Patent Ductus Arteriosus

Ramachandra

The bottle neck of large PDA:Occasional missed large PDAs with or without Eisenmenger syndrome by even renowned cardiologist.

Time line1939:Surgical ligation by Gross and Hubbard1980:Maturation stages of ductus by

Gittenberger-De Groot AC et.al1989: Krichenko A, Benson LN, Burrows P, et al:

classification1967:First transcatheter closure by Portsmann

and coworkers1979:doubleumbrella device by Rashkind2003:Amplatzer device

Define

If ductus remains patent beyond 3 months of

life in full-term infants and beyond 1 year in premature infants, it is termed persistent PDA

Signature of PDA

• Most of them small• Seesaw murmur• TTE is enough for Dx and Rx• PDA with noise needs closure• Percutaneus closure is Rx-98% success• No IE prophylaxis

Foetal Life

PDA is life thread in normal developing heart like

part of series connection in electrical circuit shunting 60-70% oxygenated umbilical venous return to aorta

Post natal

After birth the duct closes functionally in 12 to 18 hours and anatomically in 2 to 3 weeks.

Embryology day 29 6th aortic /pulmonary arch develops 8th week of gestation, the ventral portions of the RT

and LT 6th AA form the proximal part of the RPA and the proximal part of LT MPA ,respectively. The dorsal portion of the right sixth arch is obliterated along with the right dorsal aorta. Sometimes the dorsal portion of the left 6th arch persists as a vascular conduit called PDA arising from the roof of the junction between the main and LPA and joining the left dorsal aorta just distal to the LSCA in normal left-sided aorta

Anatomy

• Usually LPDA• PDA and DTA angle at junction is 30 degree• Angiographic class: A to E (90 degree LL) by

Krichenko & colleagues®• 80% of PDA : A or B, Rx=Percutaneus closure• Siblings: Reverse , Rt AA,aneurysm•

Krichencko et.al:1989• Angiography • Dead left lateral• Left angiograms• Types– A:conical– B:window(L< 2 to 3 mm)– C:Tubular(both ends narrowing)– D:complex(multiple narrowing)– E :Elongated=a beaklike constriction at the

pulmonary end

Hemodynamic classification

• Small PDA :QP:QS <1.5 to 1• moderate PDA: QP:QS :1.5 and 2.2 to 1• large PDA:QP:QS >2.2 to 1.43• silent PDA :shunt is minimal/no murmur

detected on echocardiography

Reverse PDA

• Pulmonary atresia• Tricuspid atresia• Inferior angle near 90 degree OK but if <60

deree ,needs ductal stenting

Ductal aneurysm

90% spontaneous closure except large size causing pressure effect

Up to 8% reported of all PDA

Phenotypes Rt-sided PDA X RPA to the RT DTALPDA X RT Brachiocephalic A. LSCA X LPA Dual PDALPDA from LSCAVascular ring: SCA from RT DTA and runs behind

the trachea and esophagus, forming a around them by the right aortic arch anteriorly, and to the RT,the LSCA at the back and the PDA to the left.

Histology

• Mature:SMC are arranged longitudinally and circularly helping close by spasm

Physiology in foetus

• Life thread• Tunnels 70% saturate blood into DA• Only 7% of volume enters unexpanded lungs• Patency:Immature duct,low O2 ,high O2/PGE-2

from placenta• Functional closure:15th day• Anatomical closure:21st day=placenta turn off,

high O2 stops Ik ,intracellular ca2+ increase add to spasm in mature duct

Incidence

1/2000 births5% to 10% of CHDWith silent PDA ,Incidence is 1:500F>M(2:1)

Etiologic factors

• Sporadic• Multifocal(genetic+environmental+ low

O2(Asphyxia),rubella(First 4 weeks)/chemicals

Genetics

Chromosomal aberrations:Trisomy 21Single-gene mutations:Holt-Oram syndrome/

Char syndrome(TFAP2B mutations )X-linked mutations

Pathophysiology Small PDA :asymptomatic throughout life.Accidental detection by ECHO

for murmur Moderate PDA:compensate well throughout childhood and may remain completely asymptomatic in early adulthood but will eventually

present with exercise intolerance and symptoms related to left ventricular failure, usually starting in the third decade. Moderate to large:Large volume of blood leads to the very early

development of pulmonary congestion,decreased lung compliance, and failure of the left ventricle, often presenting within weeks after birth with failure to thrive, recurrent pulmonary infections, and even death. Pulmonary overcirculation remains uncorrected,the arteriolar medial hypertrophy, intimal proliferation,and eventual obliteration of pulmonary arterioles and capillaries will lead to an irreversible marked increase in pulmonary arterial pressure. When pulmonary vascular resistance exceeds the systemic vascular resistance, ductal shunting is reversed and becomes right to left (Eisenmenger syndrome)

Natural History

• Spontaneous closure may be delayed until 3 months of life, after which the closure rate is less than 0.6%/Yr

• Silent PDA remain undetected for life• premature :Closure could be delayed up to

1 year and more PDA• Sibling :1% and 5%• Parents:3%

Physical Examination

• Small PDA:Gr-II/III continuous murmur engulfing and peaking around S2

• Thrill :moderate to large PDA• S1 normal,S2 usual split with P2 accentuated• S3 and diastolic rumble : moderate/ large PDA• Eisenmenger syndrome:P2 loud/PSL/Graham

Still’s murmur• wide pulse :large shunt• Cyanosis/clubbing: Eisenmenger

ECG

• LAE• LVH• RVH

Chest Radiograph

• Small PDA: normal• moderate to large: increased pulmonary

vascular markings with prominent ascending aorta, and enlarged cardiac silhouette with prominence of the left atrium, left Ventricle and peripheral pruning

• Calcification

ECHO

• TTE allows the assessment of ductal size,geometry, the degree of shunt, and pulmonary artery pressures

• A left atrium/aorta ratio greater than 1.3/1 is considered to be a reliable marker of a hemodynamically significant ductal shunt

• Shunt ratio: continuity equation

Catheterization

• PDA closure• Hypertensive PDA

Management

• Ignore• Follow• Transcathetor closure• Surgical closure• IE prophylaxis

Class I closure

Evidence of volume overload on the left atrium or left ventricle (LAE/LVH)

Development of PAH but the pressure and the resistance still remain less than two-thirds of the systemic levels

Endarteritis

Class IIa closure

Small PDAs with normal PA pressures andnormal heart size with a shunt ratio less than1.5/1 or followed with repeat evaluationsevery 3 to 5 year

Class III closure

Silent PDAPDA with net right-to-left shunting

Closure method

• Cox inhibitors has no role in grown up• Percutaneus Methods: Coil and device• Surgical

Transcathetor

• Coils :<3 mm• Device:3-12mm

Post closure follow up

Six months with IE prophylaxis

The basic of transcathetor technique

• Coils :Retrograde aortic • Device :Antegrade veno-arterial• 7Fr venous and 6Fr arterial sheath• Pigtail angio in dead left lateral to decide• Device size is 2mm more than PA end• Cross with multipurpose and Terumo• Confirm with repeat angio• 6month F/U SBE prophylaxis

Success story of TCC

• ADO is 99% • immediate closure at the time of

implantation of 76%• day 1 of 89%• 6 to 12 months of 99% by echocardiography.

Complication

• Mortality in 1 / 439 cases• major events 2.3%• Device embolisation 2%

Surgicalvery large PDA unusual ductal anatomyDuctal aneurysmSignificant endarteritisAbscess• Methods: lateral thoracotomy,median

sternotomy, or VAT ligation• 100% success• Morbidity:long hospital stay,laryngial palsy

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