pda jurnal.pptx

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Congenital heart Disease for the Adult CardiologistPatent Ductus Arteriosus

Douglas J. Schneider, and John W. Moore

Journal ReadingSeptember 2014

Bahagian KardiovaskularFakultas Kedokteran

Universitas Hasanuddin


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The patent ductus arteriosus (PDA) is avascular structure that connects the

proximal descending aorta to the roof ofthe main pulmonary artery near theorigin of the left branch pulmonaryartery.

Essential fetal structure normally closesspontaneously after birth.


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After the first few weeks of life, persistenceof ductal patency is abnormal.

The physiological impact and clinicalsignificance of the PDA depend largely onits size and the underlying cardiovascularstatus of the patient.

The PDA may be silent (not evidentclinically but diagnosed incidentally byechocardiography done for a different

reason), small, moderate, or large


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Normal and essential fetal structure

Abnormal if it remains patent after the

neonatal period. This transformation is complete by 8

weeks of fetal life. (Figure 1)


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Figure 1. Schematic of embryonicaortic arch system.

The 6 pairs of embryonic aorticarches are demonstrated (left-sided arches are numbered).

The portions that normallyinvolute are indicated by brokenlines.

The distal left sixth embryonicarch normally persists andbecomes the PDA, connecting

the left pulmonary artery to theproximal descending aorta.

The right distal sixth arch normallyinvolutes, as does the eighthsegment of the right dorsal aorta(*), which results in a leftward

aortic arch. RCA indicates right carotid artery;

LCA, left carotid artery; RSCA,right subclavian artery; and LSCA,left subclavian artery.


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Fetal Circulation

65% of the fetal CO is from RV

5% to 10% passes through the lungs

Ventricular output -> DA -> descending

aorta The fetal ductus arteriosus is thus an

important structure that is essential fornormal fetal development, permitting right

ventricular output to be diverted away fromthe high-resistance pulmonary circulation.

Premature constriction or closure -> rightheart failure -> fetal hydrops.


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Histology and Mechanisms of NormalClosure

Aorta & pulmonary artery : surroundedmediae are composed mainly ofcircumferentially arranged layers ofelastic fibers

Ductus arteriosus : the media iscomposed longitudinally and spirallyarranged layers of smooth muscle fiberswithin loose, concentric layers of elastic

tissue. The intima of the ductus arteriosusis thickened and irregular, with abundantmucoid material,sometimes referred toas intimal cushions.


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Before birth

Fetal patency of the ductus arteriosus is

controlled by many factors ; low fetal oxygen tension

cyclooxygenase-mediated products of

arachidonic acid metabolism (primarilyprostaglandin [PGE2] and prostacyclin [PGI2] -> vasodilator DA via ductal prostanoidreceptor)

Placenta -> PGE & PGI -> decreasedmetabolism in the fetal lungs.

ft bi th


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After birthIncrease oxygen tension

ductal constriction & PGE2 and PGI2 levels fall

lungs metabolism now functioning

ductus contract & wall thickening, lumen obliteration &shortening of the ductus arteriosus

Functional complete within 24 to 48 hours of birth in termneonates

next 2 to 3 weeks ->

endothelium infolding, subintimal disruption & proliferation->

fibrosis & a permanent seal ->

ligamentum arteriosum.


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The factors responsible for persistentpatency of the ductus arteriosus beyondthe first 24 to 48 hours of neonatal life arenot completely understood

Prematurity clearly increases theincidence of PDA

In term infants -> sporadically, but there

is increasing evidence with geneticfactors

Prenatal infection appear to play a role

in some cases.


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Incidence

PDA has been reported to be 1 in 2000

births This accounts for 5% to 10% of all

congenital heart disease

Children with silent patent ductus, theincidence has been estimated to be ashigh as 1 in 500.

Female : male ratio is 2:1 in most reports.


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Genetic Factors

Increased frequency in several genetic

syndromes(such as trisomy 21 and 4psyndrome), single-gene mutations (suchas Carpenters syndrome and Holt-Oramsyndrome), and X-linked mutations (suchas incontinentia pigmenti).

