertension, atherosclerotic CVD, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy).
Stage B: Pre-HF No symptoms or signs of HF and evidence of 1 of the following:
Structural heart disease*
- Reduced left or right ventricular systolic function
- Reduced ejection fraction, reduced strain
- Ventricular hypertrophy
- Chamber enlargement
- Wall motion abnormalities
- Valvular heart disease
Evidence for increased filling pressures*
- By invasive hemodynamic measurements
- By noninvasive imaging suggesting elevated filling pressures (eg, Doppler echocardiography)
Patients with risk factors and
- Increased levels of BNPs* or
- Persistently elevated cardiac troponin in the absence of competing diagnoses resulting in such biomarker elevations such as acute coronary syndrome, CKD, pulmonary embolus, or myopericarditis
Stage C: Symptomatic HF Structural heart disease with current or previous symptoms of HF.
Stage D: Advanced HF Marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize GDMT.
Diagnostic tests
Medical history and physical examination.
12-lead ECG – LVH, LBBB, LAE, AF, sinus tachy.
Echocardiogram
Laboratory tests – BNP (protein indicates myocyte stretch)
Chest X-ray – normal size/slightly enlarged, calcified aortic valve, pulmonary congestion.
What is BNP?
The main stimulus for BNP synthesis and secretion is myocyte stretch and levels are elevated in HF and other conditions such as atrial flutter/fibrillation.
These peptides regulate the circulation. They dilate blood vessels. They also work on the kidneys, causing them to excrete more salt and water. In addition, they reduce the production of hormones that narrow blood vessels, boost the heart rate, or affect fluid retention; examples includeadrenaline, angiotensin,andaldosterone.
Diagnosis of HF (ACC)
- Diagnostic algorithm for patients with suspected HF
Assessment: Clinical hx, Physical Examination, ECG, labs
-> Natriuretic Peptide: NT-proBNP >125pg/mL / BNP > 35pg/mL
–> TTE (indicated with assessment/ assessment and)
-> HF diagnosis confirmed: determine cause and classify
-> HFrEF: LVEF less/equal to 40%
HFmrEF: 41%-49%
HFpEF: LVEF greater than or more than 50%
-> Evaluate for precipitating factors and initiate treatment
Diagnosis of HF (NICE)
Chronic HF suspected -> Take a detailed hx and perform a clinical examination -> measure NT-pro BNP and perform ECG, consider chest X-Ray, blood tests, urinalysis, peak flow or spirometry.
-> NT-proBNP >2,000 ng/l (235 pmol/l) -> refer urgently to be be seen within 2 weeks
-> NT-proBNP 400-2,000ng/l (47-236 pmol/l) -> refer urgently to be seen within 6 weeks
-> specialist clinical assessment including transthoracic echocardiography
-> HF confirmed; assess severity, establish aetiology and identify correctable causes
-> NT-proBNP <400ng/l (47pmol/l) -> HF not confirmed; consider other causes of symptoms with specialist input if concern persists
Diagnosis of HF ESC guidelines
Electrocardiogram (ECG). A normal ECG makes the diagnosis of HF unlikely.63 The ECG may reveal abnormalities such as AF, Q waves, LV hypertrophy (LVH), and a widened QRS complex (Table 7) that increase the likelihood of a diagnosis of HF and also may guide therapy.
Measurement of NPs are recommended, if available. A plasma concentration of B-type natriuretic peptide (BNP) <35 pg/mL, N-terminal pro-B-type natriuretic peptide (NT-proBNP) <125 pg/mL, or mid-regional pro-atrial natriuretic peptide (MR-proANP) <40 pmol/L68 make a diagnosis of HF unlikely. These will be discussed in more detail in section 4.2.69,70
Basic investigations such as serum urea and electrolytes, creatinine, full blood count, liver and thyroid function tests are recommended to differentiate HF from other conditions, to provide prognostic information, and to guide potential therapy.
Echocardiography is recommended as the key investigation for the assessment of cardiac function. As well as the determination of the LVEF, echocardiography also provides information on other parameters such as chamber size, eccentric or concentric LVH, regional wall motion abnormalities (that may suggest underlying CAD, Takotsubo syndrome, or myocarditis), RV function, pulmonary hypertension, valvular function, and markers of diastolic function.16,71
A chest X-ray is recommended to investigate other potential causes of breathlessness (e.g. pulmonary disease). It may also provide supportive evidence of HF (e.g. pulmonary congestion or cardiomegaly).
