scholarly journals Differential Expression of TXNIP Isoforms in the Peripheral Leukocytes of Patients with Acute Myocardial Infarction

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Yujing Zhang ◽  
Peng Zhong ◽  
Yingze Xu ◽  
Baokui Wang ◽  
Tao Zhu ◽  
...  

Background. Acute myocardial infarction (AMI) is the most serious type of coronary atherosclerotic heart disease (CAD). The pathological changes are characterized by atherosclerosis. Oxidative stress plays an important role in atherosclerosis. Thioredoxin-interacting protein (TXNIP), an endogenous inhibitor and regulator of thioredoxin, could bind thioredoxin to regulate its expression and antioxidant activity negatively. The NCBI data show that there are two isoforms in TXNIP gene, namely, TXNIP1 and TXNIP2. Our previous studies have shown that TXNIP expression levels in patients with unstable angina pectoris (UAP) were increased compared with controls (CTR). However, no upregulation of TXNIP was detected in AMI patients. Methods. The leucocytes were isolated from peripheral venous blood, and total RNA of the leucocytes was extracted. Then, real-time quantitative PCR was performed. Results. mRNA levels of TXNIP2 in AMI were significantly increased compared with CTR (P<0.05). However, the expression of TXNIP1 was downregulated in AMI, but the difference was not statistically significant (P>0.05). Logistic regression analysis showed that TXNIP2 mRNA levels were significantly associated with AMI (OR = 2.207, P<0.05). Conclusions. The expression of TXNIP2, not TXNIP1, is upregulated in leukocytes of AMI patients, indicating that only TXNIP2 in circulating leucocytes may be involved in the pathogenesis of AMI.

Author(s):  
Shashank S Sinha ◽  
Nicholas M Moloci ◽  
Andrew M Ryan ◽  
Brahmajee K Nallamothu ◽  
John M Hollingsworth

Objective: Spending for acute myocardial infarction (AMI) episodes varies widely across hospitals, driven primarily by payments made more than 30 days after discharge. Through collective incentives and an emphasis on care coordination, Medicare accountable care organizations (ACOs) may help reduce this variation. To test this hypothesis, we analyzed national Medicare data. Methods: Using a 20% random sample, we identified Medicare beneficiaries admitted for AMI from January 2010 to December 2013. We distinguished admissions to hospitals affiliated with a Medicare ACO from those that were not. We then calculated 90-day, price-standardized, risk-adjusted episode payments made on behalf of beneficiaries, differentiating between early (index admission to 30 days post-discharge) and late payments (31 to 90 days). We also calculated component payments, including those for the index hospitalization, readmissions, physician services, and post-acute care. Finally, we used difference-in-differences estimation to measure the effect of admission to an ACO-affiliated hospital on early and late episode payments. Results: Over the study period, 15,219 beneficiaries were admitted to 299 eventual ACO-affiliated hospitals and 73,910 were admitted to 1,685 never ACO-affiliated hospitals ( p <0.001). While beneficiaries admitted to eventual ACO-affiliated hospitals tended to be younger than those admitted to never ACO-affiliated hospitals (mean age: 79.2 ± 8.6 versus 80.0 ± 8.5, respectively; p =.003), they had similar levels of comorbidity (mean Elixhauser score: 2.7 ± 1.4 versus 2.7 ± 1.4, respectively; p =0.526). Mean 90-day episode payments were greater for ACO-affiliated hospitals [$24,887 versus $23,966; p <0.001]. In the period after ACO implementation (2012 and 2013), total payments for AMI episodes fell by $1259 (Figure; p <0.001). Most of this savings was attributable to decreases in early ($1118) versus late ($141) episode payments. However, none of these savings differed based on admission to an ACO-affiliated hospital ( p =0.363 for the difference). Conclusions: Early Medicare ACOs have not affected 90-day episode payments for AMI admissions. Future studies should explore the possibility of heterogeneity in effect based on ACO structure.


