The ‘Fontan circulation' has evolved to include a variety of surgical procedures designed
to overcome the absence of two distinct ventricular chambers.1
w1–w3 Inherent to this circulation is chronic elevation of right atrial and vena caval
pressure, and absence of a dedicated power source to serve the pulmonary circulation,
making low pulmonary vascular resistance and optimal systemic ventricular function
the essential ingredients of a successful Fontan circulation.2 Originally designed
for the single left ventricle, modifications to the original atriopulmonary connections
extended repairs to complex ventricular anatomy, and are now most commonly performed
for single right ventricular anatomy associated with hypoplastic left heart syndrome.
Together with improved perioperative management, creation of the Fontan circulation
in two stages (superior cavopulmonary anastomosis followed by later Fontan completionw4),
and performance of Fontan procedures at a younger age, have led to reduced operative
mortality associated with the Fontan procedure of ≤5% (compared with 15–30% in earlier
decades); survival at 20 years is presently 85%.3
w5
Over the last two decades, the initial survivors of the atriopulmonary Fontan repairs
have reached adulthood, bringing a multiplicity of haemodynamic complications and
sequelae of their abnormal circulatory status. The atriopulmonary connection is now
obsolete as a surgical option, and the current surviving adults with this circulation
do not reflect contemporary Fontan outcomes. Nonetheless, their attendant compendium
of complications and sequelae provides a daunting array of management challenges,
and stigmatises the current perception of long term Fontan outcomes.
The ‘Fontan circulation’ now encompasses a spectrum of anatomic substrates, staging
options, and operative techniques. Problems classified as ‘Fontan failure’ may represent
problems inherent to the morphologic substrate, operative variables, and inevitable
sequelae of the Fontan circulation: chronic venous congestion and progressively declining
functional status. This review will separate complications into those where intervention
may optimise clinical status while maintaining the Fontan circulation—the ‘failing
Fontan’—and those conditions which have progressed to a ‘failed Fontan’, where options
are limited to cardiac transplantation or attempts to minimise the impact of irreversible
functional deterioration. Finally, we will discuss strategies which may alter the
incidence and time course of Fontan failure.
The failing Fontan circulation
Evaluation of the failing or failed Fontan circulation requires knowledge of the anatomic
substrate, surgical intervention details, cardiac imaging and assessment of haemodynamic
status, assessment of rhythm status, and evaluation of other organ systems and metabolic
function. Late Fontan failure may present insidiously over years. It is a failure
of medical management to interpret the absence of overt symptoms or ascites as evidence
of optimal haemodynamic status in the functionally univentricular circulation. In
contrast to other forms of operated congenital heart disease, Fontan patients have
lived with less than ideal cardiac output their entire lives, and may neither recognise
nor show overt manifestations of progressive decline in functional status until deterioration
is quite advanced (table 1).
Table 1
Failing Fontan circulation
Constitutional
Growth failure
Inadequate cardiac output
Exercise intolerance
Chronotropic incompetence, pronounced atrial distension
Depression
Secondary to limitations on functional status
Haemodynamic
Obstruction
Systemic venous
Systemic outflow
Atriopulmonary, pulmonary arterial
Pulmonary venous return, atrioventricular (AV) valve inflow
Ventricular outflow, aortic arch
AV valve function
≥Moderate regurgitation
≥Mild stenosis
Ventricular dysfunction
Secondary: atrial dilatation/distortion; AV valve or semilunar valve dysfunction,
chronic arrhythmias or antiarrhythmic medications; impaired myocardial perfusion due
to coronary sinus hypertension
Thrombosis
Systemic venous, atrial, pulmonary
Rhythm
Arrhythmias
Sinus node dysfunction, predominant junctional rhythm, AV block, supraventricular
tachycardia/atrial tachycardia, ventricular tachycardia
Pulmonary
Cyanosis
Intracardiac right to left shunt, veno-venous collaterals, pulmonary arteriovenous
malformations (AVMs)
Pleural effusions
Gastrointestinal
Ascites
Secondary to portal hypertension related to obstruction, versus cirrhosis
Metabolic
Metabolic markers
Declining albumin; thrombocytopenia; hyperbilirubinaemia; coagulopathy
Growth
In general, the Fontan patient population is shorter in height than the normal population;
there is increased recognition that failure to gain weight appropriately is an early
indicator of suboptimal cardiac output in childhood.4 Growth failure should prompt
a thorough investigation of haemodynamic status, with early efforts to optimise haemodynamic
status with catheter or surgical intervention for residual obstruction or valve abnormalities.