Symptoms and signs:
Diagnosis includes assessing patient’s signs and symptoms.
Examination generally difficult in: Obese, Elderly, Lung disease.
Typical symptoms: breathlessness, Orthpnoea (SOB) when lying down and paroxysmal nocturnal dyspnoea (SOB at night which awakens a patient)., dyspnoea, reduced exercise tolerance, fatigue/tiredness/increased time to recover after exercise, ankle swelling, anorexia, confusion/delirium (elderly)
Signs:
Elevated jugular venous pressure
Hepatojugular reflux –distension of jugular vein induced by applying manual pressure over the liver
Third heart sound - gallop rhythm
Laterally displaced apical impulse
Cardiac murmur
Peripheral oedema, ascites (fluid collects in abdomen)
Tachycardia
Irregular pulse
Hepatomegaly (back up of blood into hepatic veins – liver becomes congested and grows)
Cachexia and muscle wasting
Most common ECG changes in HF
Sinus tachycardia; causes decompensated HF, anaemia, fever, hyperthyroidism
Sinus bradycardia; causes beta-blockade, digoxin, ivabradine, verapamil, diltiazem, antiarrhythmics, hypothyroidism, sick sinus syndrome
Atrial tachy/flutter/fib ; hyperthyroidism, infection, mitral valve disease, decompensated HF, infarction
Ventricular arrhythmias; ischaemia, infarction, cardiomyopathy, myocarditis, hypokalaemia, digitalis OD, hypomagnesaemia
M isch/ infarction; coronary artery disease
Q waves; infarction, hypertrophic cardiomyopathy, LBBB, pre-excitation
LV hypertrophy; HTN, AV disease, hypertrophic cardiomyopathy
AV block; infarction, drug toxicity, myocarditis, sarcoidosis, genetic cardiomyopathy, Lyme disease
Low QRS voltage; obesity, emphysema, pericardial effusion, amyloidosis
QRS duration >120ms and LBBB morphology
Most common Echo findings in HF
Parameters related to systolic function;
- LVEF Reduced (<50%)
Parameters related to diastolic function;
- LV diastolic dysfunction parameters
Parameters related to valvular function
- valvular structure and function
Other parameters;
RV function (e.g. TAPSE) (reduced TAPSE<16mm)
TR peak velocity
Common Lab Tests in HF
BNP (biologically active hormone; short half-life).
NT pro-BNP (not biologically active; longer half-life).
Different thresholds for acute/worsening HF and non-acute.
Acute = 300 pg/ml for NT pro-BNP. 100 pg/ml for BNP.
Non-acute = 125 pg/ml for NT pro-BNP. <35 pg/ml for BNP.
Diagnosis HF REF / HF PEF
HF has recently been classified into two main subtypes, namely HF with reduced ejection fraction (HFrEF), HF with preserved ejection fraction (HFpEF) and HF mid-range ejection fraction (HFmrEF).
HF also classified based on severity of patient symptoms with I being the most mild and IV being the most severe.
The diagnosis of HF-REF requires three conditions to be satisfied:
1. symptoms typical of HF
2. Signs typical of HF
3. Reduced LVEF
The diagnosis of HF-PEF requires 4 conditions to be satisfied:
1. Symptoms typical of HF
2. Signs typical of HF
3. Normal or only mildly reduced LVEF and LV not dilated
4. Relevant structural heart disease (LV hypertrophy/ LA enlargement) and/or diastolic dysfunction
NYHA classification:
Class I - No limitation of physical activity. Ordinary physical activity does not cause undue breathlessness, fatigue, or palps.
Class II - Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in undue breathlessness, fatigue or palpitations
Class III - Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in undue breathlessness, fatigue or palpitations
Class IV - Unable to carry on any physical activity without discomfort. Symptoms at rest can be present. If any physical activity is undertaken, discomfort is increased
Pathophysiology of HF-REF
Long-term hypertension can contribute to HF-REF.
Can induce LV remodelling and dilatation and reduced cardiac output.
Stretching and altering of the conduction system.
May lead to electrical and mechanical dyssynchrony.
The change in LV shape and size may lead to tricuspid and mitral annulus dilatation and resultant functional tricuspid and mitral regurgitation.
Myocyte stretching in response to hypertension and valvular disease can lead to atrial dilatation and an increased susceptibility to Aflutter/AF.
