MRI detects increased aortic stiffening and myocardial dysfunction after TEVAR of blunt injury in young patients.

Background: Thoracic endovascular aortic repair (TEVAR) is a well-established technique for the management of blunt thoracic aortic injury (BTAI). Despite improvements in vascular imaging, graft material properties, and implant techniques, stent-graft deployment artificially induces aortic stiffening. This study aimed to evaluate the midterm effect of thoracic endovascular aortic repair after blunt thoracic aortic injury on aortic stiffness and cardiac function in young patients using cardiovascular magnetic resonance (CMR) imaging. Patients and methods: From all patients who underwent TEVAR for BTAI between 2009 and 2019 in a single institution, 10 patients with no other comorbidities affecting arterial stiffness were sex-, age-, height-, and body surface area-matched to 10 healthy controls. Comprehensive CMR examination was performed in all controls and patients. The mean follow-up period was 5.4±1.8 years; the mean age at the time of TEVAR was 30.3±8.7 years. Results: Four patients who underwent TEVAR developed arterial hypertension. 4D flow CMR-based analysis demonstrated higher global pulse wave velocity (PWV) in TEVAR patients than in controls (p=0.012). Segmental analysis showed a higher PWV in the descending and abdominal aorta. The indexed diameter of the ascending aorta was larger in TEVAR patients than in controls (p=0.007). The CINE acquisitions demonstrated increased left ventricular myocardial thickness (p<0.001). The 3D global diastolic strain rate and diastolic longitudinal velocity (e') decreased, and the A-wave velocity increased. Native myocardial T1 values were significantly higher in TEVAR patients (p=0.037). Conclusions: Young patients with TEVAR after BTAI are at an increased risk of developing vascular and myocardial dysfunction due to increased aortic stiffness. CMR follow-up allows for a comprehensive and radiation-free evaluation of vascular stiffness and associated myocardial changes, especially at the early and subclinical stages.

[Unclear Abdominal Pain - Not Always a Gastroenterological Emergency]. / Der unklare Bauchschmerz ­ nicht immer ein gastroenterologischer Notfall.

History and admission findings An 84-year old patient with persistent atrial fibrillation and chronic renal failure received a subcutaneous injection with low molecular weight heparin (LMWH) during a hospital stay. Over the course of her hospitalization, the patient developed abdominal pain. There was a marked hematoma at the injection site. A large tumor was palpable in the right abdominal quadrant. Examinations Due to the significant reduction in hemoglobin, we performed a CT-angiogram of the abdomen. Diagnosis We were able to visualize an intramuscular hematoma within the rectus abdominis muscle. Therapy and clinical course After visualization with digital subtraction angiography and application of microcoils and histoacryl-glue, we were able to stop bleeding. After implantation of left atrial appendage occluder, oral anticoagulation therapy could be stopped. Conclusion LMWH-treated patients with nonspecific abdominal pain should be meticulously examined to exclude iatrogenic abdominal muscle hematoma.

Porcine aortic endothelial cells show little effects on smooth muscle cells but are potent stimulators of cardiomyocyte growth.

Smooth muscle cells (SMC) and endothelial cells (EC) play a pivotal role in arteriogenesis and atherosclerosis. We evaluated the role of EC on the growth of SMC and neonatal cardiomyocytes (NEO) by using serum-free EC-supernatant (AoCM). Five percent fetal calf serum was used in order to mimic growth effects of blood. EC and SMC purities were 99% as determined by absence or presence of markers such as CD31, desmin, alpha-smooth muscle actin and tropomyosin using immunostaining and FACS analysis. AoCM markedly influenced the morphology of NEO as determined by alpha-actinin staining but showed only little effect on the phenotype of SMC. Protein synthesis after 2 days increased 2.5-fold in SMC and 3.7-fold in NEO as determined by tritium incorporation. The values for serum (2.8 and 2.3-fold, respectively) were comparable. The induction of DNA-synthesis by serum in NEO was twice that of AoCM (3.9-fold). However, proliferative effects of serum and AoCM on SMC differed markedly: Serum induced a 66-fold increase in DNA-synthesis resulting in a 54% higher cell number. DNA-synthesis after AoCM treatment lead to a nonsignificant small increase and no proliferation was detected. Platelet derived growth factor (PDGF-AB), present in blood, induced a 47-fold increase in DNA-synthesis and a 38% increase in cell number. Our data suggest that EC in the absence of physical forces exert strong morphogenic effects on cardiomyocytes but they lack specific effects on smooth muscle cells. In vessels EC might function as a border to isolate SMC from key regulators in blood such as PDGFs.