The role of Val66Met single nucleotide polymorphism in brain-derived neurotropic factor gene in prediction of adverse outcomes after ST-segment elevation myocardial infarction

2019 ◽  
Vol 3 (1) ◽  
pp. 7
Author(s):  
AlexanderE Berezin ◽  
OlgaV Petyunina ◽  
MykolaP Kopytsya ◽  
OlgaV Skrynnyk
Keyword(s):  
Myocardial Infarction ◽  
Adverse Outcomes ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Factor Gene ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Neurotropic Factor

scholarly journals The role of single nucleotide polymorphism Val66Met in BDNF gene in the formation of end points after ST segment elevation myocardial infarction

2019 ◽  
Vol 27 (3) ◽  
pp. 19-25
Author(s):  
Olga Petyunina ◽  
Mykola Kopytsya ◽  
Olga Skrynnyk
Keyword(s):  
Myocardial Infarction ◽  
Single Nucleotide Polymorphism ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Bdnf Gene ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment

The purpose of this study was to research the possible associations of single-nucleotide polymorphism of Val66Met BDNF gene with the occurrence of endpoints after 6 months of follow-up after a myocardial infarction with ST elevation segment — ST segment elevation myocardial infarction (STEMI). To participate in the study, 256 patients which met all the inclusion criteria were hospitalized in the department of intensive care, State Institution “L. T. Malaya Therapy National Institute NAMSU” from January 2016 to February 2019. Blood fl ow to all patients was restored at the level TIMI III. The frequency of genotypes Val66Met gene for BDNF in STEMI patients (n = 256) was the following: 66ValVal — 74.2 % (n = 190), 66ValMet + 66MetMet — 25.8 % (n = 66). The study of single-nucleotide polymorphism of Val66Met gene BDNF (rs6265) was performed by real-time polymerase chain reaction using the “TacMan TMSNP Genotyping Assays” production of Thermo Fisher Scientifi c Assay IDC_11592758_1. The emotional state of the patients and its relationship with stress were assessed with the questionnaire “Depression, Anxiety and Stress Scale-21”. It turned out that the 66ValMet + 66MetMet polymorphism of the BDNF gene, stress and anxiety 10—14 days before the event, as well as reduced left ventricular ejection fraction, are associated with an unfavorable prognosis of the combined end point 6 months after STEMI and are its independent predictors.

Novel role of platelet reactivity in adverse left ventricular remodelling after ST-segment elevation myocardial infarction: The REMODELING Trial

2017 ◽  
Vol 117 (05) ◽  
pp. 911-922 ◽  
Author(s):  
Yongwhi Park ◽  
Udaya Tantry ◽  
Jin-Sin Koh ◽  
Jong-Hwa Ahn ◽  
Min Kang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Reactivity ◽  
Left Ventricular ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Hs Crp

SummaryThe role of platelet-leukocyte interaction in the infarct myocardium still remains unveiled. We aimed to determine the linkage of platelet activation to post-infarct left ventricular remodelling (LVR) process. REMODELING was a prospective, observational, cohort trial including patients (n = 150) with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. Patients were given aspirin plus clopidogrel therapy (600 mg loading and 75 mg daily). Platelet reactivity (PRU: P2Y12 Reaction Units) was assessed with VerifyNow P2Y12 assay on admission. Transthoracic echocardiography was performed on admission and at one-month follow-up. The primary endpoint was the incidence of LVR according to PRU-based quartile distribution. LVR was defined as a relative ≥ 20 % increase in LV end-diastolic volume (LVEDV) between measurements. Adverse LVR was observed in 36 patients (24.0 %). According to PRU quartile, LVR rate was 10.8 % in the first, 23.1 % in the second, 27.0 % in the third, and 35.1 % in the fourth (p = 0.015): the optimal cut-off of PRU was ≥ 248 (area under curve: 0.643; 95 % confidence interval: 0.543 to 0.744; p = 0.010). LVR rate also increased proportionally according to the level of high sensitivity-C reactive protein (hs-CRP) (p = 0.012). In multivariate analysis, the combination of PRU (≥ 248) and hs-CRP (≥ 1.4 mg/l) significantly increased the predictive value for LVR occurrence by about 21-fold. In conclusion, enhanced levels of platelet activation and inflammation determined the incidence of adverse LVR after STEMI. Combining the measurements of these risk factors increased risk discrimination of LVR. The role of intensified antiplatelet or anti-inflammatory therapy in post-infarct LVR process deserves further study.

Sign in / Sign up

Export Citation Format

Share Document