Heart failure

Heart failure describes the clinical syndrome that

develops when
the heart cannot maintain adequate output, or can
do so only
at the expense of elevated ventricular filling
pressure. In mild to
moderate forms of heart failure, symptoms occur
only when the
metabolic demand increases during exercise or
some other form
of stress. In severe heart failure, symptoms may be
present at
rest. In clinical practice, heart failure may be
diagnosed when
a patient with significant heart disease develops
the signs or
symptoms of a low cardiac output, pulmonary
congestion or
systemic venous congestion at rest or on exercise.
Three types
of heart failure are recognised.
Left heart failure
This is characterised by a reduction in left
ventricular output and an
increase in left atrial and pulmonary venous
pressure. If left heart
failure occurs suddenly – for example, as the result
of an acute
MI – the rapid increase in left atrial pressure causes
pulmonary
oedema. If the rise in atrial pressure is more
gradual, as occurs
with mitral stenosis, there is reflex pulmonary
vasoconstriction,
which protects the patient from pulmonary
oedema. However,
the resulting increase in pulmonary vascular
resistance causes
pulmonary hypertension, which in turn impairs
right ventricular
function.
Right heart failure
This is characterised by a reduction in right
ventricular output and
an increase in right atrial and systemic venous
pressure. The most
common causes are chronic lung disease,
pulmonary embolism
and pulmonary valvular stenosis. The term ‘cor
pulmonale’ is
used to describe right heart failure that is
secondary to chronic
lung disease.
Biventricular heart failure
In biventricular failure, both sides of the heart are
affected.
This may occur because the disease process, such
as dilated
cardiomyopathy or ischaemic heart disease, affects
both ventricles
or because disease of the left heart leads to
chronic elevation
of the left atrial pressure, pulmonary hypertension
and right
heart failure.
Epidemiology
Heart failure predominantly affects the elderly; the
prevalence
rises from 1% in those aged 50–59 years to over
10% in those
aged 80–89 years. In the UK, most patients
admitted to hospital
with heart failure are more than 70 years old; they
typically remain
hospitalised for a week or more and may be left
with chronic
disability. Although the outlook depends, to some
extent, on
the underlying cause of the problem, untreated
heart failure
generally carries a poor prognosis; approximately
50% of patients
with severe heart failure due to left ventricular
dysfunction will
die within 2 years because of either pump failure or
malignant
ventricular arrhythmias. The most common causes
are coronary
artery disease and myocardial infarction but almost
all forms of
heart disease can lead to heart failure, as
summarised in Box
16.12. An accurate diagnosis is important because
treatment
of the underlying cause may reverse heart failure
or prevent its
progression.
Pathogenesis
Heart failure occurs when cardiac output fails to
meet the
demands of the circulation. Cardiac output is
determined by
preload (the volume and pressure of blood in the
ventricles at
the end of diastole), afterload (the volume and
pressure of blood
in the ventricles during systole) and myocardial
contractility,
forming the basis of Starling’s Law (Fig. 16.24). The
causes of
heart failure are discussed below
entricular dysfunction
Ventricular dysfunction is the most common cause
of heart
failure. This can occur because of impaired systolic
contraction
due to myocardial disease, or diastolic dysfunction
where there
is abnormal ventricular relaxation due to a stiff,
non-compliant
ventricle. This is most commonly found in patients
with left
ventricular hypertrophy. Systolic dysfunction and
diastolic
dysfunction often coexist, particularly in patients
with coronary
artery disease. Ventricular dysfunction reduces
cardiac output,
which, in turn, activates the sympathetic nervous
system (SNS)
and renin–angiotensin–aldosterone system (RAAS).
