https://caltcm.memberclicks.net/assets/documents/acc_aha_chf_2013_guidelines.pdf

2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Matrix metalloproteinases (MMPs), also designated matrixins, hydrolyze components of the extracellular matrix. These proteinases play a central role in many biological processes, such as embryogenesis, normal tissue remodeling, wound healing, and angiogenesis, and in diseases such as atheroma, arthritis, cancer, and tissue ulceration. Currently 23 MMP genes have been identified in humans, and most are multidomain proteins. This review describes the members of the matrixin family and discusses substrate specificity, domain structure and function, the activation of proMMPs, the regulation of matrixin activity by tissue inhibitors of metalloproteinases, and their pathophysiological implication.

Matrix metalloproteinases and tissue inhibitors of metalloproteinases: structure, function, and biochemistry.

https://www.medpagetoday.com/upload/2014/3/3/02536-1.pdf

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease

Matrix metalloproteinases (MMPs), also called matrixins, function in the extracellular environment of cells and degrade both matrix and non-matrix proteins. They play central roles in morphogenesis, wound healing, tissue repair and remodelling in response to injury, e.g. after myocardial infarction, and in progression of diseases such as atheroma, arthritis, cancer and chronic tissue ulcers. They are multi-domain proteins and their activities are regulated by tissue inhibitors of metalloproteinases (TIMPs). This review introduces the members of the MMP family and discusses their domain structure and function, proenyme activation, the mechanism of inhibition by TIMPs and their significance in physiology and pathology.

Structure and function of matrix metalloproteinases and TIMPs

The need for advancing therapeutic strategies with respect to post myocardial infarction (MI) remodeling and the subsequent prevention to progressive left ventricular (LV) failure was well articulated in the editorial by Kloner and colleagues. Specifically, the editorialists identified the need to focus our attention on how localized delivery of stem cells and other strategies can favorably alter the structure and function of the MI region. In this commentary, reference was made to our study regarding the use of a localized delivery strategy by which a recombinant tissue inhibitor of the matrix metalloproteinases (rTIMP-3) was encapsulated in a degradable hydrogel biomaterial and injected directly into the MI region of pigs. In this study, we developed a method by which rTIMP-3 would continuously elute into the MI region with no detectable release into adjacent viable myocardium or the systemic circulation. The key findings were that rTIMP-3 release into the newly formed MI region attenuated key indices of adverse LV remodeling and failure, which included a reduction in LV dilation and pulmonary capillary wedge pressure. At the cellular/molecular level, rTIMP-3 release into the MI region reduced indices of inflammation, such as cytokine expression and macrophage polarization. This was the first study to demonstrate that localized release of a recombinant TIMP could alter the natural history of post- MI remodeling. These findings provide additional evidence that targeting the MMP system in the post-MI context is a relevant therapeutic target.

Author response: new therapies for reducing post-myocardial left ventricular remodeling.

To the Editor:

We thank Schmitto et al for the insightful response to our review “Large Animal Models of Heart Failure: A Critical Link in the Translation of Basic Science to Clinical Practice.”1 The thrust of this commentary was that the use of large animal models of microembolization to produce a chronic myocardial …

Francis G. Spinale

Papers

Author response: new therapies for reducing post-myocardial left ventricular remodeling.

Response to Letter Regarding Article “Large Animal Models of Heart Failure: A Critical Link in the Translation of Basic Science to Clinical Practice”

Preventing radial artery spasm: reply

Injectable Biomaterials and Myocardial Infarction: Gaining a Toehold in an Unstable Matrix.