1. Coarctation of the aorta causes obstruction to left ventricular outflow, resulting in elevated systolic blood pressure and hypertension in the upper body. It can lead to left ventricular hypertrophy and heart failure. 2. Echocardiography is useful for visualizing the coarctation segment and assessing the severity based on peak systolic velocity and diastolic flow. Chest x-rays may show rib notching from collateral circulation in older children. 3. In neonates, features of right ventricular hypertrophy may be seen on ECG due to ductal-dependent lower body circulation. Over time, left ventricular hypertrophy patterns emerge on ECG in children and adults with coarct

1. Coarctation of Aorta

2. Pathophysiology
• Fetal hemodynamics –Least disturbed (only 10 % combined ventricular
output transverses the aortic isthmus)
• After birth , the pathophysiology depends on :-
1. Degree of obstruction
2. Type of COA
3. Rapidity of development of obstruction
4. Status of ductus arteriosus
5. State of collateral circulation
6. Associated intracardiac lesion

3. • Coarctation of aorta ->increases impedance of LVOT->Elevated systolic
pressure in LV and Asc. Aorta:-
1. Left ventricular myocardial hypertrophy
2. Upper body systolic hypertension
3. Systolic pressure gradient across the coarctation
• Myocardial hypertrophy normalizes myocardial wall stress and
ventricular afterload and maintains normal ventricular function .

4. • Perfusion to lower limb maintained via collaterals
• Patient remains asymptomatic for until complications of left
ventricular hypertrophy ,degenerative aortic changes or chronic
systemic hypertension occur.

5. • Coarctation develops rapidly ->Rapidly increasing afterload->left ventricular failure .
• Manifestations of left ventricular failure:-
1. Left ventricular systolic dysfunction
2. Ventricular dilatation
3. Mitral regurgitation
4. Elevated left ventricular end-diastolic pressure
5. Elevated atrial pressure
6. Pulmonary venous congestion
7. Potential for left to right atrial level shunting through foramen ovale
Severe hypoperfusion of organs distal to coarctation:-
• Metabolic acidosis
• Oliguria
• Gut ischemia
• Cold constricted extremities

6. • Ductus arteriosus wide open:- RV output provides lower body
perfusion via the ductus , Sev. Hypoperfusion of lower body is avoided
• Acute Left ventricular decompensation depends upon the acuteness of
ductal closure:-
1. Rapid ductal closure ->LV fails , lower body hypoperfusion
2. Gradual ductal closure-> Time for LV hypertrophy and Collateral
formation.

7. Associated Intracardiac defects
• Commonly a VSD is present
• Due to VSD pulmonary artery pressure remains elevated for more prolonged
period after birth.
• VSD + PDA-> Lower body perfusion maintained for longer period
• Due to fall in pulmonary vascular resistance and closure of PDA :- Lower body
hypoperfusion occurs
• Increased systemic afterload due to coarctation + decreased PVR-
>Ventricular level left to right shunt increases ->LV failure due to volume
overload + increased after load.
• Patients with VSD and COA always develop severe symptoms in neonatal
period or in the early infancy.

8. Abnormalities in vascular physiology
• Systolic arterial hypertension:-
1. Aortic obstruction
2. Increased reactivity of arteriolar resistance vessels
3. Reduced compliance of aortic wall
4. Resetting of the baroreceptor reflex
5. Increased plasma renin activity

10. ECG
• Standardization and speed :- 12 lead ECG , 25 MM/SEC , 1MM=0.1
MV
• RATE:- 300/LARGE BOXES , 1500/SMALL BOXES
• AXIS:-
• P WAVE
• PR INTERVAL
• QRS
• ST SEGEMENT
• T WAVES

11. Infants and neonates
• The electrocardiogram (ECG) usually shows right ventricular
hypertrophy in the first few months of life, even with isolated
coarctation.
About two thirds of infants operated on in the first year of life have
right ventricular hypertrophy or combined hypertrophy, and fewer than
25% have pure left ventricular hypertrophy.

12. ECG
• In the neonatal period , the ECG may reflect RVH rather than LVH.
• This is because the right ventricle in-utero is the dominant ventricle, and
through the PDA pumps blood to the descending aorta.
• In Infancy ECG is generally normal

13. Childhood(1-14 yrs)
• ECG shows predominantly left ventricular hypertrophy, with right
ventricular hypertrophy present only when there is pulmonary
hypertension with elevated pulmonary vascular resistance.
• ECG is normal in about one third of children.
Adolescence (Beyond 14 Years) and Adult Life
• Left ventricular hypertrophy and features of left ventricular
failure on ECG

14. • In an infant the findings of left ventricular hypertrophy with strain
pattern (ST SEGMENT DEPRESSION AND T WAVE INVERSION):-
1. Strongly suggests the associated presence of aortic stenosis or endocardial
fibroelastosis
• Older patients have findings of left ventricular hypertrophy usually
without strain.
• Bicuspid aortic valve – Q wave of left precordial AR causing LVVO

17. Electrocardiogram
1. Symptomatic (sick) neonate with
pulmonary venous congestion-
The QRS axis is rightward.
tall p wave in lead 1 (rt atrial)
Right ventricular hypertrophy is
manifested by a tall monophasic R wave
in led V1 and deep S waves in left
precordial leads.