Exercise capacity is lower in Fontan patients than in other patients with repaired
congenital heart disease, and recent studies have reported a 1–3% annual decline in
maximal oxygen consumption beginning in adolescence.5
w6–w8 In Fontan patients, the average peak oxygen consumption ranges from 19–28 ml/kg/min,
or 50–60% of predicted consumption for age. Decline in exercise function correlates
with the need for hospitalisation and symptom development.6
w8 Decreased exercise tolerance is more common in single right or indeterminant ventricular
morphology, and in patients with lateral tunnel repairs, and may be related to chronotropic
incompetence or abnormal pulmonary compliance with exertion.6
w8 w9 Serial exercise testing may objectively identify changes in haemodynamic or
rhythm status, which may be addressed with intervention such as pulmonary stenting,
atrial pacing, pulmonary vasodilator therapy, or Fontan conversion surgery.5
Cyanosis
A mild degree of desaturation is present in most Fontan patients, due to coronary
sinus drainage to the left atrium or pulmonary shunting. Resting saturations <90%
suggest the presence of right to left shunting (either intracardiac or due to veno-veno
collateral flow to the left atrium) or pulmonary arteriovenous fistulae. Coil embolisation
of collaterals or catheter based occlusion of atrial septal defects may improve saturations,
although investigation for a more compelling cause for the development of collaterals
may allow more definitive intervention. Patients with discontinuous pulmonary arteries
with a classic Glenn to the right pulmonary artery have insufficient hepatic flow
to that lung, and would benefit from surgical intervention to provide confluent pulmonary
arteries and increased hepatic flow to the right lung. Patients with atriopulmonary
connections frequently have ‘decompressing’ collateral flow or atrial level shunts,
and benefit from Fontan conversion.
Pathway obstructions and valve dysfunction
The development of haemodynamic abnormalities may be gradual and insidious in Fontan
patients, and detection is complicated by the lack of complaints from most patients
until pronounced limitation occurs. Decline in exercise tolerance, resting or exercise
desaturation, the presence of a murmur, hepatomegaly, or cardiomegaly on radiography
are indicators of haemodynamic abnormalities. Patients with atriopulmonary connections
develop marked right atrial distension over time, secondary to anatomic obstructions
at the anastomosis, or due to the notable energy loss associated with sluggish flow
(figure 1). Decompression of the atrium occurs via coronary sinus dilatation, and
atrial communications or veno-veno collaterals from the systemic veins to the left
atrium or pulmonary veins may ensue. Distension of the right atrium may result in
torsion and narrowing of the connection to the pulmonary arteries, as well as compression
of the pulmonary venous return from the right lung; the dilated atrium may impinge
on inflow in the setting of a right-sided atrioventricular valve. Anatomic obstructions
may exist at the atriopulmonary anastomosis or the branch pulmonary arteries; a gradient
of >1 mm Hg in this circuit dependent on passive flow is haemodynamically significant.
Patients with valved conduits in place, either atrioventricular or atriopulmonary,
invariably develop obstruction over time. Patients with lateral tunnel repairs in
general do not develop pronounced atrial distension, but narrowing at the pulmonary
arteries may exist. Abnormalities of atrioventricular (AV) valve function result in
elevated left atrial pressure, which will harm the pulmonary circulation. Chronic
aortic outflow obstruction will result in hypertrophy and diminished ventricular compliance;
the volume overload of aortic insufficiency will contribute to ventricular failure.
Figure 1
MRI of marked atrial dilatation with impingement on pulmonary venous return in a patient
with an atriopulmonary Fontan anastomosis for tricuspid atresia. Right atrium measures
7×7.5 cm. Image courtesy of Cynthia K Rigsby, Children's Memorial Hospital, Chicago,
Illinois, USA.