Genetic mechanism of patent ductus insome patients may be autosomal

recessive inheritance with incompletepenetrance


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In a family having 1 sibling with a PDA,

there is an 3% chance of a PDA in a

subsequent offspring. Genetic studies suggest that the

abnormalities in Char syndrome (aninherited disorder with PDA, facial

dimorphism, and hand anomalies) resultfrom derangement of neural crest cellderivatives.

There is also evidence of abnormalfibronectin-dependent smooth musclecell migration as a cause of PDA


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Infection and Environmental Factors

Rubella infection (first trimester of

pregnancy)

particularly in the first 4 weeks.

Environmental factors, such as in fetal

valproate syndrome


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The size, configuration,

and relationship toadjacent structuresare important withrespect to determiningresistance to bloodflow

Figure 2 demonstratesthe wide variability inpatent ductus size andconfiguration using theangiographicclassification originallydevised to help guidetranscatheter closureprocedures


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Figure 2. Variations in PDAconfiguration illustrated with theclassification of Krichenko et al.

A, Type A (conical) ductus, withwell-defined aortic ampulla andconstriction near the pulmonaryartery end.

B, Very large type B (window)

ductus, with very short length.

C, Type C (tubular) ductus,which is without constrictions.

D, Type D (complex) ductus,Which has multiple constrictions.

E, Type E (elongated) ductus,with the constriction remotefrom the anterior edge of the

trachea.


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Left-to-Right Shunting

The hemodynamic impact ofPDA,determined by the magnitude ofshunting(flow resistance of the ductusarteriosus, length, the narrowest diameter,

shape and configuration) Flow in the ductus is dynamic and pulsatile,

the elasticity of the ductus wall affect theblood flow

The magnitude of shunt flow depends notonly on the ductal resistance but also onthe pressure gradient between the aortaand the pulmonary artery


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Left-to-right shunting pulmonaryovercirculation and left heart volume

overload Increased pulmonary flow from the ductal

shunting increased pulmonaryfluid volume.

Shunts with moderate or largedecreased lung compliance

increased work of breathing


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Increased flow returning to the left heartincreased LA and LV end-diastolic

pressures.

LV compensates

Neuroendocrine adaptations

LVH

increased sympatheticactivity & catecholamines

(increased contractility & HR)


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EisenmengersSyndrome

long-standing left-to-right shunting

pulmonary artery system to high-pressure &increased flow

progressive morphological changes in thepulmonary vasculature (arteriolar medialhypertrophy, intimal proliferation & fibrosis)

progressive increase in pulmonary vascularresistance

ductal shunting reverses , right to left


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Medical History

Exercise intolerance

Reactive airways disease

Symptoms of congestive heart failure

Physical Examination

continuous murmur LUSB -> machinery

murmur

Murmur often radiates down the left side of

the sternum and into the back


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Thrill may be present

Diastolic rumble is audible at the cardiac

apex The peripheral pulses may be prominent

or bounding.

Auscultation may reveal a high-frequency diastolic decrescendomurmur of pulmonary regurgitationand/or a holosystolic murmur from

tricuspid valve regurgitation. Peripheral edema may be present late in

the course of disease when rightventricular dysfunction is present.


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Chest Radiograph

Cardiomegaly(specifically with signs of

left atrial and left ventricularenlargement).

Increased pulmonary vascular markings.

Main pulmonary artery is frequentlyenlarged, particularly in older adults withpulmonary hypertension, calcification ofthe ductus may be evident.

Electrocardiogram Sinus tachycardia or atrial fibrillation

LVH, LAE, RAE

Biventricular hypertrophy


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Echocardiogram

The echocardiogram is the procedure of

choiceto confirm the diagnosis and tocharacterize a PDA (Figure 3).

Echocardiogram is often useful inclassifying the PDA as silent, small,

moderate, or large. To identify and evaluate other

associated cardiac defects.

