Coarctation of the aorta

Hemodynamic disturbances and compensation

The pathogenesis of the disease is centered around a mechanical obstruction to blood flow. In the vast majority of cases (about 95%), the narrowing is located distal to the origin of the left subclavian artery from the aorta.

This creates two completely different hemodynamic beds:

• Zone above the narrowing: Persistent arterial hypertension develops here. Both systolic and diastolic blood pressure values increase. This specific factor forces the heart to work under increased load. Pressure overload inevitably leads to the development of left ventricular hypertrophy.
• Zone below the narrowing: Blood flow in the lower half of the trunk is diminished, manifesting as arterial hypotension.

To compensate for the lack of blood supply by bypassing the obstruction, the body initiates the development of collateral circulation. First and foremost, the intercostal arteries and chest wall vessels dilate and take on the load. It is worth noting that this defect is statistically significantly associated with another anomaly—a bicuspid aortic valve.

Symptoms and clinical presentation

Symptoms in patients with this defect appear quite late. As a rule, the disease first manifests as arterial hypertension at a young age—typically between 15 and 30 years.

All symptoms are clearly divided into two groups depending on the hemodynamic profile:

1. Symptoms of upper body hypertension: Patients are troubled by frequent and severe headaches, and spontaneous nosebleeds may occur.
2. Symptoms of lower body ischemia: Due to inadequate blood supply, patients complain of chronically cold feet and rapid leg fatigue during physical exertion. A characteristic sign is the onset of calf pain while walking, clinically described as intermittent claudication.

Physical examination findings

A thorough patient examination can reveal a number of specific signs pointing to coarctation.

• Palpation and inspection: Visual inspection and palpation reveal a forceful apical impulse displaced laterally—a reliable sign of an enlarged left ventricle. Visible pulsation of dilated intercostal arteries acting as collaterals can sometimes be noted on the chest.
• Blood pressure measurement and pulse assessment: The key marker is blood pressure dissociation. BP figures are high in the brachial arteries, whereas blood pressure in the femoral arteries remains normal or pathologically decreased. Asymmetry of pulse and blood pressure between the patient's right and left arms is frequently recorded.
• Auscultatory findings: Auscultation of the heart in the 2nd right intercostal space at the sternal border reveals a prominent systolic murmur. An important feature of this murmur is its radiation: it is well heard over the neck vessels and is also transmitted to the back—into the interscapular region.

Instrumental diagnostics and complications

Various instrumental visualization and functional diagnostic methods are used to confirm the diagnosis.

• Chest X-ray: Allows detection of a pathognomonic sign of the defect—notching of the inferior rib contours. This erosion of bone tissue occurs due to the constant mechanical pressure of pulsating, markedly dilated intercostal arteries.
• Electrocardiography (ECG): Reflects characteristic signs of pronounced left ventricular myocardial hypertrophy.
• Angiography (aortography): Considered the "gold standard" of diagnostics. The procedure allows precise determination of the localization and degree of narrowing of the aortic trunk, which is critically important for planning surgical intervention.

If the disease is not diagnosed in time, severe complications may develop in the late stages. These include progressive heart failure, formation of a dissecting aortic aneurysm, infective endocarditis, and fatal cerebral hemorrhages against the background of uncontrolled severe hypertension.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of collateral circulation formation via chest wall arteries.
• Pathogenesis of left ventricular hypertrophy development under pressure overload.
• Differential diagnosis of the causes of pulse and BP asymmetry in the upper extremities.
• Risk of developing a dissecting aortic aneurysm and infective endocarditis as late complications.

Other topics in the "Cardiovascular system" section

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