Hepatic and infra-diaphragmatic venous congestion is present in all Fontan patients,
to greater or lesser degrees. Sequestration of platelets by the liver and spleen result
in thrombocytopenia, present in 15–25% of adult Fontan patients. Mild elevation of
bilirubin is common, followed by abnormalities of liver enzymes. The effects of years
of venous congestion will result in hepatic cirrhosis, which becomes apparent by approximately
11 years following surgery.7 Surveillance with abdominal ultrasound may detect hepatic
nodules, with more detailed imaging provided by CT. Monitoring of α-fetoprotein may
provide early detection of hepatocellular carcinoma, now reported in a small number
of older Fontan patients.
Arrhythmias
This broad term includes sinus node dysfunction, predominant junctional rhythm, atrioventricular
block, supraventricular and ventricular arrhythmias, and the risk of arrhythmic sudden
death. Modifications to the Fontan procedure have resulted in a decreased incidence
of sinus node dysfunction and atrial arrhythmias. Sinus node dysfunction is reported
in 40% of patients with atriopulmonary connections, and is reported in up to 25% of
lateral tunnel and extracardiac cavopulmonary connection surgeries.8
9
w10 w11 Reassurance based on an ‘adequate overall heart rate’, which is usually junctional,
is a disservice to the patient, as the haemodynamic consequences of junctional rhythm
in the Fontan circulation are profound, including acute elevation of atrial pressure
with each ventricular contraction. Non-sinus rhythm has been associated with increased
risk of atrial arrhythmias, as well as an increased risk of hepatic fibrosisw12; these
data warrant vigorous attempts to maintain regular atrial rhythm in Fontan patients.
The incidence of atrial arrhythmias during long term follow-up has decreased with
surgical modifications of the Fontan procedure, from as many as 60% of atriopulmonary
patients to approximately 12% of extracardiac total cavopulmonary connection patients.9–13
w5 w13 Atrial reentrant tachycardia accounts for approximately 75% of supraventricular
tachycardia, with focal atrial tachycardia in up to 15% of patients.w13 w14 In lateral
tunnel patients, the reentrant circuit may reside in the pulmonary venous atrium.
Atrial fibrillation is becoming increasingly common in adult Fontan patients, and
is present in almost half of patients referred for Fontan conversion. Risk factors
for the development of atrial tachycardia include an atriopulmonary connection, preoperative
bradycardia, lack of sinus rhythm, older age at Fontan and longer postoperative interval,
greater than mild atrioventricular valve regurgitation, and heterotaxy syndrome.3
9
11
w11 As the incidence of atrial tachycardia increases with the postoperative interval
and is a major source of morbidity,8
10 regular surveillance of rhythm with ambulatory 24 h monitors, event monitors and
exercise testing becomes more important during long term follow-up.
Termination of an acute episode of atrial tachycardia within 24–48 h from onset is
recommended whenever possible, due to the rapid deterioration in haemodynamic status
associated with tachycardia in the single ventricle circulation. Figure 2 summarises
an algorithm for management of atrial arrhythmias.w15 Development of atrial tachycardia
is commonly associated with haemodynamic abnormalities which will require more extensive
haemodynamic, functional, and metabolic evaluation. Catheter ablation for atrial tachycardia
in Fontan patients has considerably lower success rates than in other forms of repaired
congenital heart disease. Acute success rates from catheter ablation in the Fontan
patient range from 40–75%, with recurrence of tachycardia in 60% of patients during
the first year.14
w14 Catheter ablation in this population is best suited for patients with lateral
tunnel repairs and focal atrial tachycardia, or atriopulmonary repairs who are not
suitable candidates for Fontan arrhythmia surgery. The development of significant
arrhythmias in the atriopulmonary or atrioventricular Fontan modification, when coupled
with signs of heart failure, is associated with a 3 year mortality rate of 25%.6
Figure 2
Management of atrial arrhythmias in Fontan patients. PLE, protein-losing enteropathy.
