Stent Graft Migration Causing Two Aortic Wall Injuries 10 Years After Type II Hybrid Arch Repair.

Hybrid arch repair (HAR) combines surgical reconstruction of the ascending aorta and arch debranching with stent graft deployment into the descending thoracic aorta in an effort to reduce the morbidity associated with conventional open total arch replacement. We describe a case of delayed presentation for 2 thoracic aortic wall injuries caused by stent graft migration after type II HAR. This report highlights an important late complication of HAR and the need for careful device selection.

Magnetic resonance imaging-based hemodynamic wall shear stress alters aortic wall tissue biomechanics in bicuspid aortic valve patients.

Objective: In this study we aimed to conclusively determine whether altered aortic biomechanics are associated with wall shear stress (WSS) independent of region of tissue collection. Elevated WSS in the ascending aorta of patients with bicuspid aortic valve has been shown to contribute to local maladaptive aortic remodeling and might alter biomechanics.

Methods: Preoperative 4-dimensional flow magnetic resonance imaging was performed on 22 patients who underwent prophylactic aortic root and/or ascending aorta replacement.

Normative healthy reference values for global and segmental 3D principal and geometry dependent strain from cine cardiac magnetic resonance imaging.

3-Dimensional (3D) myocardial deformation analysis (3D-MDA) enables novel descriptions of geometry-independent principal strain (PS). Applied to routine 2D cine cardiovascular magnetic resonance (CMR), this provides unique measures of myocardial biomechanics for disease diagnosis and prognostication. However, healthy reference values remain undefined.

Elastin integrity in bicuspid valve-associated aortopathy is associated with altered biomechanical properties and influenced by age.

Background: Aortic wall remodelling in bicuspid aortic valve (BAV) patients is heterogeneous and characterized by elastin fiber breakdown alongside impaired biomechanics. However, the relationship between aortic histopathological changes and biomechanics are incompletely understood. We clarify the influence of elastin fiber integrity on ex vivo aortic wall mechanical properties in BAV patients, and explore the influence of patient age.

Aorta-specific DNA methylation patterns in cell-free DNA from patients with bicuspid aortic valve-associated aortopathy.

Background: The dilation of the aorta that occurs as a consequence of a congenitally bicuspid aortic valve (BAV) is associated with a risk of dissection, aneurysm or rupture. With progressive aortopathy, surgery is often recommended, but current patient selection strategies have limitations. A blood-based assay to identify those who would most benefit from prophylactic surgery would be an important medical advance.

Effect of Active Cancer on the Cardiac Phenotype: A Cardiac Magnetic Resonance Imaging-Based Study of Myocardial Tissue Health and Deformation in Patients With Chemotherapy-Naïve Cancer.

Background The overlap between cancer and cardiovascular care continues to expand, with intersections emerging before, during, and following cancer therapies. To date, emphasis has been placed on how cancer therapeutics influence downstream cardiac health. However, whether active malignancy itself influences chamber volumes, function, or overall myocardial tissue health remains uncertain.

The science of BAV aortopathy.

The aortopathy associated with bicuspid aortic valve (BAV) is an epidemiologically relevant source of chronic and acute aortic disease (aneurysm and dissection). However, its pathogenesis is still the object of scientific uncertainties and debates. Indeed, the mechanisms determining the diseases of the ascending aorta in BAV patients are most likely complex and multifactorial, i.

Acellular bioscaffolds redirect cardiac fibroblasts and promote functional tissue repair in rodents and humans with myocardial injury.

Coronary heart disease is a leading cause of death. Tissue remodeling and fibrosis results in cardiac pump dysfunction and ischemic heart failure. Cardiac fibroblasts may rebuild damaged tissues when prompted by suitable environmental cues.

Fluoroquinolone-Associated Type A Aortic Dissection in Alpha-1 Anti-Trypsin Deficiency.

Fluroquinolone antibiotics have come under increased scrutiny given their recent association with aortic events. Although judicious use has been urged in select patient populations, such as those with Marfan and Ehlers-Danlos syndromes, that have a known predisposition for aortopathy, other at-risk patient populations may remain. We describe the atypical delayed-presentation of a type A aortic dissection in a patient with alpha-1 anti-trypsin (A1AT) deficiency and longstanding FQ exposure.

Applications of a Specialty Bicuspid Aortic Valve Program: Clinical Continuity and Translational Collaboration.

Bicuspid aortic valve (BAV) is a common congenital heart diagnosis and is associated with aortopathy. Current guidelines for aortic resection have been validated but are based on aortic diameter, which is insufficient to predict acute aortic events. Clinical and translational collaboration is necessary to identify biomarkers that can individualize the timing of prophylactic surgery for BAV aortopathy.

Direct Effects of Empagliflozin on Extracellular Matrix Remodelling in Human Cardiac Myofibroblasts: Novel Translational Clues to Explain EMPA-REG OUTCOME Results.