Chronic LV dysfunction frequently leads to increased pulmonary vascular resistance and pulmonary hypertension due to endothelial cell dysfunction, vasoconstriction and remodelling, which can ultimately result in concurrent RV dysfunction (Moraes et al., 2000).
Primary myocardial injury e.g. Due to ischaemic heart disease, leads to impaired cardiac structure or function and a reduced ability to efficiently supply blood to the body’s tissues at a rate that meets their oxygen and metabolic demands
Secondary myocardial effects
- LV remodelling
- Contractility
- Hypertrophy
- Apoptosis
- Cytokines
- Fibrosis
- NOS/ROS
- EP
Neurohormones
- Increased SNS activity
Increase RAS
Increased Endothelin
Increased ANP/BNP
Increased cytokines
Endothelium
- vasoconstriction
- NOS/ROS
- structural change
-cytokines
CHF outcomes: Sudden death, progressive pump failure, symptoms
Other useful adjunct testing summary.
DSE/ETT
Angiography
RHC / myocardial biopsy
CMR
Genetic testing
Ambulatory ECG
Treatment
Aim: Keep symptoms under control
The National Institute of Clinical Excellence (NICE) guidelines 2018 in England and Wales, and the Scottish Intercollegiate Guidelines Network (SIGN) guidelines in Scotland, recommend that heart failure patients should be considered for the following medications.
(Start low, aim high).
Stage A and Stage B HF
Stage A - At risk of HF
Patients with HTN - Optimal control of BP
Pts with T2DM and CVD or high risk for CVD - SGLT2i
Patents with CVD - Optimal management of CVD
Patients with exposure to cardiotoxic agents - MDT evaluation for management
First degree relatives of patients with genetic or inherited cardiomyopathies - genetic screening and counseling
Patients at risk for HF - Natriuretic peptide biomarker screening
Patients at risk for HF - validated multivariable risk score
Stage B - Pre-HF
Patients with LVEF <40% - ACEi
Patients with a recent MI and LVEF <40% - ARB if ACEi intolerant
Patients with LVEF <40% - beta blocker
Patients with LVEF <30%; >1y survival; >40d post MI
Patients with non-ischaemic cardiomyopathy - Genetic counselling and testing
ACE Inhibitor
(Angiotensin Converting Enzyme Inhibitor)
Traditionally a 1st line drug. Titration to target dose is essential.
– Long term studies suggest may increase survival by up to 50%.
– All NYHA classes benefit, NYHA IV have shown most benefit.
Relieves symptoms and improves exercise tolerance.
Reduces risk of death and slows disease progression.
Benefits may not be apparent for 1-2 months after initiation.
Help to relax blood vessels, making it easier for heart to pump blood around the body.
Occasional side effects may include a troublesome cough or dizziness.
Renin-angiotensin system
The liver reproduces angiotensinogen
Drop in BP/ drop in fluid volume -> renin is released from the kidney, and acts on angiotensinogen to form angiotensin I
Angiotensin converting enzyme (ACE) is released from lungs, which acts on Angiotensin I to form angiotensin II.
-> This acts on blood vessels stimulating vasoconstriction (narrowing)
->It also acts on the adrenal gland to stimulate release of aldosterone
Aldosterone acts on kidneys to stimulate reabsorption of salt (NaCl) and water (H2O)
Diuretics (water tablets)
Diuretics increase the amount of water and salt passed from the kidneys into the urine and therefore can help to get rid of any build-up of fluid.
Used to treat congestive symptoms and fluid retention.
Diuretics are best taken in the morning on an empty stomach.
Titrate up and down as needed.
Can have an impact on QoL for patient.
What are the four pillars of HF?
BMJ: ARNI, angiotensin receptor-neprilysin inhibitors; BB, beta-blocker; MRA, mineralocorticoid receptor antagonists;SGLT2i, sodium-glucose co-transporter 2inhibitors.
Sacubitril valsartan
Anangiotensin receptor-neprilysin inhibitor(ARNI).
Valsartan is an angiotensin II receptor blocker, and it works onblocking the RAAS system.
Sacubitril blocks the action of neprilysin –prevents breakdown of natriuretic peptides e.g. BNP to increase diuresis and vasodilation.
Recommended for treating symptomatic chronic HF with reduced EF and NYHA II – IV with LVEF <35% who are on stable dose of ACEi/ARB.
PROVE-HF – reverse remodelling, increases LVEF.