18. 2. Coarctation after childhood
The QRS axis is normal.
Normal P wave in lead 2 .
Left ventricular hypertrophy is suggested by
deep S wave in V1 and tall R wave in v5 with
low, flat, or inverted T waves in left precordial
leads

19. • Electrocardiography (ECG) showed sinus rhythm with features of
extreme right axis deviation with absent left ventricular forces in
leads V4 to V6 ( 20 DAY OLD TERM CHILD)

20. RIGHT VENTRICULAR HYPERTROPHY ECG
Axis: RAD for the patients age
Voltages: Tall R waves (greater than limits for patient’s age) in right-sided leads V4R and V1. Deep S waves (greater than limits for
patient’s age) in left-sided leads V5 and V6.
R/S ratio: Abnormal R/S ratio in favour of RVH.
•Increased R/S ratio (greater than upper limits for child’s age) in V1-2.
•R/S ratio < 1 in V6 (after one month of age).
Abnormal T waves: Upright T waves in V1 and V4R in children 3 days to 6 years (provided that T waves are normal elsewhere, i.e.
upright in V6). This is evidence alone of significant RVH.
Abnormal Q waves: qR pattern in V1 (small Q wave, tall R wave) = highly specific for RVH.
• Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
• Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
• Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.

22. R Wave Peak Time (Intrinsicoid deflection)
• The time from the onset of the earliest Q or R wave to the peak of the
R wave in the lateral leads (aVL, V5-6).
• Represents the time taken for excitation to spread from the
endocardial to the epicardial surface of the left ventricle.
• R-wave peak time is said to be prolonged if > 45ms FOR Left LEADS
AND >35 MS FOR RIGHT LEADS

23. COA IN 11 YRS FEMALE

26. CHEST XRAY
• VIEW
• EXPIRATORY OR INSPIRATORY
• MARKER LOCATION
• EXPOSURE
• CENTRALISATION
• ABDOMINAL SITUS
• BRONCHIAL SITUS
• CARDIAC POSITION
• CARDIAC APEX
• AORTIC ARCH sidedness
• CTR

27. X-ray
• In an infant with congestive heart failure :-X-RAY non specific except for
cardiomegaly and pulmonary congestion.
• In asymptomatic infants and young children :- x-ray is normal.
• In children and adolescents heart is only mildly enlarged

28. The x-ray in symptomatic infants
• Pulmonary venous congestion with dilation of the right
ventricle and the right and left atria
• Left ventricular size remains normal or nearly so

29. • VIEW
• ROTATED FILM
• OVER EXPOSED
• ABDOMINAL SITUS-SOLITUS
• BRONCHUS SITUS-SOLITUS
• CARDIAC POSITION-LEVOPOSITION
• CARDIAC APEX-LEVOCARDIA
• CTR-0.7
• RV TYPE APEX
• STRAIGHTENIG OF LEFT HEART BOR.
• PROMINENT PA SEGMENT
• FEATURES OF PVH AND
PULMONARY EDEMA

30. CEPHALISATION
KERLEY B
CARDIOMEGALY
1
2
3
4

31. • In children and young adults
• The post-coarctation descending
thoracic aorta has a distinctive
leftward convexity that is
accompanied by dilation of the left
subclavian artery .

32. 30 YRS FEMALE WITH COARCTATION
LSCA AND ARCH DILA.
COA
POST. STENO DILA.

33. ADULT COARCTATION CHEST XRAY (35 YRS/MALE)

34. • The figure 3 sign is seen in aortic coarctation and is formed by
prestenotic dilatation of the aortic arch and left subclavian artery,
indentation at the coarctation site (also known as the "tuck"), and
post-stenotic dilatation of the descending aorta.
FIGURE 3 SIGN

37. • On barium studies of the esophagus in patients with aortic
coarctation, a corresponding contour abnormality is demonstrated,
referred to as the reverse figure 3 sign or E sign.
REVERSE FIGURE 3 SIGN OR E SIGN

39. Notching of the ribs
Classic radiologic sign of coarctation
caused by collateral flow through
dilated, tortuous, pulsatile posterior
intercostal arteries.
Rib notching seldom appears before age
of 6 years ( 3 years, Kirklin)
Typical coarctation distal to the LSCA
results in bilateral notching between
the third and the eighth posterior ribs
When the LSCA lumen is compromised
- unilateral rib notching is confined to
the right hemithorax
Anomalous origin of the RSCA distal to
the coarctation - unilateral notching is
confined to the left

40. • PA VIEW
• WELL CENTRALISED
• APPROPRIATE EXPOSURE
•
• ABDOMINAL SITUS-SOLITUS
• BRONCHUS SITUS-SOLITUS
• CARDIAC POSITION-LEVOPOSITION
• CARDIAC APEX-LEVOCARDIA
• CTR-0.55

43. COLLATERAL CIRCULATION
• RARE IN NEONATES
• DEVELOPS IN CHILDHOOD (>5YRS)
• Rib notching is caused by erosion of the inferior surfaces of posterior ribs by dilated and tortuous
intercostal arteries
• First two are not involved as first and second intercostal arteries do not form collateral channels
• SEEN IN INF BORDER OF 3-6 (..9)RIBS
• RT SIDED RIB NOTCHING ONLY-?
• LT SIDED RIB NOTCHING ONLY- ?

