Robert M. Reed

Dr. Robert M. Reed

Associate Professor, University of Maryland School of Medicine, Baltimore, Maryland, USA

Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

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

Representative Publications

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1 February 2014 in JACC: Heart Failure
Verified
Journal Article
Closed access
Robert M. ReedRobert M. Reed
Robert M. Reed
GNGiora Netzer
Giora Netzer
LHLawrence Hunsicker
Lawrence Hunsicker
BMBraxton Mitchell
Braxton Mitchell
KRKeshava Rajagopal
Keshava Rajagopal
MEMichael Eberlein
Michael Eberlein

1 December 2012 in The American Journal of Medicine
Verified
Journal Article
Closed access
Robert M. ReedRobert M. Reed
Robert M. Reed
MEMichael Eberlein
Michael Eberlein
RGReda E. Girgis
Reda E. Girgis
SHSalman Hashmi
Salman Hashmi
AIAldo Iacono
Aldo Iacono
SSSteven Scharf
Steven Scharf

26 April 2015 in Current Pulmonology Reports
Verified
Journal Article
Open access
PDF file
LBLindsey Barnes
Lindsey Barnes
Robert M. ReedRobert M. Reed
Robert M. Reed
KPKalpaj R Parekh
Kalpaj R Parekh
JBJay K. Bhama
Jay K. Bhama
TPTahuanty Pena
Tahuanty Pena
MEMichael Eberlein
Michael Eberlein
Mechanical ventilation (MV) is an important aspect in the intraoperative and early postoperative management of lung transplant (LTx) recipients. There are no randomized-controlled trials of LTx recipient MV strategies; however, there are LTx center experiences and international survey studies reported. The main early complication of LTx is primary graft dysfunction (PGD), which is similar to the adult respiratory distress syndrome (ARDS). We aim to summarize information pertinent to LTx-MV, as well as PGD, ARDS, and intraoperative MV, and to synthesize these available data into recommendations. Based on the available evidence, we recommend lung-protective MV with low tidal volumes (≤6 mL/kg predicted body weight [PBW]) and positive end-expiratory pressure for the LTx recipient. In our opinion, the MV strategy should be based on donor characteristics (donor PBW as a parameter of actual allograft size), rather than based on recipient characteristics; however, this donor characteristics-based protective MV is based on indirect evidence and requires validation in prospective clinical studies.

1 October 2021 in The American Journal of Medicine
Verified
Journal Article
Closed access
JSJennifer Y. So
Jennifer Y. So
NONathan N. O'HAra
Nathan N. O'HAra
BKBlaine Kenaa
Blaine Kenaa
JWJohn G. Williams
John G. Williams
CDChristopher L. Deborja
Christopher L. Deborja
Robert M. ReedRobert M. Reed
Robert M. Reed

1 June 2011 in The Journal of Heart and Lung Transplantation
Verified
Journal Article
Closed access
Robert M. ReedRobert M. Reed
Robert M. Reed
AIAldo Iacono
Aldo Iacono
ADAndrew DeFilippis
Andrew DeFilippis
MEMichael Eberlein
Michael Eberlein
RGReda E. Girgis
Reda E. Girgis
SJSteven Jones
Steven Jones

15 April 2011 in COPD: Journal of Chronic Obstructive Pulmonary Disease
Verified
Journal Article
Closed access
Robert M. ReedRobert M. Reed
Robert M. Reed
AIAldo Iacono
Aldo Iacono
ADAndrew DeFilippis
Andrew DeFilippis
SJSteven Jones
Steven Jones
MEMichael Eberlein
Michael Eberlein
RGReda E. Girgis
Reda E. Girgis
Pulmonary hypertension (PH) in COPD carries a poor prognosis. Statin therapy has been associated with numerous beneficial clinical effects in COPD, including a possible improvement in PH. We examined the association between statin use and pulmonary hemodynamics in a well-characterized cohort of patients undergoing evaluation for lung transplantation. We conducted a cross-sectional analysis of 112 subjects evaluated for lung transplant with a diagnosis of COPD. Clinical characteristics, pulmonary function, cardiac catheterization findings and medical comorbidities were compared between statins users and non-users. Thirty-four (30%) subjects were receiving statin therapy. Statin users were older and had an increased prevalence of systemic hypertension and coronary artery disease (CAD). Mean pulmonary arterial pressure (mPAP) in the statin group was lower [26 ± 7 vs 29 ± 7 mmHg, p = 0.02], as was pulmonary artery wedge pressure (PAWP) [12 ± 5 vs. 15 ± 6 mmHg, p = 0.02]. Pulmonary vascular resistance did not differ between the groups. In multiple regression analysis, statin use was associated with a 4.2 mmHg (95% CI: 2 to 6.4, p = <0.001) lower PAWP and a 2.6 mmHg (95% CI: 0.3 to 4.9, p = 0.03) reduction in mPAP independent of PAWP. In patients with severe COPD, statin use is associated with significantly lower PAWP and mPAP. These finding should be evaluated prospectively.