F
Fetnat M. Fouad-Tarazi
Researcher at Cleveland Clinic
Publications - 72
Citations - 4129
Fetnat M. Fouad-Tarazi is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Blood pressure & Hemodynamics. The author has an hindex of 22, co-authored 71 publications receiving 3979 citations.
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Journal ArticleDOI
Sympathetic overactivity in patients with chronic renal failure.
Richard L. Converse,Tage N. Jacobsen,Robert D. Toto,Charles M.T. Jost,Frank Cosentino,Fetnat M. Fouad-Tarazi,Ronald G. Victor,Ronald G. Victor +7 more
TL;DR: Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.
Journal ArticleDOI
Comparative Effects of Therapy With Captopril and Digoxin in Patients With Mild to Moderate Heart Failure
Jay N. Cohn,Morton Hawkins,Herbert J. Levine,John Naughton,Elliot Rapaport,Sidney Goldstein,Bertram Pitt,Robert Cody,Prakash Deedwania,Leonard Dennick,Joseph A. Franciosa,Mark McGovern,Joseph J. Meyer,Alan Gradman,Barry M. Massie,Milton Packer,James E. Doherty,Jacquelyn Gammill,William O. Cooper,Stanford Engel,Rita Fand,Barbara Hallows,Linda Kerwin,Debra A. Soltesz,John O. Parker,Karen Lahey,Prakash Deedwania,Enrique V. Carbajal,Pat Watson,Robert DiBianco,James A. Ronan,Dennis J. Donohue,Keith M. Lindgren,Louis J. Larca,Judy Freitag,Donna Lindemuth,Jeffrey B. Lakier,Howard S. Rosman,Mary Beth Wlodkowski,Robert J. Cody,Spencer H. Kubo,Mary Clark,Katie Pondolfino,Joseph A. Franciosa,Mary Wilen,Drexel Jordan,Sunil K. Das,John M. Nicklas,Mary Kay Foley,Michael B. Higginbotham,Frederick R. Cobb,Jean D. Wilson,David M. Berkson,Dragic Obradovic,Patricia Hershinow,N. Gary Nicholls,Hamid Ikram,Ian Crozier,Carl J. Pepine,John Culp,Marion Limacher,Kathy Mulvehill-Verbust,D. John Farnham,Dorothy Adams,Norene Streicher,Carol Shanley,Mark A. Greenberg,Janet Strain,Mary Hewitt,Barbara Levine,D. Norman Sharpe,Robin Briant,Rene Coxon,Barry M. Massie,James W. Cornyn,Nina Topic,Harold Willens,Denise Antonishen,Dorothy Reinstein,Harry F. Colfer,Karen E. Graham,Gerald M. Perlow,Harvey S. Zarren,Barbara Bent,Marjorie Zicherman,Barry Zaret,Deborah Lawrason,Pat Tellier,Kathy O'Keefe,Syed M. Mohiuddin,Lois Stengel,James D. Madison,Nancy Carruthers,Fernando Elijovich,Mary Jo O'Sullivan,Uri Elkayam,Shabudin H. Rahimtoola,Laura Weber,Sheldon K. Gottlieb,Carol L. Brown,Mariell D. Jessup,Susan Ulrich,Jane Kronenthal,Denise Capaccio,Colin Grant,Edward Gillie,Pat Wood,Fetnat M. Fouad-Tarazi,Kay Petey +108 more
TL;DR: Captopril treatment is significantly more effective than placebo and is an alternative to digoxin therapy in patients with mild to moderate heart failure who are receiving diuretic maintenance therapy.
Journal ArticleDOI
Neurogenic orthostatic hypotension: A double-blind, placebo-controlled study with midodrine
Joseph Jankovic,Janice L Gilden,Bradley C. Hiner,Horacio Kaufmann,David C. Brown,Cecil Coghlan,Michael Rubin,Fetnat M. Fouad-Tarazi +7 more
TL;DR: Midodrine is an effective and well-tolerated treatment for moderate-to-severe orthostatic hypotension associated with autonomic failure and the overall side effects were mainly mild to moderate.
Journal ArticleDOI
The usefulness of head-up tilt testing and hemodynamic investigations in the workup of syncope of unknown origin.
TL;DR: The tilt test is commonly a provocative tool in the workup of patients with recurrent syncope due to vasovagal ‐ vasodepressor reactions and other abnormalities of blood pressure regulation, and its usefulness is augmented by associated hemodynamic and blood volume evaluations.
Journal ArticleDOI
Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension.
Richard L. Converse,Tage N. Jacobsen,Charles M.T. Jost,Robert D. Toto,Paul A. Grayburn,Troy M. Obregon,Fetnat M. Fouad-Tarazi,Ronald G. Victor +7 more
TL;DR: In a group of hemodialysis patients without diabetes or other conditions known to impair autonomic reflexes, he modialysis-induced hypotension is not caused by chronic uremic impairment in arterial or cardiopulmonary baroreflexes but rather by acute, paradoxical withdrawal of sympathetic vasoconstrictor drive producing vasodepressor syncope.