Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Structural remodelling in heart failure: gelatinase induction

P W Armstrong1, G W Moe, R J Howard

  • 1Department of Medicine, Samuel Nunenfeld Research Institute, University of Toronto, Ontario.

The Canadian Journal of Cardiology
|March 1, 1994
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The hospital frailty risk score in patients with heart failure is strongly associated with outcomes but less so with pharmacotherapy.

Journal of internal medicine·2019
Same author

Psychosocial stress and major cardiovascular events in patients with stable coronary heart disease.

Journal of internal medicine·2017
Same author

Effect of nesiritide in patients with acute decompensated heart failure.

The New England journal of medicine·2011
Same author

Benefit of angiographic spontaneous reperfusion in STEMI: does it extend to diabetic patients?

Heart (British Cardiac Society)·2009
Same author

Short- and long-term outcomes following atrial fibrillation in patients with acute coronary syndromes with or without ST-segment elevation.

Heart (British Cardiac Society)·2008
Same author

It's a matter of time: contemporary pre-hospital management of acute ST elevation myocardial infarction.

Heart (British Cardiac Society)·2005

Matrix metalloproteinase-92 kDa activity increases with severe heart failure, correlating with left ventricular remodeling. This suggests a role in the extracellular matrix disruption during heart failure progression and recovery.

Area of Science:

  • Cardiovascular physiology
  • Biochemistry
  • Extracellular matrix remodeling

Background:

  • Rapid ventricular pacing induces congestive heart failure, characterized by neurohumoral activation and cardiac dysfunction.
  • Heart failure involves left ventricular dilation, thinning, shape changes, and disruption of the collagen network.
  • Matrix metalloproteinases (MMPs) are implicated in tissue remodeling, but their role in pacing-induced heart failure is unclear.

Purpose of the Study:

  • To investigate matrix metalloproteinase activity in a canine model of rapid ventricular pacing-induced heart failure.
  • To determine if specific MMPs, particularly gelatinases, are associated with left ventricular structural changes.

Main Methods:

  • Twenty-one dogs underwent rapid ventricular pacing, categorized into early, severe, and recovered heart failure groups.

Related Experiment Videos

  • Measurements included echocardiographic and hemodynamic parameters, noradrenaline levels, and matrix metalloproteinase activity.
  • Gelatinase activity was quantified using specific molecular weight markers (72 kDa and 92 kDa).

    • Main Results:

    • Normal left ventricular tissue showed predominantly 72 kDa gelatinase activity (85%) with minimal 92 kDa activity (15%).
    • 92 kDa gelatinase activity significantly increased with severe heart failure, becoming over 50% of total gelatinase activity.
    • Elevated 92 kDa gelatinase activity strongly correlated with increased left ventricular systolic and diastolic areas, indicating ventricular remodeling.

    Conclusions:

    • Increased 92 kDa gelatinase activity is associated with left ventricular dilation and shape changes in heart failure.
    • This MMP may play a role in modulating the fibrillar components of the extracellular matrix during heart failure.
    • The findings suggest a potential therapeutic target for managing cardiac remodeling in heart failure.