2015 ◽  
Vol 40 (2) ◽  
pp. 79-84 ◽  
Author(s):  
T Bashar ◽  
N Akhter

In acute myocardial infarction (AMI), lack of oxygen delivery to myocardium leads to generation of reactive oxygen species (ROS) which play an important role in the pathogenesis of AMI. Endogenous anti-oxidants protect the myocardial tissues from the deleterious effect of free radical mediate injury. The study evaluates the extent of oxidative stress and antioxidant status against ROS in AMI patients and amelioration of oxidative stress after regular treatment and also assesses the association between oxidative stress and risk factors for atherosclerosis like dyslipidemia and diabetes mellitus (DM).The study was conducted on 72 AMI patients and age and sex matched 18 healthy controls. Patients were assigned to four groups, AMI without dyslipidemia or DM, with dyslipidemia, with DM and with both dyslipidemia and DM. Plasma malondialdehyde (MDA) and GSH content and vitamin E levels were determined on admission into hospital and on the 5th day of treatment. Plasma MDA level increased significantly (p<0.001) and erythrocyte GSH and plasma vitamin E levels were decreased (p<0.001) in all the groups of patients as compared to control. On the 5th day of regular treatment MDA level reduced (p<0.001) and GSH and vitamin E levels increased (p<0.001) in patients. The plasma MDA level was significantly higher (p<0.001) in patients with both dyslipidemia and DM or with only DM in comparison to patients without dyslipidemia and DM. The difference in the GSH level between patients with risk factors and without risk factors was not significant. It may be conclude that an imbalance exists between oxidant and antioxidant molecules in AMI patients which shift towards oxidative side and regular treatment restores this balance. There may be some association between oxidative stress in AMI and risk factors like dyslipidemia and diabetes mellitus.Bangladesh Med Res Counc Bull 2014; 40 (2): 79-84


2021 ◽  
Author(s):  
Kaiyang Wang ◽  
Yunjie Teng ◽  
Tingting Wu ◽  
Yitong Ma ◽  
Xiang Xie

Abstract Background:To explore the application value of thromboelastic graph (TEG) in the assessment of patients with acute myocardial infarction (AMI).Results: 1.R time (min), K time (min) and LY30(%) in the STEMI group were lower than those in the NSTEMI group, and the differences were statistically significant (P<0.05). The Angle(°) and MA values in the STEMI group were higher than those in the NSTEMI group, and the difference between the two groups was statistically significant (P<0.05). 2.R time(min), K time(min) and LY30(%) gradually decreased with the increase of the number of coronary artery lesions, while Angle(°) and MA value(mm) gradually increased. 3. R time (min), K time (min) and LY30(%) gradually decreased with the aggravation of coronary artery lesions, while Angle(°) and MA value (mm) gradually increased. 4. R time (min), K time (min) and LY30(%) were negatively correlated with Gensini score (r=-0.456, -0.418, -0.483, P<0.001).Angle(°) and MA value(mm) were positively correlated with Gensini score (r=0.531, 0.569, P<0.001).Conclusion: Thromboelastic graph (TEG) can be used as an effective indicator for predicting the condition of patients with acute myocardial infarction (AMI), evaluating the severity of coronary artery disease, and guiding clinical treatment.


2020 ◽  
Author(s):  
Safir Soukaina

Background: Acute myocarditis and acute myocardial infarction have frequently similar clinical presentations and poses an important clinical challenge in the differential diagnosis. In both cases, the electrocardiographic ST-T changes and an increase in troponins can be noted. Differential diagnosis may be very challenging and requires invasive assessment of coronary arteries and other investigations especially cardiac magnetic resonance. Case Presentation: In this report, we report a rare case of acute myocarditis misdiagnosed to an acute myocardial infarction in a patient presented to the emergency department for an acute onset of chest pain with ST-segment elevation on electrocardiogram for which he received urgent fibrinolysis. The confirmation of acute myocarditis was confirmed posteriori after a normal coronary angiogram using cardiac Magnetic Resonance Imaging cMRI. Conclusions: Clinical signs as long with Electrocardiogram may mimick a ST elevation myocardial infarction in the presence of an authentic acute myocarditis,Hence, cardiac magnetic resonance could present an intersting tools to make the difference even in acute phase.


1991 ◽  
Vol 37 (6) ◽  
pp. 845-852 ◽  
Author(s):  
Johannes Mair ◽  
Erika Artner-Dworzak ◽  
Peter Lechleitner ◽  
Jörn Smidt ◽  
Ina Wagner ◽  
...  