-similar effects to CRT
Beta blockers
Historically a ‘no-go’ in HF due to negative inotropic effect (heart beats with less force).
Now good evidence that used cautiously can reduce mortality by 35% and hospitalisations by 15%.
Contraindications to Beta blocker therapy- COPD with reversibility, Brittle asthma.
Carvedilol, Bisoprolol and Nebivolol are the only ones licensed in UK for HF (Nebivolol over 70s only).
Mechanism: slowing down heart rate and reducing the work the heart has to do.
Some relax blood vessels, making it easier to pump blood through them.
Side effects include SOB and tiredness until body adjusts.
Mineralocorticoid Receptor Antagonists (MRAs)
Historically prescribed if still symptomatic despite taking ACE inhibitors, beta blockers and diuretics, or if HF graded as moderate-severe, may be indicated.
MRAs work by blocking hormone aldosterone.
Aldosterone causes salt and water retention and so blocking its action is beneficial.
MRAs are increasingly used in people with all grades of HF as research studies have shown that they help with symptom control and increase life expectancy.
(e.g. Spironolactone and eplerenone).
SGLT2 inhibitors
e.g. dapagliflozin
Block the SGLT2 protein in the proximal tubule of the nephron, reducing the amount of reabsorbed glucose and sodium in the blood.
Traditionally known as anti-hyperglycaemic drugs, sodium-glucose co-transporter 2 (SGLT-2) inhibitors are an important therapy for symptomatic HF with reduced LVEF
Diuretics:SGLT2 inhibitors may add to the diuretic effect of thiazide and loop diuretics and may increase the risk of dehydration and hypotension.
Ivabradine
Must be in sinus rhythm > 75 bpm (slows SAN conduction) with NYHA II – IV stable chronic HF with LVSD and LVEF <35%.
Inhibits the movement of sodium into cells.
Currently the only agent shown to clinically lower heart rate with no negative inotropism or effects on conduction and contractility.
Usually prescribed if heart rate is still too fast despite taking a betablocker (may be offered if cannot tolerate a beta blocker).
Research has shown that it reduces the risk of HF hospitalisations.
Digoxin
Rapid or irregular heartbeat due to AF.
Still have symptoms despite OMT.
Enhances inotropy (energy of contractions) of cardiac muscle.
Reduces activation of SNS:
– Reduces symptoms
– Decreases risk of HF progression
– Reduces hospitalisation rates for decompensated HF
– Does not improve survival
– Trial data shows deterioration in symptoms if stopped.
ESC guidelines recommended pharmacological therapy
1) An ACEi is recommended in addition to BB for all pts with EF <40% to reduce the risk of hospitalisation and risk of premature death
2) B is recommended in addition to ACEi (or ARB if ACEi is not well tolerated) for all patients with an EF <40% to reduce the risk of HF hospitalisation and risk of premature death
3) MRA is recommended for all pts with persisting symptoms (NYHA class II-IV) and an EF <35% despite treatment with ACEi (or ARB), and a BB to reduce risk of hospitalisation and premature death.
Key Trials for Pharmacological Therapy in HF REF.
ACEi
CONSENSUS
SOLVD
ATLAS
27%, 16% and 15% reduction in mortality and hospitalisation.
BB in HFrEF
CIBIS II
COPERNICUS
MERIT-HF
SENIORS
Different types of beta-blocker.
Reduction of 34% in mortality and 28-36% in hospitalisation.
MRA
RALES
EMPHASIS-HF
Spironolactone and Eplerenone.
30% reduced death rates, 35% hospitalisation.
37% reduction in CV-related death and 24% hospitalisation.
Types of diuretics
Diuretics are used in systolic and diastolic HF
Not proven to improve life expectancy.
Do relieve symptoms of dyspnoea and oedema.
Aim for euvolaemia.
May need to adjust to prevent dehydration, hypotension and worsening HF.
Loop diuretics: Furosemide, bumetanide, torasemide
Thiazides: Indapamide, bendroflumethiazide, hydrochlorothiazide, metolazone
Potassium-sparing diuretics: Spironolactone/eplerenone, amiloride, triamterene
Non-pharmacological treatment for HF REF.
Secondary prevention - ICD recommended for a patient with a ventricular arrhythmia causing haemodynamic instability, who is expected to survive for >1year with good functional status, to reduce risk of sudden death.
Primary prevention - ICD is recommended in pt with symptomatic HF (class II-III) and an EF <35% despite >3mo treatment with optimal pharmacological therapy, expected to survive >1yr with good functional status to reduce risk of sudden death.