Fontan conversion with arrhythmia surgery
Recognition that atriopulmonary Fontan patients have associated haemodynamic limitations
in addition to atrial tachycardia led our group to incorporate arrhythmia surgery
into Fontan conversion to an extracardiac total cavopulmonary connection, beginning
in 1994.15
w16 In addition to right atrial reduction, performance of a modified right atrial
maze procedure eliminates right atrial macro-reentrant tachycardia, but is not intended
to treat focal atrial tachycardia or other mechanisms without targeted resection (figure
3). Left atrial macro-reentrant tachycardia or atrial fibrillation is treated with
an additional left atrial Cox Maze III, which effectively eliminates atrial fibrillation,
but we have noted recurrence of a slower organised atrial reentry tachycardia in about
15% of such patients.w16 Implantation of epicardial dual chamber anti-tachycardia
pacing systems is performed for virtually all patients, predominantly relying on atrial
pacing at rates of 70–80 beats/min chronically, without ventricular pacing. Our centre
has performed over 135 Fontan conversions with arrhythmia surgery at a mean interval
of 15.5±5.2 years following initial Fontan procedure, with acute mortality of 1.5%;
other centres have achieved relatively comparable results.16 Analysis of intermediate
outcomes in the initial 110 patients undergoing such surgery at our centre showed
freedom from death or transplantation at 15 years of follow-up was 80%, with freedom
from recurrent tachycardia of 85%. Risk factors for poor outcomes in this population
include right or ambiguous ventricle, presence of right atrial thrombus at time of
surgery, older age at Fontan conversion, longer post-Fontan interval, or ascites.
Patients with protein-losing enteropathy are not considered candidates for Fontan
conversion surgery, and patients without correctable causes of poor ventricular function,
or multiorgan system disease, may be better treated by transplantation. We have recently
demonstrated improved functional status at 5 years of follow-up in a subset of patients
undergoing paired pre- and post-Fontan conversion exercise testing, with an average
17% increase in maximal oxygen consumption. These results suggest that aggressive
efforts to improve flow dynamics and associated haemodynamic abnormalities, eliminate
arrhythmias, and maintain chronic atrial rhythm may favourably alter what has been
considered as an ‘inexorable decline’ in functional status in many Fontan patients.
Figure 3
Surgical modifications of atrial maze procedure in complex anatomy. Solid black lines
indicate sites of cryoablation. avn, atrioventricular node; CS, coronary sinus; FO,
foramen ovale; HV, hepatic vein; IVC, inferior vena cava; LAA, left atrial appendage;
LSVC, left superior vena cava; MV, mitral valve; PV, pulmonic vein; RAA, right atrial
appendage; RSVC, right superior vena cava; TAPVR, total anomalous pulmonary venous
return; TV, tricuspid valve. Reprinted with permission from Mavroudis C, Deal BJ,
Backer CL, Tsao S. Arrhythmia surgery in patients with and without congenital heart
disease. Ann Thorac Surg 2008;86:857–68.
In addition to atrial arrhythmias, atrioventricular block occurs, either due to intrinsic
conduction abnormalities as seen in patients with l-transposition, or as a consequence
of surgery. The incidence of pacemaker implantation in most series ranges from 3–18%,
without stratification as to implantation for AV block versus sinus node dysfunction.3
w5 w17 Limitations of venous access to the atrium, the risk of endocardial lead thrombosis,
and the morbidity of repeat sternotomy to place epicardial leads, support a preemptive
strategy of atrial lead placement at the time of primary Fontan repair, although not
a class I or II indication for pacing by current recommendations. With improved survival,
it is becoming apparent that ventricular arrhythmias are noted in 3–12% of adult patients.17
w5 w17 The contribution of ventricular arrhythmias to late sudden death, reported
in 9% of patients, is not yet known.18
Ascites
Ascites may develop as a consequence of elevated right atrial pressure, protein-losing
enteropathy or hepatic dysfunction, and requires clarification of the aetiology with
aggressive evaluation and treatment. Ascites may occur without hypoalbuminaemia, but
is an advanced indicator of a failing Fontan circulation; in this setting, Fontan
conversion with arrhythmia surgery may be feasible, although with increased risk of
later Fontan failure. A small number of patients have persistent or recurrent ascites
late after Fontan conversion, without evidence of Fontan circulation obstruction.
