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William T Rivers

Explore the profile of William T Rivers including associated specialties, affiliations and a list of published articles. Areas
Snapshot
Articles 14
Citations 208
Followers 0
Related Specialties
Cardiology & Vascular Diseases
Physiology
General Surgery
Top 10 Co-Authors
Francis G Spinale
Rupak Mukherjee
Robert E Stroud
Juozas A Zavadzkas
Christine N Koval
Richard A McKinney
Risha K Patel
Jennifer A Dixon
Michael R Zile
Eileen I Chang
Published In
Am J Physiol Heart Circ Physiol
J Thorac Cardiovasc Surg
J Cardiovasc Pharmacol
Circulation
Ann Thorac Surg
Affiliations
Soon will be listed here.
Recent Articles
1.
Cardiopulmonary Resuscitation Quality Issues
Reed-Schrader E, Rivers W, White L, Clemency B
Cardiol Clin . 2018 Oct; 36(3):351-356. PMID: 30293601
Much of the current evidence and many of the recent treatment recommendations for increasing survival from cardiac arrest revolve around improving the quality of cardiopulmonary resuscitation during resuscitation. A focus...
2.
Inhibition of class I histone deacetylase activity represses matrix metalloproteinase-2 and -9 expression and preserves LV function postmyocardial infarction
Mani S, Kern C, Kimbrough D, Addy B, Kasiganesan H, Rivers W, et al.
Am J Physiol Heart Circ Physiol . 2015 Mar; 308(11):H1391-401. PMID: 25795711
Left ventricular (LV) remodeling, after myocardial infarction (MI), can result in LV dilation and LV pump dysfunction. Post-MI induction of matrix metalloproteinases (MMPs), particularly MMP-2 and MMP-9, have been implicated...
3.
Cardiac-restricted overexpression or deletion of tissue inhibitor of matrix metalloproteinase-4: differential effects on left ventricular structure and function following pressure overload-induced hypertrophy
Yarbrough W, Baicu C, Mukherjee R, Van Laer A, Rivers W, McKinney R, et al.
Am J Physiol Heart Circ Physiol . 2014 Jul; 307(5):H752-61. PMID: 24993046
Historically, the tissue inhibitors of matrix metalloproteinases (TIMPs) were considered monochromatic in function. However, differential TIMP profiles more recently observed with left ventricular (LV) dysfunction and matrix remodeling suggest more...
4.
Progressive induction of left ventricular pressure overload in a large animal model elicits myocardial remodeling and a unique matrix signature
Yarbrough W, Mukherjee R, Stroud R, Rivers W, Oelsen J, Dixon J, et al.
J Thorac Cardiovasc Surg . 2011 Nov; 143(1):215-23. PMID: 22056365
Objective: Patients with severe left ventricular pressure overload secondary to aortic stenosis can present with signs and symptoms of heart failure despite normal left ventricular ejection fraction. This process occurs,...
5.
Direct regulation of membrane type 1 matrix metalloproteinase following myocardial infarction causes changes in survival, cardiac function, and remodeling
Zavadzkas J, Mukherjee R, Rivers W, Patel R, Meyer E, Black L, et al.
Am J Physiol Heart Circ Physiol . 2011 Jun; 301(4):H1656-66. PMID: 21666120
The membrane type 1 matrix metalloproteinase (MT1-MMP) is increased in left ventricular (LV) failure. However, the direct effects of altered MT1-MMP levels on survival, LV function, and geometry following myocardial...
6.
Continuous localized monitoring of plasmin activity identifies differential and regional effects of the serine protease inhibitor aprotinin: relevance to antifibrinolytic therapy
Reust D, Dixon J, McKinney R, Patel R, Rivers W, Mukherjee R, et al.
J Cardiovasc Pharmacol . 2011 Apr; 57(4):400-6. PMID: 21502925
Background: Antifibrinolytic therapy, such as the use of the serine protease inhibitor aprotinin, was a mainstay for hemostasis after cardiac surgery. However, aprotinin was empirically dosed, and although the pharmacological...
7.
Hemodynamics and myocardial blood flow patterns after placement of a cardiac passive restraint device in a model of dilated cardiomyopathy
Dixon J, Goodman A, Gaillard 2nd W, Rivers W, McKinney R, Mukherjee R, et al.
J Thorac Cardiovasc Surg . 2011 Mar; 142(5):1038-45. PMID: 21397269
Background: The present study examined a cardiac passive restraint device which applies epicardial pressure (HeartNet Implant; Paracor Medical, Inc, Sunnyvale, Calif) in a clinically relevant model of dilated cardiomyopathy to...
8.
Heterogeneity in MT1-MMP activity with ischemia-reperfusion and previous myocardial infarction: relation to regional myocardial function
Dixon J, Gaillard 2nd W, Rivers W, Koval C, Stroud R, Mukherjee R, et al.
Am J Physiol Heart Circ Physiol . 2010 Oct; 299(6):H1947-58. PMID: 20935147
After a myocardial infarction (MI), an episode of ischemia-reperfusion (I/R) can result in a greater impairment of left ventricular (LV) regional function (LVRF) than that caused by an initial I/R...
9.
Long-term localized high-frequency electric stimulation within the myocardial infarct: effects on matrix metalloproteinases and regional remodeling
Mukherjee R, Rivers W, Ruddy J, Matthews R, Koval C, Plyler R, et al.
Circulation . 2010 Jun; 122(1):20-32. PMID: 20566951
Background: Disruption of the balance between matrix metalloproteinases (MMP) and MMP inhibitors (TIMPs) within a myocardial infarct (MI) contributes to left ventricular wall thinning and changes in regional stiffness at...
10.
Short-term disruption in regional left ventricular electrical conduction patterns increases interstitial matrix metalloproteinase activity
Mukherjee R, Zavadzkas J, Rivers W, McLean J, Chang E, Bouges S, et al.
Am J Physiol Heart Circ Physiol . 2010 May; 299(1):H217-24. PMID: 20472759
Increased matrix metalloproteinase (MMP) abundance occurs with adverse left ventricular (LV) remodeling in a number of cardiac disease states, including those induced by long-standing arrhythmias. However, whether regionally contained aberrant...