Under normal
circumstances, activation of the SNS and RAAS
supports cardiac
function but, in the setting of impaired ventricular
function, the
consequences are negative and lead to an increase
in both
afterload and preload (Fig. 16.25). A vicious circle
may then be
Mechanisms of heart failure
Cause Examples Features
Reduced ventricular
contractility
Myocardial infarction (segmental
dysfunction) In coronary artery disease,
‘akinetic’ or ‘dyskinetic’ segments
contract poorly and may impede the
function of normal
segments by distorting their contraction
and relaxation patterns
Myocarditis/cardiomyopathy (global
dysfunction) Progressive ventricular
dilatation
Ventricular outflow
obstruction
(pressure overload)
Hypertension, aortic stenosis (left heart
failure)
Pulmonary hypertension, pulmonary valve
stenosis (right
heart failure)
Initially, concentric ventricular hypertrophy
allows the ventricle
to maintain a normal output by generating
a high systolic
pressure. Later, secondary changes in the
myocardium and
increasing obstruction lead to failure with
ventricular dilatation
and rapid clinical deterioration
Ventricular inflow
obstruction
Mitral stenosis, tricuspid stenosis Small,
vigorous ventricle; dilated, hypertrophied
atrium. Atrial
fibrillation is common and often causes
marked deterioration
because ventricular filling depends heavily
on atrial contraction
Ventricular volume
overload
Left ventricular volume overload (mitral or
aortic
regurgitation)
Ventricular septal defect
Right ventricular volume overload (atrial
septal defect)
Increased metabolic demand (high output)
Dilatation and hypertrophy allow the
ventricle to generate a
high stroke volume and help to maintain a
normal cardiac
output. However, secondary changes in the
myocardium lead
to impaired contractility and worsening
heart failure
Arrhythmia Atrial fibrillation Tachycardia
does not allow for adequate filling of the
heart,
resulting in reduced cardiac output and
back pressure
Tachycardia Prolonged tachycardia causes
myocardial fatigue
Complete heart block Bradycardia limits
cardiac output, even if stroke volume is
normal
Diastolic
dysfunction
Constrictive pericarditis Marked fluid
retention and peripheral oedema, ascites,
pleural
effusions and elevated jugular veins
Restrictive cardiomyopathy Bi-atrial
enlargement (restrictive filling pattern and
high atrial
pressures). Atrial fibrillation may cause
deterioration
Left ventricular hypertrophy and fibrosis
Cardiac tamponade
Good systolic function but poor diastolic
filling
Hypotension, elevated jugular veins, pulsus
paradoxus, poor
urine output

established because any additional fall in cardiac

output causes
further activation of the SNS and RAAS, and an
additional
increase in peripheral vascular resistance.
Activation of the RAAS causes vasoconstriction and
sodium
and water retention. This is primarily mediated by
angiotensin II, a
potent constrictor of arterioles, in both the kidney
and the systemic
circulation (Fig. 16.25). Activation of the SNS also
occurs and
can initially sustain cardiac output through
increased myocardial
contractility and heart rate. Prolonged sympathetic
stimulation has
negative effects, however, causing cardiac
myocyte apoptosis,
cardiac hypertrophy and focal myocardial necrosis.
Sympathetic
stimulation also contributes to vasoconstriction and
predisposes
to arrhythmias. Sodium and water retention is
further enhanced by
the release of aldosterone, endothelin-1 (a potent
vasoconstrictor
peptide with marked effects on the renal
vasculature) and, in
severe heart failure, vasopressin (antidiuretic
hormone, ADH).
Natriuretic peptides are released from the atria in
response to atrial
dilatation and compensate to an extent for the
sodium-conserving
effect of aldosterone, but this mechanism is
overwhelmed in
heart failure. Pulmonary and peripheral oedema
occurs because
of high left and right atrial pressures, and is
compounded by
sodium and water retention, caused by impairment
of renal
perfusion and by secondary hyperaldosteronism. If
the underlying
cause is a myocardial infarction, cardiac
contractility is impaired
and SNS and RAAS activation causes hypertrophy
of noninfarcted segments, with thinning, dilatation
and expansion
of the infarcted segment (see Fig. 16.64, p. 496).