In this setting, ascites is thought to be related to hepatic dysfunction. Diuretic
therapy and optimisation of medical therapy may minimise ascites; regular evaluation
of cirrhotic changes with abdominal ultrasound, CT or MRI, and monitoring of liver
function, is recommended. When advanced cardiac liver cirrhosis changes are noted,
the risk for hepatocellular carcinoma increases.7 Combined cardiac and liver transplantation
for a Fontan patient has been performed successfully.w18
The failed Fontan
In the unusual setting of early postoperative failure, a failed circulation requires
early takedown of the Fontan surgical circuit. Late failure, discussed here, includes
haemodynamic or multiorgan system complications of the Fontan circulation which are
not reversible by surgical or catheter interventions at acceptable risk. Strategies
to minimise/palliate complications or consideration for cardiac transplantation are
the limited therapeutic options. Table 2 summarises the conditions associated with
a failed Fontan, which are discussed in several excellent reviews.19
w19 Most studies report early operative mortality for Fontan patients undergoing cardiac
transplantation at approximately 30%, higher than that reported for other forms of
congenital heart disease,20 although one recent study showed no difference in early
mortality among Fontan patients.w20 Problems specific to the Fontan patient undergoing
transplantation include multiple prior surgeries with increased sensitisation rates
between 20–60%, with preformed antibodies to donor human leucocyte antigens (HLA),
complexities of venous anatomy, malnourishment associated with protein-losing enteropathy,
and acute graft right heart failure. After the early transplant period, there is no
difference in long term survival compared with other forms of congenital heart disease,
with survival rates at 10 years of around 54%.w21 w22 Due to the significant mortality
on the waiting list and elevated early mortality, there is interest in developing
implantable mechanical assist devices in Fontan patients as either a bridge to transplantation,
or ‘destination therapy’.w23 w24
Table 2
Failed Fontan circulation
Condition
Incidence
Manifestations
Aetiologies
Treatments
Early failure
3%
Low cardiac output, pleural effusions, chylothoraces, ascites, hepatomegaly
Pulmonary vasculature abnormalities
Incessant/refractory atrial tachycardia
Residual obstruction related to surgical technique
Early evaluation to correct obstructions, terminate tachycardia
Fontan takedown
Recreate systemic to pulmonary blood flow
Cardiac transplantation
Late failure Lymphatic dysfunction Protein-losing enteropathy (PLE)
2–13%
Ascites, peripheral oedema, pleural effusions, diarrhoea, malabsorption of fat, hypoalbuminaemia
Unknown, but associated with:
Low cardiac output
Mesenteric vascular flow abnormalities
Intestinal cellular wall damage
Autoimmune reactions
Intestinal lymphangiectasia
Risk factors: prolonged postoperative chest tube drainage, systemic right ventricle
Nutritional support with protein and medium chain triglycerides
Optimise cardiac output: atrial rhythm, pulmonary vasodilator therapy, afterload reduction,
atrial fenestration
Enteric steroids
Diuretics
Heparin
High dose aldactone
Intravenous albumin and γ-globulin infusions
Immunosuppression
Cardiac transplantation
Plastic bronchitis
<2%
Tachypnoea, cough, wheezing, expectoration of bronchial casts
Unknown; associated with leakage of proteinaceous material into the airways resulting
in bronchial casts
Urgent bronchial lavagePulmonary vasodilatorsCardiac transplantation
Primary ventricular dysfunction
∼7–10%
Progressive exercise intolerance, AV valve insufficiency, hepatomegaly, ascites
Chronic hypertrophy, abnormal ventricular morphology (systemic right or indeterminate
ventricle), older age at repair, prolonged cyanosis or volume overload, myocardial
perfusion abnormalities
ACE inhibition
Pulmonary vasodilators
Calcium channel blockers for diastolic dysfunction
β-blockers
Multisite pacing
Cardiac transplantation
Progressive increase in pulmonary resistance
Unknown
Hypoxaemia
Pulmonary arteriovenous malformations, inadequate hepatic vein effluent, lack of pulsatile
flow
Pulmonary vasodilators; stenting of pulmonary arterial narrowing
Hepato-renal insufficiency
Low cardiac output, sepsis
Supportive care, optimise cardiac output, high mortality
Hepatic failure
Unknown
Hepatomegaly, ascites; hepatocellular carcinoma
Progression of chronic cardiac cirrhosis
Cardiac and liver transplantation
Failure of medical care
At this stage in our knowledge of the natural history of the Fontan circulation, several
concepts have become clear, including: (1) the unique challenges of the functionally
univentricular circulation with progressive multiorgan system impact; (2) the inability
to definitively treat a truly ‘failed’ Fontan with measures other than cardiac transplantation;
(3) the inadequacy of traditional cardiac follow-up visits to reliably detect subtle
changes in circulation before advanced stages; and (4) the challenges in ‘cardiac’
management that present unlike any other repaired congenital cardiac anomalies. In
addition, the collective memory of the earlier high mortality or prolonged hospital
courses associated with primary Fontan surgery in past decades has made many clinicians
reluctant to recommend additional interventions, particularly without overt symptoms.
