Subcapsular hepatic hematoma as a complicating cardiac surgery

An 80-year-old woman was hospitalized for aortic valve insufficiency, paroxysmal atrial fibrillation, and ascending aortic aneurysm. She underwent aortic valve replacement, pulmonary vein isolation, left atrium appendectomy, and ascending aorta replacement. She developed a subcapsular hepatic hematoma during the surgery. The patient was managed conservatively and discharged successfully.

79 Platypnea–orthodeoxia syndrome as an uncommon cause of dyspnoea in a nonagenarian with aortic dissection

Methods and results Platypnea–Orthodeoxia syndrome (POS) is an uncommon but challenging clinical condition characterized by positional dyspnoea (platypnea) and arterial desaturation (orthodeoxia) in the upright position that improve in the supine position. POS can occur insidiously, as progressive unexplained oxygen desaturation for months or years, or as acute life-threatening unexplained hypoxaemia. The most common cause is the presence of an intracardiac shunt (patent foramen ovale and other interatrial defects) associated with a secondary anatomic or functional defect that serve as substrate for a right to left intracardiac shunt leading to oxygen desaturation. Conclusions Herein we present the case of a nonagenarian with a known history of ascending aortic aneurysm, that was admitted to the emergency department of our institution with a complaint of intermittent chest pain and dyspnoea. POS was then diagnosed, and the patient underwent a successful percutaneous closure with an Amplatzer™ device (25/25 mm) with minimal residual right-to-left shunt leading to a significant relief of the dyspnoea and improvement of arterial saturation. We also herein revise the clinical presentation, pathophysiology, diagnostic work-up, and management of patients with POS, aiming at increasing the awareness of this uncommon but often misdiagnosed treatable condition.

Computational analysis of aortic haemodynamics in the presence of ascending aortic aneurysm

BACKGROUND: The usefulness of numerical modelling of a patient’s cardiovascular system is growing in clinical treatment. Understanding blood flow mechanics can be crucial in identifying connections between haemodynamic factors and aortic wall pathologies. OBJECTIVE: This work investigates the haemodynamic parameters of an ascending aorta and ascending aortic aneurysm in humans. METHODS: Two aortic models were constructed from medical images using the SimVascular software. FEM blood flow modelling of cardiac cycle was performed using CFD and CMM-FSI at different vascular wall parameters. RESULTS: The results showed that highest blood velocity was 1.18 m/s in aorta with the aneurysm and 1.9 m/s in healthy aorta model. The largest displacements ware in the aorta with the aneurysm (0.73 mm). In the aorta with the aneurysm, time averaged WSS values throughout the artery range from 0 Pa to 1 Pa. In the healthy aorta, distribution of WSS values changes from 0.3 Pa to 0.6 Pa. CONCLUSIONS: In the case of an ascending aortic aneurysm, the maximum blood velocity was found to be 1.6 times lower than in the healthy aorta. The aneurysm-based model demonstrates a 45% greater wall displacement, while the oscillatory shear index decreased by 30% compared to healthy aortic results.

Inflammatory cells in the ascending aortic aneurysm in patients with type 2 diabetes versus patients with hypertension

Aortic aneurysms occur relatively frequently in the ascending thoracic aorta, but are rarely seen in patients with type 2 diabetes. Our aim was to evaluate inflammatory cell infiltration in the ascending aortic aneurysm wall in patients with diabetes without arterial hypertension (DM2 group, N=6) versus hypertensive non-diabetic patients (AH group, N=34). For histologic analysis, the sections were stained with hematoxylin-eosin and Movat pentachrome. The immunohistochemical staining was used to analyze the infiltration of pro-inflammatory (CD68) and anti-inflammatory macrophages (CD163), T helper (CD4) and T killer cells (CD8), and B (CD79a) and plasma cells (CD138) in all three layers of aneurysms of both groups. The statistical significance of the differences between groups was evaluated by ANOVA and the Welch test. In comparison to the AH group, the DM2 group developed less severe infiltration of pro-inflammatory macrophages (P=0.004) and B cells (P=0.025) in the tunica intima, and tunica media (P=0.049, P=0.007, respectively), and fewer plasma cells in the tunica media (P=0.024) and tunica adventitia (P=0.017). We found no significant differences in the number of T helper, T killer cells, and anti-inflammatory macrophages and in the amount of collagen and elastic fibers, ground substance, and smooth muscle cells in all three layers of the vessel wall. Except in tunica adventitia of DM2 group, there were more collagen fibers overall (P=0.025). Thus, we conclude that the histological structure of the aneurysm in diabetics without hypertension is almost the same as in hypertensive patients without diabetes. Diabetics had significantly less inflammatory infiltration in all three layers of the vessel wall, and more collagen fibers in tunica adventitia.