ICDs reduce mortality for survivors of cardiac arrest and patients with documented ventricular arrhythmias.
Must have life expectancy >1 year (aim is to increase survival).
CRT
Cardiac resynchronisation therapy (CRT) for LV systolic dysfunction.
Evidence from COMPANION and CARE-HF in moderate to severe HF.
Reduction in death and hospitalisation with CRT device and CRT + ICD in situ.
MADIT-CRT and RAFT in mild to moderately symptomatic HF.
Both studies demonstrated reduction in hospitalisation and death when compared to standard therapy alone. MADIT-CRT did not show a reduction in all cause mortality.
Treatment recommendations for patients with heart failure (HF) with left ventricular systolic dysfunction and an associated left ventricular ejection fraction (LVEF) of 35% or less. Treatment varies depending on the patient’s New York Heart Association (NYHA) class, QRS duration and presence of left bundle branch block . NICE 2014
NYHA CLASS I II III IV
QRS interval
<120ms ICD if sudden risk of SCD No recomm
120-149ms w/oLBBB ICD ICD ICD CRT-P
120-149 w LBBB ICD CRT-D CRT-P/CRT-D CRT-P
>150ms w/o LBBB CRT-D CRT-D CRT-P/CRT-D CRT-P
>150ms w LBBB CRT-D CRT-D CRT-P/CRT-D CRT-P
Exercise training
- another form of interventionLoads of evidence regarding benefits in mild to severe HF-REF.Starting to gather data showing benefit in HF-PEF (small trials).
Parameters in HF known to be modulated by Ex Training
Central adaptations:
- Improved systolic and diastolic function (contradictory evidence)
Improved O2 handling and efficiency:
- Improved muscle mitochondrial function, increased lung capacity, improved energetics within muscle cells, beneficial changes to cardiac metabolism – overall increase in VO2 max, anaerobic threshold and inefficient production of lactate.
Increased muscle strength.
Increased endurance.
Improved vascular function:
- Endothelial function, increased production of nitric oxide, reduced risk of atherosclerotic related events, correction of vasoconstrictive pathology, decreased LV afterload.
Reduced inflammation:
- Less cardiac stretch (BNP), systemic inflammatory markers reduced therefore improvements in vascular and myocardial components – less cellular apoptosis.
Improved insulin modulation:
- Improved diabetic control, insulin resistance corrected – indirectly improves BMI / % adipose abdominally, improves cardiac mitochondrial energetics, improves vascular function.
Psychology:
- Improved general health, reduced depression, lessens psychosocial impact of disease.
Prognosis:
- Decreased mortality and morbidity, reduced hospital associated costs for primary and secondary care.
Surgical Interventions
LVAD.
BiVAD
- for pts with >2mo severe symptoms despitae OMT and device therapy and 1+ following:
LVEF <25% and peak VO2 <12mL/kg/min
>3 hospitalisations in prev 12mo w/o obvious precipitating cause
Dependence on i.v. inotropic therapy
Deteriorating LV fn
Progressive end-organ dysfn
Heart transplant
What is an LVAD?
A surgically implanted mechanical pump that is attached to the heart, continuously taking blood from the left ventricle and pumping it into the aorta, which then delivers oxygen-rich blood throughout the body.
Has both internal and external components.
The pump sits on or next to the left ventricle with a tube which directs blood to the aorta.
A cable called driveline extends from the pump, out through the skin, and connects the pump to a controller and power sources worn outside the body.
The driveline must be connected to the controller, and the controller must be connected to power at all times to keep the pump working properly.
The pump is powered by batteries or electricity.
Used to ‘bridge’ patients to heart transplantation.
Transplant-eligible patients may be considered for implantation of an LVAD if their condition is deteriorating and are unlikely to receive a donor heart in time.
If a patient is not eligible for a heart transplant, an LVAD may be implanted as a permanent solution.
In a minority of cases, the recovery of LV function has been sufficient for the LVAD to be explanted without transplantation.
LVAD support may also be used to reverse renal dysfunction and pulmonary hypertension secondary to HF, thereby making the patient a better candidate for transplantation.
LVAD patients >85% one-year survival rate versus OMT 25-50%.
Heart Transplantation
Final option for end-stage HF.
Only available in carefully selected patients.
Demand significantly out-weighs availability.
Special population of patients requiring significant life-long medical evaluation.
