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Douglas A. Hettrick

Researcher at Medtronic plc

Publications -  209
Citations -  6751

Douglas A. Hettrick is an academic researcher from Medtronic plc. The author has contributed to research in topics: Hemodynamics & Atrial fibrillation. The author has an hindex of 44, co-authored 201 publications receiving 6455 citations. Previous affiliations of Douglas A. Hettrick include University of Wisconsin-Madison & Tufts University.

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Minimizing Ventricular Pacing to Reduce Atrial Fibrillation in Sinus-Node Disease

TL;DR: Dual-chamber minimal ventricular pacing, as compared with conventional dual- chamber pacing, prevents ventricular desynchronization and moderately reduces the risk of persistent atrial fibrillation in patients with sinus-node disease.
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Mechanical function of the left atrium: new insights based on analysis of pressure-volume relations and Doppler echocardiography.

TL;DR: Recent advances in the understanding of LA physiology derived from pressure–volume relations and echocardiography are reviewed, the mechanical consequences of primary LA dysfunction are discussed, and current knowledge about the actions of volatile and intravenous anesthetics on LA function in vivo is described.
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Intrathoracic Impedance vs Daily Weight Monitoring for Predicting Worsening Heart Failure Events: Results of the Fluid Accumulation Status Trial (FAST)

TL;DR: Intrathoracic impedance monitoring represents a useful adjunctive clinical tool for managing HF in patients with implanted devices and was superior to that seen for acute weight changes.
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Mechanism of myocardial protection by isoflurane. Role of adenosine triphosphate-regulated potassium (KATP) channels.

TL;DR: The results indicate that isoflurane prevents decreased systolic shortening caused by multiple episodes of ischemia and reperfusion and result in improved recovery of contractile function of postischemic, reperfused myocardium and are mediated by isofLurane‐induced activation of KATP channels.
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Three-dimensional computational fluid dynamics modeling of alterations in coronary wall shear stress produced by stent implantation.

TL;DR: The hypothesis that stent geometry may be a risk factor for restenosis by affecting local wall shear stress distributions is supported and alterations in wall shears caused by a slotted-tube stent are depicted.