This leads
to further deterioration in ventricular function and
worsening
heart failure
High-output failure
Sometimes cardiac failure can occur in patients
without heart
disease due to a large arteriovenous shunt, or
where there is an
excessively high cardiac output due to beri-beri (p.
714), severe
anaemia or thyrotoxicosis.
Valvular disease
Heart failure can also be caused by valvular
disease in which
there is impaired filling of the ventricles due to
mitral or tricuspid
stenosis; where there is obstruction to ventricular
outflow,
as occurs in aortic and tricuspid stenosis and
hypertrophic
cardiomyopathy; or as the result of ventricular
overload secondary
to valvular regurgitation.
Clinical assessment
Heart failure may develop suddenly, as in MI, or
gradually, as
in valvular heart disease. When there is gradual
impairment of
cardiac function, several compensatory changes
take place. The
term compensated heart failure is sometimes used
to describe
the condition of those with impaired cardiac
function, in whom
adaptive changes have prevented the development
of overt heart
failure. However, a minor event, such as an
intercurrent infection
or development of atrial fibrillation, may
precipitate acute heart
failure in these circumstances (Box 16.13).
Similarly, acute heart
failure sometimes supervenes as the result of a
decompensating
episode, on a background of chronic heart failure;
this is called
acute-on-chronic heart failure.
Acute left heart failure
Acute left heart failure presents with a sudden
onset of dyspnoea
at rest that rapidly progresses to acute respiratory
distress,
orthopnoea and prostration. Often there is a clear
precipitating
factor, such as an acute MI, which may be apparent
from the
history. The patient appears agitated, pale and
clammy. The
peripheries are cool to the touch and the pulse is
rapid, but in
some cases there may be an inappropriate
bradycardia that
may contribute to the acute episode of heart
failure. The BP is
usually high because of SNS activation, but may be
normal or
low if the patient is in cardiogenic shock.
The jugular venous pressure (JVP) is usually
elevated,
particularly with associated fluid overload or right
heart failure.
In acute heart failure, there has been no time for
ventricular
dilatation and the apex is not displaced. A ‘gallop’
rhythm, with
a third heart sound, is heard quite early in the
development of
acute left-sided heart failure. A new systolic
murmur may signify
acute mitral regurgitation or ventricular septal
rupture. Chest
examination may reveal crepitations at the lung
bases if there is
pulmonary oedema, or crepitations throughout the
lungs if thi
is severe. There may be an expiratory wheeze.
Patients with
acute-on-chronic heart failure may have additional
features of
chronic heart failure (see below). Potential
precipitants, such as
an upper respiratory tract infection or
inappropriate cessation
of diuretic medication, may be identified on clinical
examination
or history-taking.
Chronic heart failure
Patients with chronic heart failure commonly follow
a relapsing
and remitting course, with periods of stability and
episodes of
decompensation, leading to worsening symptoms
that may
necessitate hospitalisation. The clinical picture
depends on the
nature of the underlying heart disease, the type of
heart failure
that it has evoked, and the changes in the SNS and
RAAS that
have developed (see Box 16.12 and Fig. 16.26).
Low cardiac output causes fatigue, listlessness and
a poor
effort tolerance; the peripheries are cold and the
BP is low.
To maintain perfusion of vital organs, blood flow is
diverted
away from skeletal muscle and this may contribute
to fatigue
and weakness. Poor renal perfusion leads to
oliguria and
uraemia.
Pulmonary oedema due to left heart failure
presents with
dyspnoea and inspiratory crepitations over the
lung bases. In
contrast, right heart failure produces a high JVP
with hepatic
congestion and dependent peripheral oedema. In
ambulant
patients the oedema affects the ankles, whereas in
bed-bound
patients it collects around the thighs and sacrum.
Ascites or
pleural effusion may occur (Fig. 16.26). Heart
failure is not the
only cause of oedema (Box 16.14)
Chronic heart failure is sometimes associated with
marked
weight loss (cardiac cachexia), caused by a
combination
of anorexia and impaired absorption due to
gastrointestinal
congestion, poor tissue perfusion due to a low
cardiac output,
and skeletal muscle atrophy due to immobility.
