Aortic graft infection is a feared complication after open abdominal aortic aneurysm repair secondary to its high mortality. Perigraft air is a common finding after open aortic aneurysm repair; however, it is also associated with aortic graft infection. Delineating between graft infection and common postoperative finding is a challenge. This is further complicated by use of hemostatic agents such as Gelfoam, which is also documented to cause perigraft air. Correct diagnosis has crucial implications in management of potential aortic graft infection, which is a vascular emergency. We report a case of perigraft air in a patient status after open aortic aneurysm repair with associated clinical manifestations of infection in whom conservative management and surveillance was selected for treatment. We then discuss the timeline of perigraft air, potential causation, importance of history, and physical examination, and finally, we discuss how specific findings on computed tomography imaging for infection in other areas may be useful in aortic graft infection.

The risk of rupture, the most feared clinical consequence of abdominal aortic aneurysm, increases with the enlargement of aorta. MicroRNA-29b (miR-29b) has emerged as a key modulator of extracellular matrix (ECM) homeostasis and thereby is proposed to play a crucial role in vascular remodeling. However, agents that alter miR-29b expression are relatively inefficient in the aorta, likely due to inferior uptake. Herein we found that miR-29b was upregulated in aortic smooth muscle cells upon prostaglandin E2 (PGE2) stimulation whereas indomethacin treatment downregulated miR-29b expression. In order to obtain insight into the pathological processes associated with the vascular remodeling that accompanies aortic dilatation, we compared expression profiles of several representative ECM components in aortic walls. Notably, PGE2 induced a dramatic decline in these ECM components, which was rescued by introduction of indomethacin. In addition, COL1A1 was validated as a direct target gene of miR-29b by dual-luciferase reporter assay. In aggregate, our study suggests that PGE2 may accelerate ECM degradation through decreasing miR-29b expression. Thus those anti-inflammatory drugs that inhibit PGE2 synthesis represent an effective means of inducing an augmented profibrotic response in the aortic walls and thereby inhibiting aneurysmal expansion.

The abdominal aorta is the most common site of an aortic aneurysm. The visceral and most proximal infrarenal segment (aneurysm neck) are usually spared and considered more resistant to aneurysmal degeneration. However, if an abdominal aortic aneurysm (AAA) is left untreated, the natural history of the aortic neck is progressive dilatation and shortening. This may have significant implications for patients undergoing endovascular repair of AAAs (EVAR) as endograft stability and integrity of the repair are dependent on an intact proximal seal zone. Compromised seal zones, caused by progressive diameter enlargement and foreshortening of the aortic neck, may lead to distal endograft migration, type Ia endoleak, aortic sac repressurization, and, ultimately, aortic rupture.

The technologies and innovations applicable to endovascular treatment for complex aortic pathologies have progressed rapidly over the last two decades. Although the initial outcomes of an endovascular aortic repair have been excellent, as long-term data became available, complications including endoleaks, endograft migration, and endograft infection have become apparent and are of concern. Previously, the indication for endovascular therapy was restricted to descending thoracic aortic aneurysms and abdominal aortic aneurysms. However, its indication has expanded along with the improvement of techniques and devices, and currently, it has become possible to treat pararenal aortic aneurysms and Crawford type 4 thoracoabdominal aortic aneurysm (TAAA) using the off-the-shelf devices. Additionally, custom-made devices allow for the treatment of arch or more extensive TAAAs. Endovascular treatment is applied not only to aneurysms but also to acute/chronic dissections. However, long-term outcomes are still unclear. This article provides an overview of available devices and the results of endovascular treatment for various aortic pathologies.

Abdominal aortic aneurysm (AAA) is defined as a permanent dilatation of the abdominal aorta that exceeds 3 cm. Most AAAs arise in the portion of abdominal aorta distal to the renal arteries and are defined as infrarenal. Most AAAs are totally asymptomatic until catastrophic rupture. The strongest predictor of AAA rupture is the diameter. Surgery is indicated to prevent rupture when the risk of rupture exceeds the risk of surgery. In this review, we aim to analyze this disease comprehensively, starting from an epidemiological perspective, exploring etiology and pathophysiology, and concluding with surgical controversies. We will pursue these goals by addressing eight specific questions regarding AAA: (1) Is the incidence of AAA increasing? (2) Are ultrasound screening programs for AAA effective? (3) What causes AAA: Genes versus environment? (4) Animal models: Are they really relevant? (5) What pathophysiology leads to AAA? (6) Indications for AAA surgery: Are surgeons over-eager to operate? (7) Elective AAA repair: Open or endovascular? (8) Emergency AAA repair: Open or endovascular?