M-mode echocardiography is used tomeasure the cardiac chamber sizes andquantitate left ventricular systolicfunction


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Patient with a small ductus arteriosus,chamber sizes are usually normal,

although mild LA and/or LV enlargementmay be present.

Patient with a moderate or large patentductus, the LA and LV are enlarged.

Color Doppler is a very sensitive modalityin detecting the presence of a PDA andis frequently used to estimate the degreeof ductal shunting.

A complete pulmonary artery pressurecurve can be generated from thespectral Doppler signal of ductal flow.


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Magnetic Resonance Imaging andComputed Tomography

Computed tomography can assess thedegree of calcification, important ifsurgical therapy is considered.

To define the anatomy in patients withunusual PDA geometry, associatedabnormalities of the aortic arch (ductusarteriosus aneurysm), may present as a

chest mass.


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Cardiac Catheterization

Therapeutic catheterization is currently the

treatment of choice at most centers formost children and adults with patent ductus

Complete diagnostic assessment of

hemodynamics before transcatheter

closure.

Assessment of pulmonary vascular

resistance and its response to vasodilating

agents such as oxygen, nifedipine,prostacyclin, sildenafil, and nitric oxide may

be helpful in determining advisability of

ductus closure.


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Assessment of hemodynamics during

temporary test occlusion with a balloon

catheter may also provide important

information regarding advisability of

closure.

Detailed assessment of the ductal anatomy

is essential before transcatheter closure sothat the proper device and device size can

be chosen for the intervention (minimum

diameter, the largest diameter (usually at

the aortic ampulla), the length, and therelationship of the ductus to the anterior

border of the tracheal shadow, which helps

guide device positioning.)


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The natural history of PDA dependslargely on the size and magnitude of theshunt and the status of the pulmonaryvasculature.

patients with significant left heart volumeoverload, however, are at risk of

congestive heart failure or irreversiblepulmonary vascular disease,


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Congestive Heart Failure

Moderate to large patent ductus ->

congestive heart failure due topulmonary overcirculation and left heartvolume overload

Significant chronic volume overload ofthe left heart -> develop congestiveheart failure in adulthood, starting in the

third decade

In the adult, heart failure is frequentlyassociated with atrial flutter or fibrillation


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Hypertensive Pulmonary Vascular Disease

large nonrestrictive or minimally restrictivepatent ductus -> develop irreversible

pulmonary vascular disease. Secondary to long-standing pressure and

volume overload in the pulmonarycirculation -> Hypertensive PulmonaryVascular Disease

Endarteritis

Incidence of infective arteritis was reportedto

be 1% per year

In countries with limited health resourcesand access to health care, infectiveendarteritis associated with ductusarteriosus remains a significant health issue


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Aneurysm of Ductus Arteriosus

Reported incidence as high as 8%

Ductal aneurysm most commonlypresents in infancy

Reported in adults, and may develop

after infective endarteritis, surgicalclosure, or transcatheter coil occlusion

one fourth of patients, an underlyingdisorder such as trisomy 21, trisomy 13,Smith-Lemli- Opitz syndrome, type IVEhlers-Danlos syndrome, or Marfanssyndrome is present


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One potentially promising technique isplacement of a covered stent in theaorta to simultaneously exclude the

aneurysm and occlude the ductusarteriosus.

Other Complications Recurrent laryngeal nerve paralysis even

without aneurysm

Dissection and/or spontaneous rupture

of an aneurysmally dilated pulmonaryartery due to PDA with pulmonaryhypertension


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Symptomatic : diuretics and digoxin Afterload reduction : ACE-I

Antidysrhythmia (AF, flutter)

Cardiovertion, maintained in sinus rhythmafter closure

Anticoagulation (AF)

Infective endocarditis prophylaxis -> allpatients with PDA until 6 months afterclosure


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Patients with PDA and pulmonaryvascular disease who are considered

unacceptable candidates for definitiveclosure may be managed withpulmonary vasodilating agents such aschronic oxygen, PGI2, calcium channelblockers, endothelin antagonists, andphosphodiesterase type V inhibitors.