47. • Causes of U/L Rib Notching
• Neurofibromatosis
• Post classic BT shunt
• A-V malformation
• Left SCA origin stenosis
• Causes of B/L Rib notching
• COA
• IAA
• Multiple myeloma
• Osteogenesis imperfecta
• Osteoclastic malignancy
• SVC obstruction with venous collaterals

49. 2D ECHO

51. Echocardiogram
Echo assessment is helpful in-
1. Coarctation segment itself is visualised
2. LV changes in coarctation – Size,cavity, thickness, systolic and
diastolic function.
3. Associated lesions- VSD, BAV,etc
Supra-sternal notch window/ parasternal view
with colour flow imaging is identifies the coarctation by a zone
of localized accelerated flow
Peak systolic velocity - reflects maximal systolic gradient
Persistent high-velocity diastolic forward flow - indicates
severity

52. ECHO IN COA
• SITE OF COA
• MORPHOLOGY OF COA
• COARCTATION SHELF
• SEVERITY OF COA
• PDA
• POST STENOTIC DILATATION / ANEURYSM
• GRADIENTS
• DISSECTION
• ARCH VESSELS
• AORTIC ARCH
• LV FUNCTION
• CORONARY ARTERIES
• ASSOCIATED ABNORMALITIES

53. ASSOCIATED ABNORMALITIES
• AORTIC VALVE MORPHOLOGY-BICUSPID VALVE
• LVOT EVALUATION
• VSD
• CONGENITAL MS /PARACHUTE MITRAL VALVE
• SUPRA MITRAL RING
• TGA
• SINGLE VENTRICLE
• AVSD
• DORV
• TAPVC/PAPVC

55. SUBCOSTAL VIEW

56. SUBCOSTAL VIEW

57. APICAL 4 CHAMBER VIEW

58. DOPPLER APICAL FOUR CHAMBER MITRAL

59. DOPPLER APICAL 4 CHAMBER TRICUSPID

60. APICAL 5 CHAMBER VIEW

61. DOPPLER APICAL 5 CHAMBER VIEW

62. DOPPLER APICAL 5 CHAMBER VIEW

63. PARASTERNAL LONG AXIS VIEW

65. PARASTERNAL LONG AXIS VIEW COLOR DOPPLER

66. PSAX LV

67. PSAX ARCH

69. PSAX ARCH DOPPLER

70. PSAX NO PDA

71. PSAX AORTIC LEVEL

72. NORMAL
7-11MM
16-19 /M2
7-11 MM
19-32/M2

74. DIASTOLIC TAILING –DIFF. PATIENT

76. AMATO TYPE 1

77. MEMBRANOUS COA

78. AMATO TYPE 2

79. AMATO TYPE 3

81. MRI and CT
Currently the imaging modalities of choice for coarctation in patients beyond infancy
Utility of MR/CT is in –
• Anatomy not clear in 2d echo –Better visualization of anatomy
• Assessing Coarctation morphology
• Assessment of ascending aorta / arch / DTA
• Collaterals
• Aneurysm formation
• Aortic Dissection
• Anomalous origin of arch vessels
• Airway assessment
• Vascular rings

82. MRI
• No radiation exposure
• Useful for post-interventional structural imaging for follow-up
• In advance stages to look for LV fibrosis
• Hemodynamic assessment
• Assessment of collateral flow
• Determine the significance of coarctation or recoarctation.

83. 8 MONTHS /FEMALE

88. 4 months/ female

92. Cardiac catheterization and aortography
• Once the standard for diagnosis in older patients - now
secondary
• Now only indication is when balloon dilatation is
indicated or any other intervention .
• A withdrawal gradient is present at rest across the
coarctation- >20 mm Hg is significant

93. Gradient may be falsely assessed on cath due to
• Collateral flow may increase the pressure in the aorta
distal to the coarctation
• Poorly contracting LV
• Low output state
• Multiple left sided obstructed lesions
In such cases gradient is better measured by aortography
• CoA is evident by a decrease in diameter by 50 %
• Aortography also reveals any hypoplasia of the isthmus
or arch, arrangement of the aortic arch branches,
degree of collateral circulation, and presence of an
aneurysm.

94. COA 11 YR /F CATH ANGIOGRAM