This study was designed to determine if a viable biodegradable three-dimensional fibroblast construct (3DFC) patch implanted on the left ventricle after myocardial infarction (MI) improves left ventricular (LV) function and blood flow. We ligated the left coronary artery of adult male Sprague-Dawley rats and implanted the 3DFC at the time of the infarct. Three weeks after MI, the 3DFC improved LV systolic function by increasing (p < 0.05) ejection fraction (37 ± 3% to 62 ± 5%), increasing regional systolic displacement of the infarcted wall (0.04 ± 0.02 to 0.11 ± 0.03 cm), and shifting the passive LV diastolic pressure volume relationship toward the pressure axis. The 3FDC improved LV remodeling by decreasing (p < 0.05) LV end-systolic and end-diastolic diameters with no change in LV systolic pressure. The 3DFC did not change LV end-diastolic pressure (LV EDP; 25 ± 2 vs. 23 ± 2 mmHg) but the addition of captopril (2mg/L drinking water) lowered (p < 0.05) LV EDP to 12.9 ± 2.5 mmHg and shifted the pressure–volume relationship toward the pressure axis and decreased (p < 0.05) the LV operating end-diastolic volume from 0.49 ± 0.02 to 0.34 ± 0.03 ml. The 3DFC increased myocardial blood flow to the infarcted anterior wall after MI over threefold (p < 0.05). This biodegradable 3DFC patch improves LV function and myocardial blood flow 3 weeks after MI. This is a potentially new approach to cell-based therapy for heart failure after MI.

The 3DFC functions as a cell delivery device providing matrix support for resident cell survival and integration into the heart. The imbedded fibroblasts of the 3DFC release a complex blend of cardioactive cytokines promoting increases in microvessel density and anterior wall blood flow but does not improve ejection fraction or alter LV remodeling.

Guidelines for managing atrial fibrillation recommend systemic anticoagulation for almost all patients age 65 and older, but in practice up to 50% of older patients do not receive maintenance anticoagulation therapy. The most common reason physicians cite for withholding anticoagulation in older patients with atrial fibrillation is a perception of a high risk of falling and associated bleeding, especially intracranial hemorrhage.

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Background: Marfan syndrome (MFS) leads to aortic root aneurysm, while descending thoracic aortic aneurysm (TAA) occurs less commonly. With imaging surveillance and prophylactic surgery, lifespan in MFS has increased to near normal. Abdominal aortic aneurysm (AAA) complicating Marfan syndrome is rarely reported in the literature. There are no guidelines for routine screening for AAA in MFS. We sought to characterize AAA disease in our MFS cohort. Methods: The records of 11 adults from our MFS Clinic with MFS (by Ghent or revised Ghent Criteria) and AAA disease were reviewed. Clinical features, imaging, operative reports, and outcomes were analyzed. Results: Eleven adults (9 male) with MFS and AAA, age at AAA diagnosis 43 + 15 yrs (range 18-63 yrs), were studied. Five patients smoked cigarettes. Nine of eleven patients were being treated with beta-blockers and angiotensin receptor blockers or ACE-inhibitors at the time of AAA diagnosis. Ten underwent prior aortic root replacement at age 31 + 15 yrs (range 8-62 yrs). The AAA was diagnosed 1-21 years after aortic root repair. The AAA was suprarenal in 5 patients, juxtarenal in 2, and infrarenal in 4. The size of the AAA ranged from 3.5 to 9.7 cm at time of diagnosis. Three patients had descending TAA. One patient had a prior type B dissection, not involving the abdominal aorta. Branch vessel aneurysms present in these patients included popliteal, intercostal, hepatic, subclavian and axillary. Four patients underwent open surgical repair (AAA size from 5.5 to 9.7 cm); one underwent endovascular repair; and five are being treated medically (aortic size 4.1 + 0.6 cm). One patient died suddenly with AAA size 5.7 cm at last measurement. Conclusions: Adults with MFS are at risk for developing AAA. Our cohort is the largest to date characterizing AAA in MFS. The AAAs were often very large at the time of initial diagnosis. MFS patients with AAA have a relatively high frequency of branch vessel aneurysms. Imaging to evaluate for AAA is recommended early after the diagnosis of MFS in adults and periodically thereafter to improve outcomes in this population.

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