Complications of heart failure
Several complications may occur in advanced heart
failure, as
described below.
• Renal failure is caused by poor renal perfusion
due to low
cardiac output and may be exacerbated by diuretic
therapy, ACE inhibitors and angiotensin receptor
blockers
(ARBs).
• Hypokalaemia may be the result of treatment
with
potassium-losing diuretics or hyperaldosteronism
caused
by activation of the renin–angiotensin system and
impaired
aldosterone metabolism due to hepatic congestion.
Most
of the body’s potassium is intracellular and there
may be
substantial depletion of potassium stores, even
when the
plasma concentration is in the reference range.
• Hyperkalaemia may be due to the effects of
drugs that
promote renal resorption of potassium, in
particular the
combination of ACE inhibitors, ARBs and
mineralocorticoid
receptor antagonists. These effects are amplified if
there is renal dysfunction due to low cardiac output
or
atherosclerotic renal vascular disease.
• Hyponatraemia is a feature of severe heart
failure and is a
poor prognostic sign. It may be caused by diuretic
therapy, inappropriate water retention due to high
vasopressin secretion, or failure of the cell
membrane ion
pump.
• Impaired liver function is caused by hepatic
venous
congestion and poor arterial perfusion, which
frequently
cause mild jaundice and abnormal liver function
tests;
reduced synthesis of clotting factors can make
anticoagulant control difficult.
• Thromboembolism. Deep vein thrombosis and
pulmonary
embolism may occur due to the effects of a low
cardiac
output and enforced immobility. Systemic emboli
occur in
patients with atrial fibrillation or flutter, or with
intracardiac
thrombus complicating conditions such as mitral
stenosis,
MI or left ventricular aneurysm.
• Atrial and ventricular arrhythmias are very
common and
may be related to electrolyte changes such as
hypokalaemia and hypomagnesaemia, the
underlying
cardiac disease, and the pro-arrhythmic effects of
sympathetic activation. Atrial fibrillation occurs in
approximately 20% of patients with heart failure
and
causes further impairment of cardiac function.
Ventricular
ectopic beats and runs of non-sustained ventricular
tachycardia are common findings in patients with
heart
failure and are associated with an adverse
prognosis.
• Sudden death occurs in up to 50% of patients
with heart
failure and is most probably due to ventricular
fibrillation.
Investigations
A chest X-ray should be performed in all cases.
This may show
abnormal distension of the upper lobe pulmonary
veins with the
patient in the erect position (Fig. 16.27).
Vascularity of the lung
fields becomes more prominent and the right and
left pulmonary
arteries dilate. Subsequently, interstitial oedema
causes thickened
interlobular septa and dilated lymphatics. These
are evident as
horizontal lines in the costophrenic angles (septal
or ‘Kerley
B’ lines). More advanced changes due to alveolar
oedema
cause a hazy opacification spreading from the hilar
regions, and
pleural effusions. Echocardiography is very useful
and should be
considered in all patients with heart failure in order
to:
• determine the aetiology
• detect hitherto unsuspected valvular heart
disease, such
as occult mitral stenosis, and other conditions that
may be
amenable to specific remedies
• identify patients who will benefit from long-term
drug
therapy.
Serum urea, creatinine and electrolytes,
haemoglobin and
thyroid function may help to establish the nature
and severity of
the underlying heart disease and detect any
complications. BNP
is elevated in heart failure and is a prognostic
marker, as well
as being useful in differentiating heart failure from
other causes
of breathlessness or peripheral oedema.
Management of acute heart failure
Acute heart failure with pulmonary oedema is a
medical emergency
that should be treated urgently. The patient should
initially be kept
rested, with continuous monitoring of cardiac
rhythm, BP and
pulse oximetry. Intravenous opiates can be of
value in distressed
patients but must be used sparingly, as they may
cause respiratory
depression and exacerbation of hypoxaemia and
hypercapnia.