Background: Empagliflozin, an SGLT2 inhibitor, has shown remarkable reductions in cardiovascular mortality and heart failure admissions (EMPA-REG OUTCOME). However, the mechanism underlying the heart failure protective effects of empagliflozin remains largely unknown. Cardiac fibroblasts play an integral role in the progression of structural cardiac remodelling and heart failure, in part, by regulating extracellular matrix (ECM) homeostasis.

Induction of human aortic myofibroblast-mediated extracellular matrix dysregulation: A potential mechanism of fluoroquinolone-associated aortopathy.

Objectives: Fluoroquinolone (FQ) antibiotics are associated with adverse aortic clinical events. We assessed human aortic myofibroblast-mediated extracellular matrix (ECM) dysregulation as a possible cellular mechanism underlying FQ-associated aortopathy.

Methods: Human aortic myofibroblasts were isolated from patients with aortopathy undergoing elective ascending aortic resection (N = 9).

Bioactive Extracellular Matrix Scaffold Promotes Adaptive Cardiac Remodeling and Repair.

Structural cardiac remodeling after ischemic injury can induce a transition to heart failure from progressive loss of cardiac function. Cellular regenerative therapies are promising but face significant translational hurdles. Tissue extracellular matrix (ECM) holds the necessary environmental cues to stimulate cell-based endogenous myocardial repair pathways and promote adaptive remodeling toward functional recovery.

Aortic valve-mediated wall shear stress is heterogeneous and predicts regional aortic elastic fiber thinning in bicuspid aortic valve-associated aortopathy.

Objectives: The objectives of this study were to investigate an association between the magnitude of flow-mediated aortic wall shear stress (WSS) and medial wall histopathology in patients with bicuspid aortic valve (BAV) with aortopathy.

Methods: Patients with BAV (n = 27; 52 ± 15 years; 3 women; proximal thoracic aorta diameter = 4.4 ± 0.

Human pericardial proteoglycan 4 (lubricin): Implications for postcardiotomy intrathoracic adhesion formation.

Objective: Intrapericardial fibrous adhesions increase the risk of sternal reentry. Proteoglycan 4/lubricin (PRG4) is a mucin-like glycoprotein that lubricates tissue compartments and prevents inflammation. We characterized PRG4 expression in human pericardium and examined its effects in vitro on human cardiac myofibroblast fibrotic activity and in vivo as a measure of its therapeutic potential to prevent adhesions.

Evolution of Precision Medicine and Surgical Strategies for Bicuspid Aortic Valve-Associated Aortopathy.

Bicuspid aortic valve (BAV) is a common congenital cardiac malformation affecting 1-2% of people. BAV results from fusion of two adjacent aortic valve cusps, and is associated with dilatation of the aorta, known as bicuspid valve associated aortopathy. Bicuspid valve aortopathy is progressive and associated with catastrophic clinical events, such as aortic dissection and rupture.

Heparin Augmentation Enhances Bioactive Properties of Acellular Extracellular Matrix Scaffold.

Extracellular matrix (ECM) maintains a reservoir of bioactive growth factors and matricellular proteins that provide bioinductive effects on local cells that influence phenotype and behaviors. Bioactive acellular ECM scaffolds can be used therapeutically to stimulate adaptive tissue repair. Fibroblast growth factor-2 (FGF-2) attenuates transforming growth factor-β1 (TGF-β1)-mediated cardiac fibrosis.

Bicuspid aortic valve aortopathy: mechanistic and clinical insights from recent studies.

Purpose Of Review: This focused review summarizes key insights from the past 12 months of basic science and clinical research on bicuspid aortic valve (BAV)-associated aortopathy.

Recent Findings: Recent studies in BAV-associated aortopathy support a heterogeneous spectrum of disease with distinct phenotypes. Basic science studies provide further support for the concept of regional differences in the severity of aortopathy within the aorta of BAV patients.

Epicardial infarct repair with bioinductive extracellular matrix promotes vasculogenesis and myocardial recovery.

Background: Infarcted myocardium can remodel after successful reperfusion, resulting in left ventricular dilation and heart failure. Epicardial infarct repair (EIR) using a bioinductive extracellular matrix (ECM) biomaterial is a novel surgical approach to promote endogenous myocardial repair and functional recovery after myocardial infarction. Using a pre-clinical porcine model of coronary ischemia-reperfusion, we assessed the effects of EIR on regional functional recovery, safety, and possible mechanisms of benefit.

Monocytes increase human cardiac myofibroblast-mediated extracellular matrix remodeling through TGF-β1.

Following myocardial infarction (MI), cardiac myofibroblasts remodel the extracellular matrix (ECM), preventing mechanical complications. However, prolonged myofibroblast activity leads to dysregulation of the ECM, maladaptive remodeling, fibrosis, and heart failure (HF). Chronic inflammation is believed to drive persistent myofibroblast activity; however, the mechanisms are unclear.