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Historical Perspective

Techniques for closure of PDA haveevolved since the first report of surgicalligation by Gross and Hubbard in 1939

Transcatheter methods, to avoidthoracotomy, were pioneered byPortsmann et al, who reported use of a

conical Ivalon plug in 1967, and byRashkind and Cuaso, who reported initialresults of an umbrella-type device in1979


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After Cambier et al67 in 1992 reportedthe use of Gianturco coils for

transcatheter closure of PDA,transcatheter coil occlusion quicklybecame a widely used technique forclosure of the small to moderate patent

ductus

Indications for Closure of PDA

indicated for any child or adult who issymptomaticfrom significant left-to-rightshunting through the PDA


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In asymptomatic patients with significantleft-to right shunting that results in left

heart enlargement,closure is indicatedto minimize the risk of complications inthe future

In patients with pulmonary vascular

resistance >8 U/m2, lung biopsy hasbeen recommended to determinecandidacy for closure.

The indications for closure of patent

ductus with small shunts, including thosethat are tiny and incidentally discovered(silent), are less certain, particularly inolder adults.


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Transcatheter Closure

Treatment of choice for most patent

ductus in children and adults. Cases with calcified ductus arteriosus

with increased pulmonary vascular

resistance, transcatheter closure offersconsiderable advantages over surgicalclosure

Frequently involves cardiopulmonarybypass with an anterior approachthrough a median sternotomy


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Figure 4 demonstrates an example ofductus occlusion with a standard

Gianturco coil Nit-Occlud coil occlusion designed for

occlusion of vascular structures otherthan the patent ductus

For closure of moderate and largepatent ductus, the Amplatzer ductoccluder is frequently used (Figure 6).


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Figure 4. Example ofGianturco coilocclusion of PDA.

A, Views of a

Gianturco coil in its stretched out

configuration (top)and in its naturalcoiled configuration

(bottom). Note theattached Dacronfibers, which promotethrombosis, along itslength.

B through D, Lateralangiogramsdemonstrating closureof a PDA with a single0.038-in diameterGianturco coil.


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Figure 5. Example ofPDA closure with a Nit-OccludPDA occlusiondevice.

A, Image of a Nit-Occlud coil with itsbiconical

configuration. Notethe reversed windingon the proximal end.

B through D, Lateral

angiogramsdemonstrating closureof a PDA with a singleNit-Occlud coil.


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Figure 6. Example ofPDA occlusion withan Amplatzer ductoccluder device.

A, Image of anAmplatzer ductoccluder device.

B through D, Lateralangiogramsdemonstrating

closure of a PDA withan Amplatzer ductoccluder device.


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The availability of a variety of devices andtechniques enhances the capability toclose the vast majority of patent ductus

with catheter-based techniques. Complete closure rates at follow-up

generally exceed 90% to 95% in moststudies

The most common complication is deviceembolization

Other potentially important complications :flow disturbance in the proximal leftpulmonary artery or descending aorta froma protruding device, hemolysis, femoralartery or vein thrombosis.


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Greater pain and morbidity thantranscatheter methods

Surgical ligation and surgical division aresafe and effective procedures

Surgical ligation or division of the PDA remains the treatment of choice -> very

large ductus.

Complete closure rates of surgicalligation (often accompanied by divisionof the ductus) in published reports rangefrom 94% to 100%, with 0% to 2% mortality


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Complications : bleeding,pneumothorax, infection.


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PDA is a cardiovascular disorder found in

patients of all ages and sizes, from tinypremature infants to older adults

The clinical implications vary depending onthe anatomy of the ductus arteriosus and

the underlying cardiovascular status of thepatient

Over the past 3 decades, transcathetertechniques have replaced surgical therapy

in most patients with PDA. Echocardiography have resulted in

improved detection and characterizationof PDA in patients of all ages.


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Thank you

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