Management of floating thrombus in the aortic arch

OBJECTIVE Floating aortic thrombus is an underrecognized source of systemic emboli and carries a life-threatening risk of stroke when located in the aortic arch. Optimal treatment is not established in available guidelines. We report our experience in managing floating thrombi in the aortic arch. METHODS Consecutive patients diagnosed with a floating aortic arch thrombus at a tertiary referral center between January 2008 and December 2014 were reviewed. Perioperative and midterm outcomes were assessed. RESULTS Ten patients (8 female) with a median age of 56 years (range, 47-82 years) were identified. Eight patients presented with a symptomatic embolic event, and 2 patients were asymptomatic. One patient presenting with stroke due to embolic occlusion of all supra-aortic vessels died 2 days after admission. Three patients (2 asymptomatic and 1 unfit for surgery) were treated conservatively by anticoagulation, leading to thrombus resolution in 2 patients. In the third patient, the thrombus persisted despite anticoagulation, resulting in recurrent embolic events. The remaining 6 patients underwent open thrombectomy of the aortic arch during deep hypothermic circulatory arrest. All patients treated by surgery had an uneventful postoperative course with no recurrent thrombus or embolic event during follow-up. Median follow-up of all patients was 17 months (range, 11-89 months). CONCLUSIONS Floating aortic arch thrombus is a dangerous source of systemic emboli. Surgical removal of the thrombus is easy to perform and followed by good clinical results. Conservative treatment with anticoagulation may be considered in asymptomatic, inoperable or high-risk patients.

Connexin 43 expression in human hypertrophied heart due to pressure and volume overload

Left ventricular hypertrophy (LVH) is due to pressure overload or mechanical stretch and is thought to be associated with remodeling of gap-junctions. We investigated whether the expression of connexin 43 (Cx43) is altered in humans in response to different degrees of LVH. The expression of Cx43 was analyzed by quantitative polymerase chain reaction, Western blot analysis and immunohistochemistry on left ventricular biopsies from patients undergoing aortic or mitral valve replacement. Three groups were analyzed: patients with aortic stenosis with severe LVH (n=9) versus only mild LVH (n=7), and patients with LVH caused by mitral regurgitation (n=5). Cx43 mRNA expression and protein expression were similar in the three groups studied. Furthermore, immunohistochemistry revealed no change in Cx43 distribution. We can conclude that when compared with mild LVH or with LVH due to volume overload, severe LVH due to chronic pressure overload is not accompanied by detectable changes of Cx43 expression or spatial distribution.

Cellular actors, Toll-like receptors, and local cytokine profile in acute coronary syndromes

Inflammation plays a key role in acute coronary syndromes (ACS). Toll-like receptors (TLR) on leucocytes mediate inflammation and immune responses. We characterized leucocytes and TLR expression within coronary thrombi and compared cytokine levels from the site of coronary occlusion with aortic blood (AB) in ACS patients.

Endothelial Progenitor Cells Induce a Phenotype Shift in Differentiated Endothelial Cells towards PDGF/PDGFR Axis-Mediated Angiogenesis

BACKGROUND: Endothelial Progenitor Cells (EPC) support neovascularization and regeneration of injured endothelium both by providing a proliferative cell pool capable of differentiation into mature vascular endothelial cells and by secretion of angiogenic growth factors. OBJECTIVE: The aim of this study was to investigate the role of PDGF-BB and PDGFR in EPC-mediated angiogenesis of differentiated endothelial cells. METHODS AND RESULTS: Conditioned medium from human EPC (EPC-CM) cultured in hypoxic conditions contained substantially higher levels of PDGF-BB as compared to normoxic conditions (P<0.01). EPC-CM increased proliferation (1.39-fold; P<0.001) and migration (2.13-fold; P<0.001) of isolated human umbilical vein endothelial cells (HUVEC), as well as sprouting of vascular structures from ex vivo cultured aortic rings (2.78-fold increase; P = 0.01). The capacity of EPC-CM to modulate the PDGFR expression in HUVEC was assessed by western blot and RT-PCR. All the pro-angiogenic effects of EPC-CM on HUVEC could be partially inhibited by inactivation of PDGFR (P<0.01). EPC-CM triggered a distinct up-regulation of PDGFR (2.5±0.5; P<0.05) and its phosphorylation (3.6±0.6; P<0.05) in HUVEC. This was not observed after exposure of HUVEC to recombinant human PDGF-BB alone. CONCLUSION: These data indicate that EPC-CM sensitize endothelial cells and induce a pro-angiogenic phenotype including the up-regulation of PDGFR , thereby turning the PDGF/PDGFR signaling-axis into a critical element of EPC-induced endothelial angiogenesis. This finding may be utilized to enhance EPC-based therapy of ischemic tissue in future.