Publications by authors named "Doenst T"

A 52-year-old heart-lung transplant patient presented to the emergency department with acute onset of neurologic symptoms. MRI showed ballooning of the left ventricle, midline shift and contrast enhancement in the anterior horn of the left ventricle. Ventricle neuroendoscopy revealed whitish, floccose aerial structures within the left ventricle.

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Introduction: Acute mesenteric ischemia is a rare but often fatal complication following cardiovascular surgery. Early suspicion may reduce overall mortality. This retrospective study aims to identify predictors and risk factors that may determine the onset and evolution of acute mesenteric ischemia.

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For the year 2014, more than 17,000 published references can be found in Pubmed when entering the search term "cardiac surgery". The last year has been characterized by a vivid discussion in the fields where classic cardiac surgery and modern interventional techniques overlap. Specifically, there have been important contributions in the field of coronary revascularization with either percutaneous coronary intervention or bypass surgery as well as in the fields of interventional valve therapy.

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Objectives: This study sought to test the hypothesis that end-systolic volume (ESV), as a marker of severity of left ventricular (LV) remodeling, influences the relationship between myocardial viability and survival in patients with coronary artery disease and LV systolic dysfunction.

Background: Retrospective studies of ischemic LV dysfunction suggest that the severity of LV remodeling determines whether myocardial viability predicts improved survival with surgical compared with medical therapy, with coronary artery bypass grafting (CABG) only benefitting patients with viable myocardium who have smaller ESV. However, this has not been tested prospectively.

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Objective: Cardiac hypertrophy is characterized by changes in substrate utilization and activity of the Krebs cycle. We assessed the effects of triheptanoin, an odd-chain fat that might support the Krebs cycle, on cardiac metabolism and function in a model of cardiac hypertrophy.

Methods And Results: Rats were subjected to aortic banding (AoB) to induce pressure overload (PO).

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Rationale: In chronic heart failure, increased adrenergic activation contributes to structural remodeling and altered gene expression. Although adrenergic signaling alters histone modifications, it is unknown, whether it also affects other epigenetic processes, including DNA methylation and its recognition.

Objective: The aim of this study was to identify the mechanism of regulation of the methyl-CpG-binding protein 2 (MeCP2) and its functional significance during cardiac pressure overload and unloading.

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Aims: Hypothesis 1 of the Surgical Treatment for Ischemic Heart Failure (STICH) trial enrolled 1212 patients with an LVEF of ≤35% and CAD amenable to coronary artery bypass grafting (CABG). Patients were randomized to CABG and optimal medical therapy (MED) or MED alone. The objective was to assess whether or not patients with diabetes mellitus (DM) enrolled in the STICH trial would have greater benefit from CABG than patients without DM.

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Hypoadiponectinemia is an independent predictor of cardiovascular disease, impairs mitochondrial function in skeletal muscle, and has been linked to the pathogenesis of Type 2 diabetes. In models of Type 2 diabetes, myocardial mitochondrial function is impaired, which is improved by increasing serum adiponectin levels. We aimed to define the roles of adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2) in adiponectin-evoked regulation of mitochondrial function in the heart.

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In patients with functional/ischemic mitral regurgitation (FMR/IMR), mitral annuloplasty alone frequently results in recurrent regurgitation because of ongoing left ventricular dilatation and recurrent leaflet tethering. Adjunctive subvalvular approaches exist, but the technical shortcomings limit their clinical acceptance. A novel adjunctive technique was applied in three patients: A polytetrafluoroethylene string and noose were anchored to the posteromedial and anterolateral papillary muscle, respectively.

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Adiponectin deficiency leads to increased myocardial infarct size following ischemia reperfusion and to exaggerated cardiac hypertrophy following pressure overload, entities that are causally linked to mitochondrial dysfunction. In skeletal muscle, lack of adiponectin results in impaired mitochondrial function. Thus, it was our objective to investigate whether adiponectin deficiency impairs mitochondrial energetics in the heart.

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Background: Minimally invasive surgical procedures (MIS) may offer several advantages over conventional full sternotomy (FS) aortic valve replacement (AVR). A novel class of aortic valve prostheses has been developed for rapid-deployment AVR (RDAVR). We report a randomized, multicenter trial comparing the outcomes for MIS-RDAVR with those of conventional FS-AVR.

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Heart failure induced by myocardial infarction (MI) causes diaphragm muscle weakness, with elevated oxidants implicated. We aimed to determine whether diaphragm muscle weakness is 1) early-onset post-MI (i.e.

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Purpose: The assessment of aortic annular size is critical, and inappropriate sizing is thought to be a main reason of paravalvular aortic regurgitation. Multidetector computed tomograph is associated with the risk of contrast nephropathy. For optimal evaluation of the complex structure of the aortic annulus, three-dimensional (3D)-methods should be used.

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Objectives: Patients undergoing coronary bypass grafting (CABG) are at higher risk if they suffer from atrial fibrillation (AF). It was suggested that performing CABG without the use of cardiopulmonary bypass (off-pump) would reduce perioperative risk. We assessed the influence of preoperative AF on outcome in a randomized cohort of patients above the age of 75 undergoing either on-pump or off-pump CABG.

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The hemodynamic performance of prosthetic tissue valves is influenced by valve design and valve-specific sizing strategies. Design determines the actual geometric opening area (GOA) of the prosthetic valve and sizing strategy its actual chosen size. Currently, hemodynamic performance is assessed by determining the effective orifice area (EOA; derived from the continuity equation by relating flow velocities with the area of the left ventricular outflow tract [LVOTA]).

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We investigated the impact of cardiac reactive oxygen species (ROS) during the development of pressure overload-induced heart failure. We used our previously described rat model where transverse aortic constriction (TAC) induces compensated hypertrophy after 2 weeks, heart failure with preserved ejection fraction at 6 and 10 weeks, and heart failure with systolic dysfunction after 20 weeks. We measured mitochondrial ROS production rates, ROS damage and assessed the therapeutic potential of in vivo antioxidant therapies.

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Transcatheter aortic valve implantation (TAVI) has become an established procedure for patients with aortic valve stenosis and significant comorbidities. One option offered by this technique is the implantation of a transcatheter valve inside a surgically implanted bioprosthesis. Many reports address the feasibility but also the pitfalls of these valve-in-valve (VIV) procedures.

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Background: Diastolic dysfunction in heart failure with preserved ejection fraction (HFpEF) may result in pulmonary congestion and lung remodeling. We evaluated the usefulness of major diastolic echocardiographic parameters and of the deceleration rate of early transmitral diastolic velocity (E/DT) in predicting lung remodeling in a rat model of HFpEF.

Methods And Results: Rats underwent aortic banding (AoB) to induce pressure overload (PO).

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The heart has a high rate of ATP production and turnover that is required to maintain its continuous mechanical work. Perturbations in ATP-generating processes may therefore affect contractile function directly. Characterizing cardiac metabolism in heart failure (HF) revealed several metabolic alterations called metabolic remodeling, ranging from changes in substrate use to mitochondrial dysfunction, ultimately resulting in ATP deficiency and impaired contractility.

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