Peter E. Hammer

Dr. Peter E. Hammer

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Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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27 October 2023 in Science Advances
Verified
Journal Article
Open access
JRJacob Rogatinsky
Jacob Rogatinsky
DRDominic Recco
Dominic Recco
JFJoseph Feichtmeier
Joseph Feichtmeier
YKYuchen Kang
Yuchen Kang
NKNicholas Kneier
Nicholas Kneier
TRTommaso Ranzani
Tommaso Ranzani
In minimally invasive endovascular procedures, surgeons rely on catheters with low dexterity and high aspect ratios to reach an anatomical target. However, the environment inside the beating heart presents a combination of challenges unique to few anatomic locations, making it difficult for interventional tools to maneuver dexterously and apply substantial forces on an intracardiac target. We demonstrate a millimeter-scale soft robotic platform that can deploy and self-stabilize at the entrance to the heart, and guide existing interventional tools toward a target site. In two exemplar intracardiac procedures within the right atrium, the robotic platform provides enough dexterity to reach multiple anatomical targets, enough stability to maintain constant contact on motile targets, and enough mechanical leverage to generate newton-level forces. Because the device addresses ongoing challenges in minimally invasive intracardiac intervention, it may enable the further development of catheter-based interventions.

25 February 2011 in Annals of Biomedical Engineering
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Journal Article
Closed access
PDF file
PHPeter E. Hammer
Peter E. Hammer
MSMichael S. Sacks
Michael S. Sacks
PNPedro J. del Nido
Pedro J. del Nido
RHRobert D. Howe
Robert D. Howe

19 February 2020 in Science Translational Medicine
Verified
Journal Article
Closed access
PDF file
SHSophie C. Hofferberth
Sophie C. Hofferberth
MSMossab Y. Saeed
Mossab Y. Saeed
LTLara Tomholt
Lara Tomholt
MFMatheus C. Fernandes
Matheus C. Fernandes
CPChristopher J. Payne
Christopher J. Payne
PNPedro Jose del Nido
Pedro Jose del Nido
A biomimetic prosthetic heart valve is geometrically adaptable to accommodate somatic growth and structural asymmetries within the hearts of sheep.

1 June 2005 in American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Verified
Journal Article
Closed access
PDF file
PHPeter E. Hammer
Peter E. Hammer
JSJ. Philip Saul
J. Philip Saul
A mathematical model of the arterial baroreflex was developed and used to assess the stability of the reflex and its potential role in producing the low-frequency arterial blood pressure oscillations called Mayer waves that are commonly seen in humans and animals in response to decreased central blood volume. The model consists of an arrangement of discrete-time filters derived from published physiological studies, which is reduced to a numerical expression for the baroreflex open-loop frequency response. Model stability was assessed for two states: normal and decreased central blood volume. The state of decreased central blood volume was simulated by decreasing baroreflex parasympathetic heart rate gain and by increasing baroreflex sympathetic vaso/venomotor gains as occurs with the unloading of cardiopulmonary baroreceptors. For the normal state, the feedback system was stable by the Nyquist criterion (gain margin = 0.6), but in the hypovolemic state, the gain margin was small (0.07), and the closed-loop frequency response exhibited a sharp peak (gain of 11) at 0.07 Hz, the same frequency as that observed for arterial pressure fluctuations in a group of healthy standing subjects. These findings support the theory that stresses affecting central blood volume, including upright posture, can reduce the stability of the normally stable arterial baroreflex feedback, leading to resonance and low-frequency blood pressure waves.

1 April 2012 in Journal of Biomechanics
Verified
Journal Article
Closed access
PHPeter E. Hammer
Peter E. Hammer
PCPeter C. Chen
Peter C. Chen
PNPedro J. del Nido
Pedro J. del Nido
RHRobert D. Howe
Robert D. Howe

25 August 2021 in Children
Verified
Journal Article
Open access
PDF file
PHPeter E. Hammer
Peter E. Hammer
KMKerry McEnaney
Kerry McEnaney
RCRyan Callahan
Ryan Callahan
CBChristopher W. Baird
Christopher W. Baird
DHDavid M. Hoganson
David M. Hoganson
Kathy J. JenkinsKathy J. Jenkins
Kathy J. Jenkins
Pulmonary vein stenosis is a serious condition characterized by restriction or blockage due to fibrotic tissue ingrowth that develops in the pulmonary veins of infants or children. It is often progressive and can lead to severe pulmonary hypertension and death. Efforts to halt or reverse disease progression include surgery and catheter-based balloon dilation and stent implantation. Its cause and mechanism of progression are unknown. In this pilot study, we propose and explore the hypothesis that elevated wall shear stress at discrete pulmonary venous sites triggers stenosis. To assess this theory, we retrospectively analyzed cardiac catheterization, lung scan, and X-ray computed tomography data to estimate wall shear stress in the pulmonary veins at multiple time points during disease progression in two patients. Results are consistent with the existence of a level of elevated wall shear stress above which the disease is progressive and below which progression is halted. The analysis also suggests the possibility of predicting the target lumen size necessary in a given vein to reduce wall shear stress to normal levels and remove the trigger for stenosis progression.