Comparison of aortic valve annulus diameter determination through 3-dimensional transesophageal echo with cardiac MDCT and assessment of predictors for annulus sizing.

Objectives: The long-term success of CoreValve stent prosthesis (Medtronic) implantation for severe aortic valve stenosis is limited in determination of correct aortic valve annulus.

Methods: We retrospectively investigated preinterventional cardiac 256-slice computed tomography (cardiac CT) scans and 3-dimensional transesophageal echocardiography (3D TEE) for assessment of aortic valve annulus to (i) compare both methods as well as (ii) to define predictors for annulus sizing.

Results: We investigated 200 consecutive patients with a mean aortic valve annulus (AA) of 24mm and a mean age of 81 years.

Non-invasive and invasive predictors of paravalvular regurgitation post CoreValve® stent prosthesis implantation in aortic valves.

Objectives: The long-term success of CoreValve® stent prosthesis (Medtronic) implantation for severe aortic valve stenosis is limited by postprocedural paravalvular regurgitation (PVR).

Methods: We have retrospectively investigated preinterventional cardiac 256-slice computed tomography (CT) scans and aortography to define predictors for mild, moderate, or severe PVR, in a blinded fashion.

Results: We investigated 100 consecutive patients with a mean aortic valve area (AVA) of 0.

Non-invasive and invasive evaluation of aortic valve area in 100 patients with severe aortic valve stenosis: comparison of cardiac computed tomography with ECHO (transesophageal/transthoracic) and catheter examination.

Background: Current guidelines place emphasis on the determination of aortic valve area (AVA) for defining an appropriate treatment strategy. Invasive and non-invasive modalities are used to perform planimetric [transesophageal echocardiography (TEE) and cardiac multidetector computed tomography (MDCT)] and calculated [catheter examination (CE), transthoracic echocardiography (TTE)] AVA measurements.

Purpose And Methods: We investigated 100 patients admitted to evaluate the AVA using cardiac MDCT (CT), TEE/TTE as well as invasive CE.

Image quality and radiation exposure with prospectively ECG-triggered axial scanning for coronary CT angiography: the multicenter, multivendor, randomized PROTECTION-III study.

Objectives: The purpose of this study was to evaluate image quality and radiation dose using a prospectively electrocardiogram (ECG)-triggered axial scan protocol compared with standard retrospective ECG-gated helical scanning for coronary computed tomography angiography.

Background: Concerns have been raised regarding radiation exposure during coronary computed tomography angiography. Although the use of prospectively ECG-triggered axial scan protocols may effectively lower radiation dose compared with helical scanning, it is unknown whether image quality is maintained in a clinical setting.

Atherosclerotic inflammation triggers osteogenic bone transformation in calcified and stenotic human aortic valves: still a matter of debate.

Sclerotic calcification of the aortic valve is a common disease in advanced age. However, pathophysiologic processes leading to valve calcifications are poorly understood. Transformation of atherosclerotic triggers to osteogenic differentiation is controversially discussed and is thought as a trigger of bone transformation in end stage disease.

Role of endogenous RGS proteins on endothelial ERK 1/2 activation.

Endothelial cells are maintaining atherosclerotic signaling mediated by Extracellular Regulated Kinases 1 and 2 (ERK). Signaling gets activated upon stimulation of G protein-coupled receptors mediated by G(q) and G(i/o) proteins subjected to regulation by RGS proteins. The goal of the study was to delineate the specificity of RGS proteins modulating induced ERK phosphorylation.

Statins stimulate RGS-regulated ERK 1/2 activation in human calcified and stenotic aortic valves.

The signal transduction activating extracellular-regulated kinases (ERK) is triggered by G protein-coupled receptors (GPCR). In turn, the GPCR are mediated by G(q) and G(i/o) proteins subjected to regulation of regulators of G protein-mediated signaling (RGS) proteins. This network compiles extracellular growth signals to intracellular targets of sclerosis on calcified and stenotic human aortic valves (CSAV).

Interleukin-10 improves left ventricular function in rats with heart failure subsequent to myocardial infarction.

Evidence has shown that pro-inflammatory cytokines, especially TNF-alpha, are involved in the inflammatory response in the remodelling process after myocardial infarction (MI). Although IL-10, an anti-inflammatory cytokine, has been shown to antagonize some of the deleterious effects of TNF-alpha, little is known about its role in post-MI left ventricular (LV) dysfunction. The aim of the present study was to investigate whether a therapy with rhIL-10 could be beneficial in an animal model of post-MI heart failure (HF).

RGS protein specificity towards Gq- and Gi/o-mediated ERK 1/2 and Akt activation, in vitro.

Extracellular Regulated Kinases (ERK) and Protein Kinase B (Akt) are intermediaries in relaying extracellular growth signals to intracellular targets. Each pathway can become activated upon stimulation of G protein-coupled receptors mediated by G(q) and G(i/o) proteins subjected to regulation by RGS proteins. The goal of the study was to delineate the specificity in which cardiac RGS proteins modulate G(q)and G(i/o)-induced ERK and Akt phosphorylation.

VAP-1, Eotaxin3 and MIG as potential atherosclerotic triggers of severe calcified and stenotic human aortic valves: effects of statins.

Sclerotic calcification of the aortic valve is a common disease in advanced age. Its pathophysiology is unclear. However, pathobiological similarities to atherosclerosis have been shown in several studies.

[Gene polymorphisms leading to calcified and stenotic aortic valves].

In the Caucasian world calcified and stenosed aortic valves are a common disease. Due to increasing life expectancy prevalence of aortic valve disease will increase dramatically. In order to establish alternative therapeutic approaches to valve replacement, we have to get a better understanding of the pathophysiological process and genetic determinations leading to calcified and stenotic valve disease.

Selective loss of fine tuning of Gq/11 signaling by RGS2 protein exacerbates cardiomyocyte hypertrophy.

Alterations in cardiac G protein-mediated signaling, most prominently G(q/11) signaling, are centrally involved in hypertrophy and heart failure development. Several RGS proteins that can act as negative regulators of G protein signaling are expressed in the heart, but their functional roles are still poorly understood. RGS expression changes have been described in hypertrophic and failing hearts.

Emergence of dendritic cells in rupture-prone regions of vulnerable carotid plaques.

Dendritic cells (DC), which are critically involved in various immunological disorders, were detected in atherosclerotic plaques in 1995. Since DC might be related to the immunological processes in atherosclerosis (AS), we analyzed the emergence of DC and other inflammatory cells in different stages of AS. Serial cross-sections of 44 carotid specimens were immunohistochemically analyzed for the presence of DC, T cells, macrophages, and HLA-DR.

Differential contribution of GTPase activation and effector antagonism to the inhibitory effect of RGS proteins on Gq-mediated signaling in vivo.

RGS proteins act as negative regulators of G protein signaling by serving as GTPase-activating proteins (GAP) for alpha subunits of heterotrimeric G proteins (Galpha), thereby accelerating G protein inactivation. RGS proteins can also block Galpha-mediated signal production by competing with downstream effectors for Galpha binding. Little is known about the relative contribution of GAP and effector antagonism to the inhibitory effect of RGS proteins on G protein-mediated signaling.