Extracellular Matrix Marker of Arrhythmia Risk (EMMA)

The recruitment status of this study is unknown because the information has not been verified recently.
Verified May 2008 by Thomas Jefferson University.
Recruitment status was  Recruiting
Information provided by:
Thomas Jefferson University
ClinicalTrials.gov Identifier:
First received: September 14, 2006
Last updated: May 28, 2008
Last verified: May 2008

The primary objective of this study is to assess whether serum levels of MMP 2, 9, and evaluation of the genomic promoter sequence polymorphisms, correlate with episodes of VT/VF in patients who have implantable cardioverter defibrillator devices.

Condition Intervention
Ischemia, Myocardial
Death, Sudden, Cardiac
Device: 2 ARM Event vs. Non-Event

Study Type: Observational
Study Design: Observational Model: Case Control
Time Perspective: Prospective
Official Title: The Role of MMP-9 and MMP-2 in Risk Stratification for VT/VF in Patients With Implanted Cardioverter Defibrillator Devices.

Resource links provided by NLM:

Further study details as provided by Thomas Jefferson University:

Biospecimen Retention:   Samples With DNA


Estimated Enrollment: 100
Study Start Date: September 2006
Estimated Study Completion Date: September 2008
Groups/Cohorts Assigned Interventions
2 observational
Subject with an ICD event of pacing or shock vs. subjects without an event
Device: 2 ARM Event vs. Non-Event
Comparison of MMP Levels and Genetic Promoter Sequence in event (pacing or shock) vs. non-event subjects

Detailed Description:

Sudden cardiac death (SCD) is responsible for 300,000-450,000 deaths per year in the United States. While it is well known that patients with both ischemic and non-ischemic cardiomyopathy (ICM, NICM) are at increased risk for SCD, there is little beyond ejection fraction which has proven useful as a noninvasive predictor to risk stratify these patients.

Myocardial scar has been validated as an arrhythmic substrate in ischemic populations; the majority of successful ablations for lethal ventricular arrhythmias are performed on tissues in peri-infarct regions. Scar provides an anatomic electrical boundary where peri-infarct zones may lead to areas of slow conduction due to the disruption of inter-myocyte electrical conduction.

Myocardial scar is a less organized collagen deposition which disrupts the typical cardiac extracellular matrix. The collagen matrix provides mechanical support to the myocardium dictating ventricular shape, size and stiffness. While typically relatively dormant, the fibrillar collagen matrix reflects a dynamic relationship between collagen synthesis mediated by fibroblasts and collagen degradation performed by matrix metalloproteinases.

A marker for scar burden or a marker which could assess a patient's predilection to form scar after either an ischemic or non-ischemic insult may be useful in further risk stratifying this population. Since MMP levels may fluctuate in the course of ischemic or nonischemic injury a static promoter sequence which confers a higher level of MMP expression to an ischemic or nonischemic insult may prove to be a reliable marker. Functional polymorphisms of the MMP-9 gene promoters have been shown in multivariate analysis to be an independent predictor of cardiac mortality regardless of the mechanism of heart failure.


Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population

Inpatients or outpatients with the ICD device of interest implanted prior to enrollment.


Inclusion Criteria:

  • LVEF of ≤ 35% measured within 6 months of ICD implantation
  • NYHA class II-IV at the time of ICD implantation
  • ICD implantation at least 1 year prior to enrollment

Exclusion Criteria:

  • Status post heart transplant
  • Known malignancy in the past 2 years.
  • Recent procedure, intervention or surgery within the past 90 days
  • Acute MI, CABG, or PTCA/stent within the past 2 months.
  • Active rheumatoid arthritis or pulmonary or hepatic fibrosis.
  • Taking chronic steroid therapy for a medical condition Currently pregnant Enrolled in a concurrent study that may confound the results of this study
  Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT00376532

Contact: Suzanne Adams, RN MPH 215-955-8848 suzanne.adams@jefferson.edu
Contact: Shaw Natan, MD 215-955-5050 shaw.natan@mail.tju.edu

United States, Pennsylvania
Jefferson Heart Institute Recruiting
Philadelphia, Pennsylvania, United States, 19107
Contact: Suzanne Adams, RN MPH    215-955-8848    suzanne.adams@jefferson.edu   
Principal Investigator: David J. Whellan, MD MHS FACC         
Sub-Investigator: Shaw Natan, MD         
Sub-Investigator: Arnold Greenspon, MD         
Sub-Investigator: Behzad Pavri, MD         
Sub-Investigator: Reginald Ho, MD         
Sub-Investigator: Arthur M. Feldman, MD PhD         
Sponsors and Collaborators
Thomas Jefferson University
Principal Investigator: David J. Whellan, MD MHS FACC Thomas Jefferson University
  More Information

No publications provided

Responsible Party: David J. Whellan MD MHS, Thomas Jefferson University, Jefferson Heart Institute
ClinicalTrials.gov Identifier: NCT00376532     History of Changes
Other Study ID Numbers: TJU 06U.282
Study First Received: September 14, 2006
Last Updated: May 28, 2008
Health Authority: United States: Institutional Review Board

Keywords provided by Thomas Jefferson University:
Cardiac Ischemia
Cardiac Arrhythmia
Matrix Metalloproteinase
Genetic Polymorphism

Additional relevant MeSH terms:
Arrhythmias, Cardiac
Death, Sudden
Death, Sudden, Cardiac
Myocardial Ischemia
Heart Diseases
Cardiovascular Diseases
Pathologic Processes
Heart Arrest
Vascular Diseases

ClinicalTrials.gov processed this record on April 22, 2014