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January 31, 2008European Journal of Heart FailureOpen Access

Circulating Stromelysin-1 (MMP-3): A Novel Predictor of LV Dysfunction, Remodelling and All-Cause Mortality After Acute Myocardial Infarction

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Key result

Elevated pre-discharge plasma MMP-3 levels were associated with adverse left ventricular remodeling and an increased risk of death or heart failure after acute myocardial infarction (P<0.001).

Why the study?

Does circulating MMP-3 predict LV dysfunction, remodelling, and mortality in patients with acute myocardial infarction?

Population

382 patients with acute myocardial infarction (AMI)

Design

Cohort

Follow-up

median 148 days for echocardiography, median 313 days for…

Authors

DKD. KellyUniversity of LeicesterSKSQ KhanUniversity of LeicesterGCGillian CockerillUniversity of London

Discussion

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Implication

May refine post-MI risk stratification; hypothesis-generating and should not yet change practice.

Study Design

Type

Cohort (n=382)

Structured PICO

Does circulating MMP-3 predict LV dysfunction, remodelling, and mortality in patients with acute myocardial infarction?

P
Population
382 patients with acute myocardial infarction followed for a median of 313 days for clinical endpoints.
E
Exposure
Measurement of plasma MMP-3 levels (0-12, 12-24 h and subsequent 24 h periods during admission)
O
Outcome
Left ventricular function (LVEF) and composite clinical endpoints (death or heart failure) at a median of 313 dayscomposite

Main Result

p-value: p=<0.001

Elevated pre-discharge plasma MMP-3 levels predict left ventricular dysfunction, adverse remodeling, and increased risk of death or heart failure following acute myocardial infarction.

Cite This Study

Kelly et al. (2008) conducted a cohort in Acute Myocardial Infarction (n=382). Plasma MMP-3 vs. Lower MMP-3 levels was evaluated on Death or heart failure (p=<0.001). Elevated pre-discharge plasma MMP-3 levels were associated with adverse left ventricular remodeling and an increased risk of death or heart failure after acute myocardial infarction (P<0.001).

synapsesocial.com/papers/6a71cbd05671bbf00bc2f515https://doi.org/10.1016/j.ejheart.2007.12.009
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Lower serum concentration of matrix metalloproteinase‐3 in the acute stage of myocardial infarction2006 · 30 citations
  2. 2Contribution of Plasma Matrix Metalloproteinases to Development of Left Ventricular Hypertrophy and Diastolic Dysfunction in Hypertensive Subjects2006 · 25 citations
  3. 3Time-Dependent Changes in Matrix Metalloproteinase Activity and Expression During the Progression of Congestive Heart Failure1998 · 372 citations
  4. 4Selective Matrix Metalloproteinase Inhibition Reduces Left Ventricular Remodeling but Does Not Inhibit Angiogenesis After Myocardial Infarction2002 · 187 citations
  5. 5Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction2000 · 813 citations