Publications by authors named "Julia Kelley Hahn"

The aim was to assess the mid-term results of the E-iliac branched device. Baseline and follow-up data of this monocentric retrospective cohort study including all consecutive patients with aortoiliac aneurysms treated with iliac branched devices between 2016 and 2023 were extracted from the hospital records. Preoperative and follow-up CT scans were analyzed regarding endoleaks, migration, aneurysm sac remodeling, and device patency.

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Background: Left atrioventricular valve (LAVV) stenosis following an atrioventricular septal defect (AVSD) repair is a rare but potentially life-threatening complication. While echocardiographic quantification of diastolic transvalvular pressure gradients is paramount in the evaluation of a newly corrected valve function, it is hypothesized that these measured gradients are overestimated immediately following a cardiopulmonary bypass (CPB) due to the altered hemodynamics when compared to postoperative valve assessments using awake transthoracic echocardiography (TTE) upon recovery after surgery.

Methods: Out of the 72 patients screened for inclusion at a tertiary center, 39 patients undergoing an AVSD repair with both intraoperative transesophageal echocardiograms (TEE, performed immediately after a CPB) and an awake TTE (performed prior to hospital discharge) were retrospectively selected.

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Purpose: During our transthoracic echocardiography (TTE) courses, medical students showed difficulty in spatial orientation. We implemented the use of 3D printed cardiac models of standard TTE views PLAX, PSAX, and A4C and assessed their efficacy in TTE-teaching.

Methods: One hundred fifty-three participants were split into two groups.

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We report a case of a 3-week-old infant who presented a heart murmur and low oxygen saturation. An echocardiography was performed and presented a common arterial trunk type B4 with an interrupted aortic arch and intact ventricular septum. We describe the surgical management and short-term follow-up.

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The leading cause of genetic dilated cardiomyopathy (DCM) is due to mutations in the TTN gene, impacting approximately 15-20% of familial and 18% of sporadic DCM cases. Currently, there is potential for a personalized RNA-based therapeutic approach in titin-based DCM, utilizing antisense oligonucleotide (AON) mediated exon-skipping, which attempts to reframe mutated titin transcripts, resulting in shortened, functional protein. However, the TTN gene is massive with 363 exons; each newly identified TTN exon mutation provides a challenge to address when considering the potential application of AON mediated exon skipping.

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Apoptosis (type I programmed cell death) of cardiomyocytes is a major process that plays a role in the progression of heart failure. The early response gene regulates apoptosis in a wide variety of cells and organs. However, its role in heart failure is largely unknown.

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Background: Dilated cardiomyopathy (DCM) is the result of maladaptive cardiac remodeling, which involves microRNA regulation. In turn, microRNAs can contribute to the remodeling process by post-transcriptional modulation of gene expression networks. The exact role of microRNAs in the pathogenesis of DCM is largely unknown.

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