The key elements of management are summarised
in Box 16.15.
If these measures prove ineffective, inotropic
agents such as
dobutamine (2.5–10 μg/kg/min) may be required to
augment
cardiac output, particularly in hypotensive patients.
Insertion
of an intra-aortic balloon pump may be beneficial
in patients
with acute cardiogenic pulmonary oedema and
shock.
Following management of the acute episode,
additional measures
must be instituted to control heart failure in the
longer term, as
discussed below.
Management of chronic heart failure
The aims of treatment in chronic heart failure are
to improve
cardiac function by increasing contractility,
optimising preload
or decreasing afterload, and controlling cardiac
rate and rhythm
(see Fig. 16.25). This can be achieved by a
combination of drug
treatment or non-drug treatments, as discussed
below.
Education
Education of patients and their relatives about the
causes and
treatment of heart failure can improve adherence
to a management
plan (Box 16.16). Some patients may need to
weigh themselves
daily, as a measure of fluid load, and adjust their
diuretic therapy
accordingly.
Drug treatment
A wide variety of drug treatments are now
available for the
treatment of heart failure. Drugs that reduce
preload are
appropriate in patients with high end-diastolic
filling pressures
and evidence of pulmonary or systemic venous
congestion,
whereas those that reduce afterload or increase
myocardial
contractility are more useful in patients with signs
and symptoms
of a low cardiac output.
Diuretics Diuretics promote urinary sodium and
water excretion,
leading to a reduction in blood plasma volume (p.
354), which
in turn reduces preload and improves pulmonary
and systemic
venous congestion. They may also reduce afterload
and ventricular
volume, leading to a fall in ventricular wall tension
and increased
cardiac efficiency. Although a fall in preload
(ventricular filling
pressure) normally reduces cardiac output,
patients with heart
failure are beyond the apex of the Starling curve,
so there may
be a substantial and beneficial fall in filling
pressure with either no
change or an improvement in cardiac output (see
Figs 16.24 and
16.28). Nevertheless, the dose of diuretics needs to
be titrated
carefully so as to avoid excessive volume
depletion, which can
cause a fall in cardiac output with hypotension,
lethargy and
renal failure. This is especially likely in patients
with a marked
diastolic component to their heart failure.
Oedema may persist, despite oral loop diuretic
therapy, in
some patients with severe chronic heart failure,
particularly
if there is renal impairment. Under these
circumstances an
intravenous infusion of furosemide (5–10 mg/hr)
may initiate a
diuresis. Combining a loop diuretic with a thiazide
diuretic such
as bendroflumethiazide (5 mg daily) may also
prove effective but
care must be taken to avoid an excessive diuresis.
Mineralocorticoid receptor antagonists, such as
spironolactone
and eplerenone, are potassium-sparing diuretics
that are of
particular benefit in patients with heart failure with
severe left
ventricular systolic dysfunction. They have been
shown to improve
long-term clinical outcome in individuals with
severe heart failure
or heart failure following acute MI but may cause
hyperkalaemia,
particularly when used with an ACE inhibitor.
ngiotensin-converting enzyme inhibitors ACE
inhibitors play a
central role in the management of heart failure
since they interrupt
the vicious circle of neurohumoral activation that is
characteristic
of the disease by preventing the conversion of
angiotensin I to
angiotensin II. This, in turn, reduces peripheral
vasoconstriction,
activation of the sympathetic nervous system (Fig.
16.29), and
salt and water retention due to aldosterone
release, as well as
preventing the activation of the renin–angiotensin
system caused
by diuretic therapy.
In moderate and severe heart failure, ACE
inhibitors can
produce a substantial improvement in effort
tolerance and in
mortality. They can also improve outcome and
prevent the onset
of overt heart failure in patients with poor residual
left ventricular
function following MI.
