Clinical trial NCT00430885: Effect of Intravenous Immunglobulin (IVIG) After Myocardial Infarction
Official title: Phase III Study of Intravenous Immunglobulin (IVIG) in Patients With Heart Failure After Myocardial Infarction
Study type: INTERVENTIONAL
Overall status: COMPLETED
Phase: PHASE3
Conditions: Acute Myocardial Infarction
Keywords: Heart failure
Myocardial infarction
Patients with acute myocardial infarction
Lead sponsor: Oslo University Hospital
Sponsor class: OTHER
Collaborators: name: Helse Stavanger HF
First posted: 2007-02-02
Enrollment: 62
Sex: ALL
Minimum age (years): 18
Maximum age (years): 18
Standard ages: ADULT
Accepts healthy volunteers: no
Allocation: RANDOMIZED
Intervention model: PARALLEL
Primary purpose: TREATMENT

Brief summary: The instigators hypothesize that IVIG, given in the acute phase following MI in patients at risk for developing HF, will improve cardiac performance, and by attenuating cardiac remodeling in this phase, such therapy will prevent the development of chronic HF resulting in long term beneficial effect also after the therapy has been stopped.

Detailed description: This double-blind placebo-controlled study represents a new approach to cardiovascular disease. The project deals with unresolved issues in the intersection between cardiology, immunology and molecular biology.

IVIG/placebo will be given as an induction therapy for 5 days and thereafter as monthly infusions for 5 months. Change in left ventricular remodeling will be assessed at baseline, and 6 and 12 months with MRI and echocardiography.

The objectives are:

1. The primary objective of this study is to evaluate the effect on IVIG on LV remodeling and function: LV remodeling will be evaluated with magnetic resonance imaging (MRI) which offers an unsurpassed precision in the measurements of heart volumes and function. End points will be LV-end systolic and diastolic volume (LVESV, LVEDV), regional wall motion score index (WMSI), and LV-ejection fraction (LV-EF).
2. The secondary objective of this study is to evaluate the effect on IVIG on the myocardial marker B-Type Natriuretic Peptide (BNP). BNP is a sensitive marker of the degree of HF besides being a prognostic indicator 18-20.
3. The tertiary objective of this study is to evaluate the effect on IVIG on:

   a. Quality of life. b. Effect on New York Heart Association (NYHA) functional class. c. Effect on immunological variables. i. Inflammatory cytokines such as TNF-alpha, IL-6, IL-18. ii. Anti-inflammatory cytokines such as IL-10 and transforming growth factor beta iii. Chemokines such as monocyte chemoattractant protein 1, IL-8 and CCL21. iv. Regulators of hypertrophy such as matrix metalloproteinases, their endogenous inhibitors (i.e., TIMPs) and procollagen III N-terminal.

   d. Effect on neurohormones. e. Withdrawals. f. Side effects.

Eligibility criteria: Inclusion Criteria:

* Age of 18-80 years
* Have a recent MI (\<5days)
* Have ASAT \>100 U/L or CKMB \> 50 U/L.
* Have LVEF \<40%.
* Are on optimal medical treatment and considered unsuitable for surgical intervention.

Exclusion Criteria:

* Evidence of unstable disease, concomitant ischemia or unstable angina during the hospitalization.
* Significant concomitant disease such as infections, pulmonary disease or connective tissue disease.
* Participating in other studies.
* Inability to participate.
* Diseases that require surgery.
* Planned revascularisation.
* Known hypersensitivity to IVIG.

Primary outcomes:
measure: 1. The effect on IVIG on LV remodeling (volume and ejection fraction) and function as assessed by MRI
timeFrame: 2009
Secondary outcomes:
measure: 2. Effect on IVIG on B-Type Natriuretic Peptide (BNP).
timeFrame: 2009
Other outcomes:
Locations:
city: Oslo
country: Norway
facility: Rikshospitalet University Hospital
Study officials:
name: Lars Gullestad, MD, PhD
role: PRINCIPAL_INVESTIGATOR
References:
citation: Gullestad L, Orn S, Dickstein K, Eek C, Edvardsen T, Aakhus S, Askevold ET, Michelsen A, Bendz B, Skardal R, Smith HJ, Yndestad A, Ueland T, Aukrust P. Intravenous immunoglobulin does not reduce left ventricular remodeling in patients with myocardial dysfunction during hospitalization after acute myocardial infarction. Int J Cardiol. 2013 Sep 20;168(1):212-8. doi: 10.1016/j.ijcard.2012.09.092. Epub 2012 Oct 6.