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Tor Skibsted Clemmensen

Researcher at Aarhus University Hospital

Publications -  55
Citations -  770

Tor Skibsted Clemmensen is an academic researcher from Aarhus University Hospital. The author has contributed to research in topics: Heart failure & Heart transplantation. The author has an hindex of 14, co-authored 44 publications receiving 481 citations.

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Changes in Longitudinal Myocardial Deformation during Acute Cardiac Rejection: The Clinical Role of Two-Dimensional Speckle-Tracking Echocardiography

TL;DR: GLS is significantly reduced during moderate (2R) ACR and improves significantly in the resolving period and the present results provide encouraging evidence to consider the routine use of GLS as a marker of graft function involvement during ACR.
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Layered Fibrotic Plaques Are the Predominant Component in Cardiac Allograft Vasculopathy: Systematic Findings and Risk Stratification by OCT.

TL;DR: OCT enables the detection of CAV-associated plaque compositions and allows early detection and differentiation of vessel wall disease not visible on angiography, and may be associated with stepwise CAV progression caused by organizing mural thrombi.
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Evaluation of longitudinal myocardial deformation by 2-dimensional speckle-tracking echocardiography in heart transplant recipients: Relation to coronary allograft vasculopathy

TL;DR: GLS is suggested as a new method to be included in the monitoring of graft function in relation to CAV in HTx patients, in contrast to LVEF and conventional pulsed mitral Doppler flow parameters used in the CAV classification.
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Prognostic implications of left ventricular myocardial work indices in cardiac amyloidosis.

TL;DR: LV myocardial work may be of prognostic value in CA patients by predicting both MACE and all-cause mortality by combining LVMWI and apical-to-basal segmental work ratio, and in contrast, LVGLS did not predict all- Cause mortality.
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Left Ventricular Pressure-Strain–Derived Myocardial Work at Rest and during Exercise in Patients with Cardiac Amyloidosis

TL;DR: Even though LVMWI increased with exercise, LVMWE decreased, suggesting inefficient myocardial energy exploitation in patients with CA, suggesting LV global longitudinal strain does not adjust for loading conditions.