In addition to standard haemodynamic evaluations, more global assessment of the impact
of the Fontan physiology on other organ systems needs to become part of routine surveillance
(table 2). It cannot be assumed that the patient has other healthcare providers with
adequate knowledge of the impact of the Fontan circulation to monitor these systems.
Growth failure in childhood and weight loss in adulthood are advanced manifestations
of inadequate haemodynamic status. In adulthood, exercise intolerance may result in
extremes of a sedentary lifestyle and result in obesity. By contributing to alterations
in pulmonary functionw22 and increased systemic vascular resistance, overweight contributes
rapidly to Fontan failure. Patients should be counselled on the importance of regular
aerobic activity for conditioning, and avoidance of overweight as essential to limiting
Fontan failure.
In the USA, the cardiologist caring for Fontan patients is now asked to routinely
monitor and assess other organ systems, including haematologic, endocrine, pulmonary,
hepatic and gastrointestinal, within the confines of decreased reimbursement for testing
and shorter office visits. The barriers to sophisticated medical care for the older
Fontan patient encompass difficulties in education of the patient relative to the
need for regular cardiac care, availability of comprehensive integrated care centres
with sufficient expertise, and in many countries the lack of healthcare coverage.
Nonetheless, it is apparent that a change in practice for the routine long term follow-up
of Fontan patients is necessary in order to detect progressive subtle decline in status
and to have a favourable impact on the functional status of these unique survivors
(table 3). Failure to change our standard methods of routine cardiac care in this
setting constitutes a failure of optimal medical management. Chronic pulmonary vasodilator
therapy, in addition to chronic diuresis, may become part of routine long term medical
therapy as this population ages.w25 Better strategies for improving vascular endothelial
function and liver protection, including the usage of polyphenols and thiazolidinediones,
will become areas for future studies.w26
Table 3
Long term Fontan surveillance
Parameters
Monitoring
Constitutional
Adequate growth in childhood
Weight or muscle loss in adulthood
Avoid overweight
Blood pressure: normotensive
Functional classification,
Aerobic activity
Daily napping
Aerobic activity
Exercise testing
Cardiac haemodynamics
Heart size
Atrial dilatation
Atriopulmonary anastomosis
Pulmonary narrowing, distortion
Pulmonary venous or atrioventricular (AV) inflow obstruction
AV valve regurgitation or stenosis
Aortic insufficiency
Ventricular outflow obstruction
Arch obstruction
Ventricular function
Echocardiogram
Periodic chest radiograph
Cardiac MRI or CT
Rhythm
Presence of atrial versus junctional rhythm
Resting heart rate
Chronotropic response to exertion
Arrhythmia development
Periodic 24 h ambulatory monitoring; event monitoring
Pulmonary
HypoxaemiaVascular resistance
Oxygen saturation, resting and exertional
Endocrine
Thyroid function
Thyroid stimulating hormone (TSH), thyroxine (T4)
Renal
Blood urea nitrogen, creatinine
Hepatic
Hepatomegaly
Cardiac cirrhosis
Synthetic function
Liver function: enzymes, coagulation
Abdominal ultrasound, CT or MR
Liver biopsy
Serum α-fetoprotein
Gastrointestinal
Bloating, distension, diarrhoea, ascites, gallstones
Stool α-1 anti-trypsin
Haematologic
Anaemia, polycythaemia, thrombocytopenia
Blood count, platelets
Metabolic
B-type natriuretic peptide, albumin, alkaline phosphatase
Neurologic
Cerebrovascular accident
Depression
Management of the failing Fontan circulation: key points
Symptoms develop at an advanced stage of declining Fontan circulation.
Identification of the ‘failing’ Fontan before the development of ascites or protein-losing
enteropathy is essential to improve outcomes.
Monitoring functional status, rhythm, serum biomarkers, and liver changes is essential
to long term assessment of ‘cardiac’ status.
Ablation procedures for atriopulmonary Fontan patients have a low likelihood of success.
Aggressive therapy for rhythm and haemodynamic abnormalities may improve long term
functional status.
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