Adverse effects of ACE inhibitors include
symptomatic
hypotension and impairment of renal function,
especially in patients
with bilateral renal artery stenosis or those with
pre-existing renal
disease. An increase in serum potassium
concentration may also
occur, which can be beneficial in offsetting the
hypokalaemia
associated with loop diuretic therapy. Short-acting
ACE inhibitors
can cause marked falls in BP, particularly in the
elderly or
when started in the presence of hypotension,
hypovolaemia or
hyponatraemia. In stable patients without
hypotension (systolic BP
over 100 mmHg), ACE inhibitors can usually be
safely started i
he community. In other patients, however, it is
usually advisable
to withhold diuretics for 24 hours before starting
treatment with a
small dose of a long-acting agent, preferably given
at night (Box
16.18). Renal function and serum potassium must
be monitored
and should be checked 1–2 weeks after starting
therapy.
Angiotensin receptor blockers ARBs act by blocking
the action
of angiotensin II on the heart, peripheral
vasculature and kidney.
In heart failure, they produce beneficial
haemodynamic changes
that are similar to the effects of ACE inhibitors (Fig.
16.29) but
are generally better tolerated. They have
comparable effects on
mortality and are a useful alternative for patients
who cannot
tolerate ACE inhibitors. Like ACE inhibitors they
should be started
at a low dose and titrated upwards, depending on
response
(Box 16.18). Unfortunately, they share all the more
serious
adverse effects of ACE inhibitors, including renal
dysfunction
and hyperkalaemia. ARBs are normally used as an
alternative
to ACE inhibitors, but the two can be combined in
patients with
resistant or recurrent heart failure.
Neprilysin inhibitors The only drug currently in this
class is
sacubitril, a small-molecule inhibitor of neprilysin,
which is
esponsible for the breakdown of the endogenous
diuretics
ANP and BNP. Used in combination with the ARB
valsartan
(sacubitril–valsartan), it has been shown to
produce additional
symptomatic and mortality benefit over ACE
inhibition and is
now recommended in the management of resistant
heart failure.
Vasodilators These drugs are valuable in chronic
heart failure,
when ACE inhibitors or ARBs are contraindicated.
Venodilators,
such as nitrates, reduce preload, and arterial
dilators, such as
hydralazine, reduce afterload (see Fig. 16.28).
Their use is limited
by pharmacological tolerance and hypotension.
Beta-adrenoceptor blockers Beta-blockade helps to
counteract
the deleterious effects of enhanced sympathetic
stimulation and
reduces the risk of arrhythmias and sudden death.
When initiated
in standard doses β-blockers may precipitate
acute-on-chronic
heart failure, but when given in small incremental
doses they
can increase ejection fraction, improve symptoms,
reduce the
frequency of hospitalisation and reduce mortality in
patients with
chronic heart failure. A typical regimen is
bisoprolol, starting
at a dose of 1.25 mg daily and increased gradually
over a
12-week period to a target maintenance dose of 10
mg daily.
Beta-blockers are more effective at reducing
mortality than ACE
inhibitors, with a relative risk reduction of 33%
versus 20%,
respectively.
Ivabradine Ivabradine acts on the If inward current
in the SA
node, resulting in reduction of heart rate. It
reduces hospital
admission and mortality rates in patients with
heart failure due to
moderate or severe left ventricular systolic
impairment. In trials,
its effects were most marked in patients with a
relatively high
heart rate (over 77/min), so ivabradine is best
suited to patients
who cannot take β-blockers or whose heart rate
remains high
despite β-blockade. It is ineffective in patients with
atrial fibrillation.
Digoxin Digoxin (p. 482) can be used to provide
rate control in
patients with heart failure and atrial fibrillation. In
patients with
severe heart failure (NYHA class III–IV, see Box
16.5), digoxin
reduces the likelihood of hospitalisation for heart
failure, although
it has no effect on long-term survival.
