Myocardial infarction causes necrosis of myocardial cells and reduces cardiac function. Today, there are treatments such as primary angioplasty and thrombolysis that are effective in limiting cell death after acute myocardial infarction. However, the post-infarct scar often conditions a global ventricular remodeling that can evolve clinically towards heart failure and in more advanced stages the only therapy that completely restores cardiac function is heart transplantation. Mesenchymal stem cells are multipotent cells found from embryonic mesoderm and found in all tissues. In the field of cardiac regeneration, studies have shown a certain degree of benefit when treated with MSCs from different origins. Our approach is based on a decellularized matrix that carries the cells directly over myocardial infarction.
Myocardial infarction causes necrosis of myocardial cells and reduces cardiac function. Today there are treatments such as primary angioplasty and thrombolysis that are effective in limiting cell death after acute myocardial infarction. However, the post-infarct scar often conditions a global ventricular remodeling that can evolve clinically towards heart failure and, in more advanced stages, the only therapy that completely restores cardiac function is heart transplantation. Experimental studies are evaluating new therapeutic approaches based on tissue engineering for myocardial regeneration. Cardiac tissue engineering attempts to create functional tissue constructs that can restore the structure and function of damaged myocardium. Mesenchymal stem cells (MSCs) are multipotent cells that develop from embryonic mesoderm and are found in all structural tissues of the body. In the field of cardiac regeneration, studies have shown a certain degree of benefit when treated with MSCs from different origins. The investigators approach is based on a decellularized matrix that carries the cells directly over myocardial infarction. Among the different types of MSC currently available, the investigators propose the use of those derived from the connective tissue surrounding the great vessels (2 arteries and one vein) of the umbilical cord called Wharton's gelatin (MSC, WJ) whose immunomodulatory properties are described extensively in the literature. These MSC, WJ cells have a PEI approved by the Spanish Agency for Medicines and Healthcare Products (AEMPS) (PEI 16-017) that guarantees an optimal manufacturing process for a clinical trial.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
DOUBLE
Enrollment
12
A matrix-cell construct (PeriCord) will be placed on the ischemic area of the non-candidate revascularization area during a surgery by sternotomy to perform the surgical revascularization of the arteries candidates for revascularization.
The patient will undergo surgery by sternotomy to perform the surgical revascularization of the arteries candidates for revascularization. No additional procedure will be performed only the by-pass.
Hospital Universitari Germans Trias i Pujol
Badalona, Barcelona, Spain
Rate of death or rehospitalization due to any cause and / or adverse reactions related to the procedure / product under investigation.
Safety measured with a combined endpoint of serious clinical events (death or rehospitalization due to any cause) and serious adverse reactions related to the investigational treatment.
Time frame: at 12 months of follow-up
Rate of death or rehospitalization due to any cause and / or adverse reactions related to the procedure / product under investigation.
Safety measured with a combined endpoint of serious clinical events (death or rehospitalization due to any cause) and serious adverse reactions related to the investigational treatment
Time frame: At 1 week, 3 and 6 months
Death rate or rehospitalization due to cardiovascular causes
Death rate or rehospitalization due to cardiovascular causes at week, 3, 6 and 12 months.
Time frame: At 1 week, 3 , 6and 12 months
Rate of relevant arrhythmias in Holter of 24 hours
Rate of relevant arrhythmias in Holter of 24 hours a week, 3 and 12 months.
Time frame: At 1 week, 3 and 12 months
Relevant changes in N-terminal B-type natriuretic peptide (NT-proBNP) and High sensitivity troponin I (hsTnI) levels
Relevant changes in NT-proBNP and hsTnI levels at week, 3 and 12 months.
Time frame: At 1 week, 3 and 12 months
Changes in the necrotic myocardial mass ratio
Changes in the necrotic myocardial mass ratio due to gadolinium retention at 3 and 12 months.
Time frame: At 3 and 12 months
Changes of regional contractility
change of regional contractility by nuclear magnetic resonance (NMR) at 3 and 12 months.
Time frame: At 3 and 12 months
Changes in ejection fraction of the left ventricle
Changes in ejection fraction of the left at 3 and 12 months
Time frame: At 3 and 12 months
changes in left and right ventricular geometric remodeling
changes in left and right ventricular geometric remodeling at 3 and 12 months
Time frame: At 3 and 12 months
Changes in the score on the quality of life test Short Form 36 Healthy Survey (SF-36).
Changes in the score on the quality of life test SF-36 will be used at 3 and 12 months. The mínimum value is 0 and the máximum value is 100. Higher scores mean a better outcome.
Time frame: At 3 and 12 months
Changes in the score on the quality of life Kansas City Cardiomyopathy Questionnaire (KCCQ) test in cases of participants with heart failure will be used.
Changes in the score on the quality of life test KCCQ in cases of participants with heart failure will be used at 3 and 12 months. The test is composed of 23 items. The options for the answers are Likert scales of 1 to 5, 6 or 7 points and the score of each of its dimensions has a theoretical range from 0 to 100, 100 being the best outcome.
Time frame: At 3 and 12 months
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