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Aortic coarctation (CoAo) is a common congenital heart disease that may occur isolated or associated to complex malformations. Giovan Battista Morgagni first described it in the XVIII letter of his book De sedibus and causis morborum per anatomen indagatis published in Venice in 1761. This publication represented one of the first systematical efforts to use anatomopathology as a tool to understand and explain clinical manifestations. In fact, before Morgagni, a disease was considered as an imbalance of ‘humours’ and fluids.
Nowadays, following a mechanistic approach, treatment of CoAo aims to get rid of the stenotic segment.
Treatment depends on many factors including patient size and age, type of lesion and individual anatomy. In older children, adolescents and adults, a transcatheter approach is usually preferred to the surgical treatment. Percutaneous procedures include balloon angioplasty and stent implantation. Even if balloon angioplasty has been shown favourable results, it may be complicated by aortic wall injury and a higher rate of recurrence.1 Therefore, in suitable anatomy and patient size, stent placement has become the treatment of choice.
Nevertheless, even after a ‘perfect’ anatomical repair, up to 30%–40% of patients may develop systemic arterial hypertension, irrespective of the approach used.1
Implantable stents are metallic frames and are considered stiffer than native tissue or surgical scar. Therefore, do stents work in reducing the impact of arterial systemic hypertension and its complications?
Meijs and colleagues2 made an interesting effort to add more evidences about that controversial topic. They performed a systematic literature review and meta-analysis about systemic blood pressure (BP) fate after stenting of CoAo. They selected, after careful review, 26 studies with a total of 1157 patients. They showed a median 20.3 mm Hg (95% CI 16.4 to 24.1 mm Hg) reduction in systolic blood pressure (SBP) from baseline to a median follow-up of 26 months (range 12–120 months). Also, an 8.2 mm Hg decrease in diastolic BP was observed. In particular SBP decreased from 152 mm Hg (132–178 mm Hg) at baseline to 129 (124–141 mm Hg) after stenting. Although various definitions of hypertension were used across studies, the rate of subjects with hypertension decreased from 78% (53%–100%) to 27% (5%–82%) after stenting. This was associated to a 40% reduction in patients using any antihypertensive treatment (75% at baseline vs 35% at follow-up), drug dose reduction in 70% of cases and drug number reduction from 1.6 to 1.1.
However, as also reported by authors, several and significant limitations exist. Some of them are typical to systematic review and meta-analysis studies. In fact, the quality of results depends on the quality of original studies. First, BP assessment mostly consisted in office measurements. This may have an effect both in the sense of increased and decreased values. As clearly reported by Morgan et al,3 significant hypertension is more frequently seen on BP monitoring and exercise test as opposed to one-off office BP evaluations.
Second, side matters in many issues in life and also in CoAo. In fact, in many studies it was not reported if either the right or left arm was used to check BP. Finally, publication bias was present as shown by funnel plot analysis and Egger’s test.
If stent implantation does not provide the solution, then a more valid alternative exists?
Unfortunately, similar problems occur even after surgical treatment. In fact, arterial hypertension may be found in up to 57% of subjects during long-term follow-up even in absence of restenosis and prosthetic material.4 Furthermore, several studies showed no differences in rate of hypertension between surgery and stent.5 6 Interesting studies in porcine model7 and computational fluid dynamic simulations8 have also shown that stent implantation does not impact on compliance, ventricular workload and blood flow.
Therefore, the causes of hypertension in this cohort of patients are not completely understood. Many abnormalities may be involved and they include impaired vascular function, hyperactivation of the renin–angiotensin system, autonomous nervous system imbalance, abnormal arterial compliance and abnormal activation of baroreceptors located in the convexity of aortic arch and in the carotid arteries.1 Interesting studies have shown that it is also possible that pre-existing histological anomalies and abnormal arterial stiffness indices are present in the prestenotic aortic tissue, while no differences were found in the descending aorta compared with control groups. It is possible that prenatal or early postnatal anomalies have an impact on the occurrence of systemic arterial hypertension even after perfect repair regardless of procedure performed.
In some way, CoAo could be considered as a systemic vascular disease of the precoarctation arteries.
Therefore, the puzzling answer to the occurrence of arterial systemic hypertension in subjects treated for CoAo is still unknown.
Probably, it is the time, in a modern way, to try to put together the mechanistic principles of Morgagni to a more holistic approach.
Further studies, aimed to compare different approaches and to understand the fine mechanisms, are needed to catch answers and propose new solutions.
In the meantime, in the field of interventional cardiology, we keep on implanting stents and carefully looking after results and follow-up of our patients.
Contributors GB conceived and wrote the paper.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
Patient consent for publication Not required.
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