Thoracic aortic surgery and TEVAR
Thoracic aortic aneurysm is most commonly (in 70% of cases) located in the ascending aorta and remains asymptomatic for a long time. The risk of rupture directly correlates with diameter: at sizes over 6 cm, the annual risk reaches 3.6%. The main goal of treatment is to prevent rupture by excluding the aneurysmal sac from the bloodstream.
Endovascular repair (TEVAR) demonstrates excellent results with a 30-day mortality rate of 2–5% in elective procedures. The threshold for TEVAR is 5.5 cm (or 4.3 cm in Marfan syndrome), whereas for open surgery it is higher at 6 cm due to greater invasiveness.
Absolute contraindications for endovascular treatment include patient refusal, extremely low life expectancy or cardiopulmonary reserve, hemodynamic instability, and pathology localization in the ascending aorta (if a surgical alternative exists). At the same time, vessel rupture, mycotic aneurysms, or malignancy are not obstacles to the procedure. Spinal cord ischemia due to occlusion of the artery of Adamkiewicz remains a significant risk in thoracic aorta interventions (~3% probability of paraplegia). Unlike open surgery, TEVAR does not allow for reimplantation of intercostal vessels.
Cyanosis in congenital heart defects
Patients with congenital heart disease (CHD) may present with cyanosis caused by three main pathophysiological mechanisms:
- Decreased pulmonary blood flow. Occurs in right ventricular outflow tract obstruction (e.g., Tetralogy of Fallot). Outflow resistance forces deoxygenated blood to shunt right-to-left through septal defects. Pulmonary function is preserved, but the volume of oxygenated blood is critically low.
- Parallel circulation. Observed in transposition of the great arteries (TGA). The aorta arises from the right ventricle, and the pulmonary artery from the left. Without an intracardiac shunt (such as a patent ductus arteriosus), this condition is incompatible with life.
- Intracardiac mixing. Occurs in single atrium, single ventricle, or truncus arteriosus (truncus arteriosus). The degree of cyanosis depends on the proportion of deoxygenated blood in the common pool.
Many CHDs are successfully operated on in childhood, but adult patients require lifelong monitoring due to the risk of residual lesions or pulmonary arterial hypertension, which develops secondary to prolonged pulmonary bed overload.
Single-ventricle palliative surgery
The concept of a "single ventricle" encompasses defects where creating two independent, fully functioning circulatory loops is surgically impossible. The goal of treatment is the staged separation of systemic and pulmonary circulations so that the single ventricle drives the systemic circuit, while venous return passively enters the lungs.
Stages of Fontan circulation formation:
- Stage I (neonatal period): Creation of a systemic-to-pulmonary shunt (e.g., modified Blalock-Taussig shunt). This is a temporary measure until pulmonary vascular resistance naturally decreases.
- Stage II (3–9 months): Bidirectional cavopulmonary anastomosis (Glenn procedure). The superior vena cava is connected to the pulmonary arteries, and previous shunts are taken down.
- Stage III (1.5–5 years): Total cavopulmonary connection (TCPC). The inferior vena cava is routed to the pulmonary arteries via an extracardiac conduit or intracardiac tunnel.
Despite extending life, a "failing Fontan" syndrome may develop over time, characterized by systemic venous hypertension, plastic bronchitis, and protein-losing enteropathy. Heart transplantation is frequently required in such cases.
To remember the three causes of cyanosis in CHD: "Low (decreased blood flow), Miss (parallel circulation), Mixed (mixing)."
Class and exam questions
When is immediate surgical treatment indicated for an asymptomatic aneurysm?
Intervention is mandatory in cases of rapid aneurysm growth (1 cm or more per year) or when compression symptoms of surrounding tissues appear, regardless of absolute size.
Why does the risk of paraplegia occur during TEVAR?
Stent-graft placement may occlude radicular arteries (especially the artery of Adamkiewicz) supplying the spinal cord, leading to ischemia.
How is atrial situs determined on ultrasound?
Atrial situs is determined by the morphology of the atrial appendages. The right atrial appendage has a wide base and prominent pectinate muscles, whereas the left appendage is tubular with a less prominent muscular relief.
What else to study on this topic
- Organization of three-phase cardiac rehabilitation after valve replacement
- Specific TEVAR complications: types of endoleaks and stent-graft migration
- Sequential segmental analysis algorithm for diagnosing complex CHD
- Imaging methods in anomalous pulmonary venous drainage (ultrasound, MRI)
- Hemodynamic parameters and collateral blood flow assessment prior to TCPC
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