scholarly journals Serum Copeptin as the Predictor for Acute Heart Failure Complication of Acute Myocardial Infarction in Patients with ST-Segment Elevation

Author(s):  
Ardi Putranto Ari Supomo ◽  
JB. Suparyatmo ◽  
Dian Ariningrum

Acute Myocardial Infarction (AMI) is necrotic cardiac muscle cells due to unstable ischemic syndrome. Therapy monitoring is needed because various complications may occur (Heart Failure/HF). ST-Segment Elevation Myocardial Infarction (STEMI) can develop to Acute Heart Failure (AHF) due to myocardial dysfunction, transmural heart disease, pathological cardiac remodeling. Copeptin is an antidiuretic hormone which increases in the cardiac event. It can be used as a predictor of a further cardiac event. This study aimed to determine the role of serum copeptin level as a predictor of AHF complication in STEMI patients. A prospective cohort study was performed in 85 adult STEMI patients admitted to The Clinical Pathology Installation of Dr. Moewardi Hospital, Surakarta. Data with normal and abnormal distribution were presented in mean±Standard Deviation (SD) and median (min-max), respectively. Statistical analysis was performed using Kolmogorov-Smirnov, bivariate, and multivariate analysis for RR with Confidence Interval (CI) of 95% and p < 0.05 was considered significant. The copeptin cut-off point was determined using the ROC curve. Bivariate and multivariate analysis showed a higher copeptin level in STEMI patients with AHF compared to that of non-AHF (RR=5.172, CI 95% 1.795-14.902, p=0.002 and RR=1.889, CI 95% 1.156-3.086, p=0.001; respectively). The STEMI patients with an elevated level of copeptin showed an increased risk of AHF (STEMI with elevated copeptin level vs STEMI with normal copeptin level; 28.74% vs. 88.91%). Copeptin level is significantly related to AHF complication in STEMI patient, the higher level of copeptin led to the higher the risk of AHF.

2014 ◽  
Vol 20 (8) ◽  
pp. S117
Author(s):  
Ricardo Mourilhe-Rocha ◽  
Marcelo L.S. Bandeira ◽  
Nathalia F. Araujo ◽  
Ana Rafaela M. Santos ◽  
Roberta Ribeiro ◽  
...  

2013 ◽  
Vol 19 (8) ◽  
pp. S31
Author(s):  
Ricardo Mourilhe-Rocha ◽  
Marcelo L.S. Bandeira ◽  
Nathalia F. Araujo ◽  
Ana R.M. Santos ◽  
Roberta Ribeiro ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
B Van Tassell ◽  
C R Trankle ◽  
D Kadariya ◽  
J M Canada ◽  
S Carbone ◽  
...  

Abstract Background ST-segment elevation myocardial infarction (STEMI) is associated with an intense acute inflammatory response and an increased risk of death and heart failure (HF). C-reactive protein (CRP) is the inflammatory biomarker most commonly used for risk stratification in patients with cardiovascular diseases. CRP levels are known to rise and fall during STEMI in response to myocardial injury. In this study, we analyzed whether admission CRP or delayed CRP (measured at 72 hours after admission) held a greater predictive value for adverse HF events in patients with STEMI. Methods We analyzed data from the VCUART3 clinical trial enrolling 99 patients with STEMI within 12 hours of presentation at 3 sites in the United States of America treated with anakinra or placebo. CRP levels were measured with a high-sensitivity assay at time of admission and again at 72 hours later. A dedicated committee composed of individuals not involved in the conduct of the trial adjudicated HF events including a composite endpoint of death from any reason or incidence of HF defined as new-onset HF requiring hospital admission or a new prescription for a loop diuretic (D+HF) and a composite endpoint of death and HF hospitalization (D+HHF) at 1 year. We used a time-dependent Cox-regression analysis to determine the association of CRP at admission or at 72 hours with the outcomes of interest in univariate and multivariate analysis. Data are presented as median and interquartile range. (ClinicalTrials NCT01950299) Results CRP levels from admission and 72 hours were available in 90 and 87 subjects respectively and they increased from 4.6 [2.8–8.5] mg/L to 11.6 [4.6–24.5] mg/L (P<0.001). Both admission CRP (CRP0) and CRP at 72 hours (CRP72) were associated with the risk of D+HF (P=0.011 and <0.001, respectively) and of D+HHF (P=0.010 and P<0.001, respectively); however at multivariate analysis, only CRP72 remained significantly associated with the risk of D+HF (P=0.001) and D+HHF (P=0.004) while CRP0 was not. CRP72 significantly correlated with NTproBNP levels at 72 hours (NTproBNP72, Spearman rho R=+0.37, P=0.001). NTproBNP72 predicted D+HF (P=0.030) but not independently of CRP72 (P=0.096 for NTproBNP72 and P=0.007 for CRP72 at multivariate analysis including the 2 variables). NTproBNP72 did not predict D-HHF. Conclusions Among contemporary patients with STEMI, the levels of CRP at 72 hours after admission was superior to admission CRP levels for predicting the incidence of HF events, and independent of NTproBNP levels. Our results indicate the importance of the inflammatory response during STEMI, supporting the concept of inhibiting the inflammatory response as a therapeutic strategy. Acknowledgement/Funding Funded by NHLBI 1R34HL121402; Drug supply from Swedish Orphan Biovitrum