Amiodarone This is a potent anti-arrhythmic drug
(p. 481)
that has little negative inotropic effect and may be
valuable in
patients with poor left ventricular function. It is
effective only in the
treatment of symptomatic arrhythmias and should
not be used
as a preventative agent in asymptomatic patients.
Amiodarone
is used for prevention of symptomatic atrial
arrhythmias and
of ventricular arrhythmias when other
pharmacological options
have been exhausted.
Non-pharmacological treatments
Implantable cardiac defibrillators These devices are
indicated
in patients with symptomatic ventricular
arrhythmias and heart
failure, since they improve prognosis and survival
(p. 483).
Resynchronisation devices In patients with marked
intraventricular
conduction delay, prolonged depolarisation may
lead to
uncoordinated left ventricular contraction. When
this is associated
with severe symptomatic heart failure, cardiac
resynchronisation
devices may be helpful. Here, both the LV and RV
are paced
simultaneously (Fig. 16.30) to generate a more
coordinated
left ventricular contraction and improve cardiac
output. This is
associated with improved symptoms and survival.
Coronary revascularisation Coronary artery bypass
surgery or
percutaneous coronary intervention may improve
function in
areas of the myocardium that are ‘hibernating’
because of
inadequate blood supply, and can be used to treat
carefully
selected patients with heart failure and coronary
artery disease.
If necessary, ‘hibernating’ myocardium can be
identified by
stress echocardiography and specialised nuclear or
magnetic
resonance imaging.
Cardiac transplantation Cardiac transplantation is
an established
and successful treatment for patients with
intractable heart failure.
Coronary artery disease and dilated
cardiomyopathy are the
most common indications. The use of
transplantation is limited
by the efficacy of modern drug and device
therapies, as well
as the availability of donor hearts, so it is generally
reserved for
young patients with severe symptoms despite
optimal therapy.
Conventional heart transplantation is
contraindicated in patients
with pulmonary vascular disease due to long-
standing left heart
failure, complex congenital heart disease such as
Eisenmenger’s
syndrome, or primary pulmonary hypertension
because the RV of
the donor heart may fail in the face of high
pulmonary vascular
resistance. However, heart–lung transplantation
can be successful
in patients with Eisenmenger’s syndrome, and lung
transplantation
has been used for primary pulmonary
hypertension.
Although cardiac transplantation usually produces
a dramatic
improvement in the recipient’s quality of life,
serious complications
may occur:
• Rejection. In spite of routine therapy with
ciclosporin A,
azathioprine and glucocorticoids, episodes of
rejection are
common and may present with heart failure,
arrhythmias
or subtle ECG changes. Cardiac biopsy is often
used to
confirm the diagnosis before starting treatment
with
high-dose glucocorticoids.
• Accelerated atherosclerosis. Recurrent heart
failure is often
due to progressive atherosclerosis in the coronary
arteries
of the donor heart. This is not confined to patients
who
underwent transplantation for coronary artery
disease and
is probably a manifestation of chronic rejection.
Angina is
rare because the heart has been denervated.
Infection. Opportunistic infection with organisms
such as
cytomegalovirus or Aspergillus remains a major
cause of
death in transplant recipients.
Ventricular assist devices Because of the limited
supply of donor
organs, ventricular assist devices (VAD) may be
employed as a
bridge to cardiac transplantation and as short-term
restoration
therapy following a potentially reversible insult
such as viral
myocarditis. In some patients, VADs may be used
as a long-term
therapy if no other options exist.
These devices assist cardiac output by using a
roller, centrifugal
or pulsatile pump that, in some cases, is
implantable and portable.
They withdraw blood through cannulae inserted in
the atria or
ventricular apex and pump it into the pulmonary
artery or aorta.
They are designed not only to unload the ventricles
but also to
provide support to the pulmonary and systemic
circulations.
Their more widespread application is limited by
high complication
rates (haemorrhage, systemic embolism, infection,
neurological
and renal sequelae), although some improvements
in survival
and quality of life have been demonstrated in
patients with
severe heart failure