Low FXIII levels impairs wound healing, causes cardiac rupture and remodeling after myocardial infarction (MI). Molecular imaging demonstrates FXIII in the MI area. We recently recognized acute FXIII drops in the first post-MI days, and this was genotype dependent. Our objective is to investigate if FXIII drop, and/or late recovery, could be a novel MI marker and if a FXIII prognostic threshold could exist. We recruited 250 MI patients from Coronary Care Unit of Hospital-University of Ferrara: 72% male; 65.5±12.5yy; STEMI 78.5%; PCI 95%. We performed 1-year follow-up and the combined end-point was re-MI, death, heart failure, stroke, u-angina (MACE). FXIII level was assessed by a commercial kit [Instrumentation Laboratory, Italy] at the recruitment (t0) and every 24-hour for 5 days (t1-5) post-MI. Control samples were drawn at 30-day (t30) to have steady state levels. Patients were V34L-genotyped. Globally, t0 had 100.5±33.5 FXIII mean level; the lowest value was at t4-5 (85.3±27.3) and t30 was 99.4±25.7. Stratifying data by genotype, L-carriers had the highest fall when compared to VV-genotype. Stratifying patients by FXIII-(t4-5) median level (73.2%) there was a non-significant MACE overrepresentation among low FXIII levels (31% vs 15%). Conversely, by using ROC-FXIII-cutoff (81.3%), the difference was significant (30% vs 9.5%; P=0.03). We conclude that, despite excellent therapy for MI, post-MI MACE still remain critical influencing survival. Understanding whether FXIII level monitoring may be useful to select cases with poor clinical outcome could pave the way to utilize FXIII as tailored treatment to improve myocardial healing, recovery of functions and survival.
FXIII levels and genotypes in myocardial infarction: a potential novel prognostic biomarker?
ZERI, Giulia;MARI, Rosella;ORIOLI, Elisa;BERNARDI, Francesco;MALAGU', Michele;FERRARI, Roberto;SERINO, Maria Luisa;GEMMATI, Donato
2012
Abstract
Low FXIII levels impairs wound healing, causes cardiac rupture and remodeling after myocardial infarction (MI). Molecular imaging demonstrates FXIII in the MI area. We recently recognized acute FXIII drops in the first post-MI days, and this was genotype dependent. Our objective is to investigate if FXIII drop, and/or late recovery, could be a novel MI marker and if a FXIII prognostic threshold could exist. We recruited 250 MI patients from Coronary Care Unit of Hospital-University of Ferrara: 72% male; 65.5±12.5yy; STEMI 78.5%; PCI 95%. We performed 1-year follow-up and the combined end-point was re-MI, death, heart failure, stroke, u-angina (MACE). FXIII level was assessed by a commercial kit [Instrumentation Laboratory, Italy] at the recruitment (t0) and every 24-hour for 5 days (t1-5) post-MI. Control samples were drawn at 30-day (t30) to have steady state levels. Patients were V34L-genotyped. Globally, t0 had 100.5±33.5 FXIII mean level; the lowest value was at t4-5 (85.3±27.3) and t30 was 99.4±25.7. Stratifying data by genotype, L-carriers had the highest fall when compared to VV-genotype. Stratifying patients by FXIII-(t4-5) median level (73.2%) there was a non-significant MACE overrepresentation among low FXIII levels (31% vs 15%). Conversely, by using ROC-FXIII-cutoff (81.3%), the difference was significant (30% vs 9.5%; P=0.03). We conclude that, despite excellent therapy for MI, post-MI MACE still remain critical influencing survival. Understanding whether FXIII level monitoring may be useful to select cases with poor clinical outcome could pave the way to utilize FXIII as tailored treatment to improve myocardial healing, recovery of functions and survival.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
