Journal of Marine Medical Society

CASE REPORT
Year
: 2019  |  Volume : 21  |  Issue : 1  |  Page : 94--96

Angioplasty for coarctation of the aorta: A case series


Jnanaprakash B Karanth1, R Ananthakrishnan1, Ravi Kalra2,  
1 Department of Medicine and Cardiology, INHS Asvini, Mumbai, India
2 Director and Commandant, Armed Forces Medical College, Pune, Maharashtra, India

Correspondence Address:
Surg VAdm Ravi Kalra
Director and Commandant, AFMC, Pune - 411 040, Maharashtra
India

Abstract

Coarctation of the aorta (CoA) is a constriction of the thoracic aorta commonly located distal to the left subclavian artery. It is more common in males and is associated with Turner syndrome, bicuspid aortic valve, and ventricular septal defect. It presents as angina on exertion, lower limb claudication along diminished femoral pulses, and unequal limb blood pressure records. Balloon angioplasty with or without stenting is the preferred treatment in native coarctation or recoarctation after surgery. Here, we report four cases that were successfully managed with balloon aortoplasty for CoA.



How to cite this article:
Karanth JB, Ananthakrishnan R, Kalra R. Angioplasty for coarctation of the aorta: A case series.J Mar Med Soc 2019;21:94-96


How to cite this URL:
Karanth JB, Ananthakrishnan R, Kalra R. Angioplasty for coarctation of the aorta: A case series. J Mar Med Soc [serial online] 2019 [cited 2020 Jul 5 ];21:94-96
Available from: http://www.marinemedicalsociety.in/text.asp?2019/21/1/94/260663


Full Text



 Introduction



Coarctation of the aorta (CoA) is a discrete narrowing of the thoracic aorta. The constriction is commonly just distal to the origin of the left subclavian artery (postductal). CoA can be either congenital or acquired. It may also be associated with other cardiac defects such as bicuspid aortic valve, mitral valve anomalies, and subaortic stenosis. Aortic narrowing can be an acquired, as in Takayasu arteritis or rarely, severe atherosclerosis.[1] We report four cases illustrating a spectrum of presentation of CoA.

 Case Reports



Case 1

A term male, appropriate for gestational age born to 28-year-old Gravida 2 Para 1 mother by spontaneous vaginal delivery. There was meconium-stained liquor. The neonate cried immediately after birth, and no resuscitation was required. He developed respiratory distress soon after delivery and was managed as a case of suspected meconium aspiration syndrome in the newborn intensive care unit.

On day 3 of life, the neonate developed anasarca, hypoxemia, bradycardia, and hypotension. On examination, lower limb pulses and blood pressures were not recordable, and oxygen saturations were low. Urgent bedside echocardiography done was suggestive of ductus-dependent complex congenital heart defect [Figure 1]. It revealed bicuspid aortic valve, biventricular dysfunction, left ventricle mildly hypoplastic, and severe discrete juxtaductal CoA with a gradient of 20 mm across the coarctation. He underwent surgical repair of CoA and defect was augmented with bovine pericardium patch on day 5 of life. Patent ductus arteriosus (PDA) was ligated. The neonate was shifted back to this center on the 2nd postoperative day for postoperative care and further management. During the course of hospital stay, oxygen saturation and blood pressure were normalized. The neonate was discharged home on breastfeeds. However, he was diagnosed to have a recurrence of coarctation on the 5th month of life during routine follow-up. The neonate underwent balloon dilatation [Figure 2] and is healthy and on the regular follow-up.{Figure 1}{Figure 2}

Case 2

A male neonate, term baby born to 28-year-old primigravida developed signs of respiratory distress at day 10 of life. On examination, he had tachycardia, peripheral pulses absent in lower limbs, tachypneic, bilateral basal crackles, and hepatomegaly 4 cm below the right costal margin. Bedside echocardiography revealed CoA with systolic pressure gradient of 49.22 mmHg across the narrowed segment, severe tricuspid regurgitation, and biventricular dysfunction. He was intubated and started on injection prostaglandin E1 infusion. Due to severe biventricular dysfunction, the neonate was taken up for urgent balloon dilatation. Pressure gradient was 10 mmHg across the segment postdilatation [Figure 3].{Figure 3}

Case 3

A 6-year-old female child was diagnosed with mid-muscular ventricular septal defect (VSD) and aortic arch hypoplasia at 1 year of life. She was operated with patch closure of VSD at AIIMS. She was asymptomatic and lost to follow-up for 4 years. On routine examination, her pulses were absent in both popliteal and dorsalis pedis with radiofemoral delay. The systolic blood pressure difference of more than 40 mmHg was noted in the upper and lower limbs. Computed tomography aortogram revealed CoA [Figure 4]. She underwent balloon dilatation. Her echocardiography revealed systolic pressure gradient of 51.64 mmHg predilatation which reduced to 8.8 mmHg postdilatation.{Figure 4}

Case 4

A 21-year-old woman, with no known comorbidities, was found to be hypertensive during her first antenatal checkup at 16 weeks. On examination, the pulsation in femoral, popliteal, and dorsalis pedis was feeble on palpation in both the legs with a radiofemoral delay. The blood pressure was 170/96 in right upper lobe (RUL), 210/100 in left upper lobe (LUL), and 100/70 mmHg in both lower limbs. There was an ejection systolic murmur at the aortic area and a soft systolic murmur over the back. Chest radiograph with an abdominal shield showed borderline cardiomegaly and rib notching of the inferior margins.

Echocardiography revealed a left-sided aortic arch, with severe coarctation after the origin of the left subclavian artery with thin antegrade flow, and a peak systolic gradient across the coarcted segment of 75 mmHg. The narrowest diameter of the coarcted segment was 4 mm. There was no other congenital defect. There was mild concentric left ventricular hypertrophy with good biventricular systolic and diastolic functions.

She was taken up for an aortography which revealed severe aortic coarctation with the ledge of tissue opposite the origin of the left subclavian and left common carotid arteries [Figure 5]. The ascending aortic pressure was 179/97 mmHg, and the femoral artery pressure was 104/79 mmHg. A percutaneous transluminal balloon aortoplasty was performed with a 20 mm × 40 mm balloon with the disappearance of the waist during dilatation [Figure 6]. Postprocedure, the ascending aortic pressure was 133/73 mmHg, and the femoral artery pressure was 113/67 mmHg. There were no postprocedural complications. The gradient reduced to 14 mmHg across the coarcted segment. She subsequently delivered a healthy baby by a lower segment cesarean section at term. She is presently asymptomatic with mild hypertension requiring low dose of beta-blockers.{Figure 5}{Figure 6}

 Discussion



CoA accounts for 6%–8% of all congenital heart defects.[2] When the PDA and patent foramen ovale are closed at birth, the entire cardiac output to the lower extremity must cross the narrowed aortic segment leading to heart failure or cardiogenic shock.

The classic findings are systolic hypertension in the upper extremities, diminished or delayed femoral pulses, and low or unobtainable arterial blood pressure in the lower extremities.[3] Patients with CoA have an increased frequency of intracranial aneurysms.[4] Females are at increased risk of death from rupture or dissection of the aorta during pregnancy.[5]

The management guidelines by the American Heart Association 2011, for adult and pediatric patients with CoA, recommend correction of coarctation to be performed in early childhood to prevent the development of systemic hypertension. If coarctation escapes early detection, the repair should be performed at the time of diagnosis.[6]

 Conclusion



CoA is one of the common congenital anomalies and often missed if the newborn is asymptomatic. The repair of CoA during early childhood is associated with less systemic hypertension and improved long-term outcome.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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