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2591-2591
Author(s):  
Carolina Fossati ◽  
Giuseppe Patti ◽  
Vincenzo Pasceri ◽  
Barbara Giannetti ◽  
Annunziata Nusca ◽  
...  

Abstract In patients with acute myocardial infarction, a persistently occluded infarct related coronary artery, despite a correct thrombolysis, is associated with an unfavourable prognosis. Therefore, identification of variables predictive of ineffective thrombolysis is crucial to identify patients at higher risk of thombolysis failure. To investigate whether or not acquired or congenital thrombophilic factors had a role in the ineffective thrombolysis we designed this study in which patients treated with intravenous thrombolysis for a ST segment elevation myocardial infarction were blind tested for the thrombophilic factors on the occasion of the coronary angiography performed within 30 days from the thrombolytic treatment. Patients with known factors influencing metabolism and circulating levels of homocysteine were excluded from this study. From October 2003 to May 2004, 104 consecutive patients treated with intravenous thrombolysis for a ST segment elevation myocardial infarction were available for this study, 3of these refused to participate in the study All patients underwent,within 30 days from thrombolysis, a coronary angiography and of the 101 participating in the study, 40 resulted occluded while 61 had a patent artery. In these 101 patients we blind tested the levels of ATIII,PC,PS; moreover, we determined also the levels of homocysteine, the presence of Lupus Anticoagulant (by mean of DRVVT and Silica Clotting Time) and ACA of IgG type as well as the Plasminogen levels. Furthermore, blood samples were also analysed by PCR technique for the presence of Factor V Leiden, the G20210A Factor II mutation and the C677T mutation in the MTHFR gene. Surprisingly, patients with MTHFR 677TT homozygosis had a significantly higher prevalence of occluded infarct artery (73%) vs those with MTHFR 677CT/CC genotype (30%, P=0.0008); frequency of MTHFR 677TT homozygosis was 4-fold higher in patients with occluded vs those with a patent vessel (40% vs 10%, P=0.0008). MTHFR 677TT genotype predicted the risk of failed thrombolysis with a specificity of 90% and multivariate analysis showed that MTHFR 677TT homozygosis was independently associated with an occluded artery (odds ratio 3.8, 95% confidence interval 1.1–9.1; P=0.03). None of the other studied factors at multivariate analysis influenced the thrombolysis failure. Moreover, patients with occluded infarct vessel and MTHFR 677TT genotype had the highest homocysteine levels (P=0.011). Our findings indicate that in patients with acute myocardial infarction, MTHFR 677TT homozygous is independently associated with a persistently occluded infarct-related artery after thrombolysis.


Kardiologiia ◽  
2018 ◽  
Vol 17 (S8) ◽  
pp. 20-28
Author(s):  
E. M. Mezhonov ◽  
◽  
Y. A. Vyalkina ◽  
K. A. Vakulchik ◽  
S. V. SHalaev ◽  
...  

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