Abstract Troponin T is a structurally bound protein found in striated muscle cells. We tested concentrations of its cardiac-specific isotype in peripheral venous blood samples serially drawn from 72 patients with confirmed myocardial infarction. Fifty-nine patients received thrombolytic treatment with intravenous streptokinase, urokinase, or recombinant tissue-type plasminogen activator; because of contraindications, the remaining 13 patients did not. Concentrations of troponin T in plasma, measured by an enzyme-linked immunosorbent assay, started increasing within a few hours after the onset of symptoms (median, 4 h; range, 1-10 h). The sensitivity of troponin T for detecting myocardial infarction was 100% from 10 to 120 h after the onset of symptoms; sensitivity on the seventh day after admission was 84%. Concentrations were increased for up to three weeks in some patients with late or high peak values. Successful reperfusion in Q-wave infarction obviously influences the release of troponin T into plasma, with all such cases showing peak values less than or equal to 26 h (median, 14 h) after the onset of symptoms. Troponin T concentrations in these patients returned to within the reference interval more rapidly than in nonreperfused subjects. In the 13 patients without fibrinolytic therapy, troponin T tended to peak approximately 48 h (median) after the onset of chest pain. Troponin T concentrations in patients for whom thrombolysis was unsuccessful resembled those in patients without fibrinolytic therapy. The specificity of the assay was 96% as tested in samples of 96 emergency-room patients. The reference interval (less than 0.5 micrograms/L) was established from samples of 100 healthy blood donors. Troponin T measurements are a specific and sensitive method for the early and late diagnosis of acute myocardial infarction and could, therefore, provide a new criterion in laboratory diagnosis of its occurrence.


2013 ◽  
Vol 305 (2) ◽  
pp. E263-E270 ◽  
Author(s):  
Sevasti Zervou ◽  
Tanmoy Ray ◽  
Natasha Sahgal ◽  
Liam Sebag-Montefiore ◽  
Rebecca Cross ◽  
...  

Creatine is important for energy metabolism, yet excitable cells such as cardiomyocytes do not synthesize creatine and rely on uptake via a specific membrane creatine transporter (CrT; SLC6A8). This process is tightly controlled with downregulation of CrT upon continued exposure to high creatine via mechanisms that are poorly understood. Our aim was to identify candidate endogenous CrT inhibitors. In 3T3 cells overexpressing the CrT, creatine uptake plateaued at 3 h in response to 5 mM creatine but peaked 33% higher ( P < 0.01) in the presence of cycloheximide, suggesting CrT regulation depends on new protein synthesis. Global gene expression analysis identified thioredoxin-interacting protein (Txnip) as the only significantly upregulated gene (by 46%) under these conditions ( P = 0.036), subsequently verified independently at mRNA and protein levels. There was no change in Txnip expression with exposure to 5 mM taurine, confirming a specific response to creatine rather than osmotic stress. Small-interfering RNA against Txnip prevented Txnip upregulation in response to high creatine, maintained normal levels of creatine uptake, and prevented downregulation of CrT mRNA. These findings were relevant to the in vivo heart since creatine-deficient mice showed 39.71% lower levels of Txnip mRNA, whereas mice overexpressing the CrT had 57.6% higher Txnip mRNA levels and 28.7% higher protein expression compared with wild types (mean myocardial creatine concentration 124 and 74 nmol/mg protein, respectively). In conclusion, we have identified Txnip as a novel negative regulator of creatine levels in vitro and in vivo, responsible for mediating substrate feedback inhibition and a potential target for modulating creatine homeostasis.


Diagnostics ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 2035
Author(s):  
Kuang-Che Kuo ◽  
Ya-Ling Yang ◽  
Mao-Hung Lo ◽  
Xin-Yuan Cai ◽  
Mindy Ming-Huey Guo ◽  
...  

Background: Kawasaki disease (KD) is a form of febrile vasculitis that primarily occurs in children. It can cause inflammation of the coronary arteries, which leads to aneurysms. The pathogenesis of coronary arteries may be associated with apoptosis or pyroptosis mediated by caspases activity, but this idea has not been discussed much in KD. Materials and Methods: We enrolled 236 participants in this study. In the Affymetrix GeneChip® Human Transcriptome Array 2.0 study, there were 18 KD patients analyzed prior to receiving intravenous immunoglobulin (IVIG) treatment, at least 3 weeks after IVIG treatment, and 36 non-KD control subjects. We also recruited 24 KD patients prior to receiving IVIG treatment, at least 3 weeks after IVIG treatment, and 24 non-KD control subjects for Illumina HumanMethylation450 BeadChip study. A separate cohort of 134 subjects was analyzed to validate real-time quantitative PCR. Results: The mRNA levels of caspase-1, -3, -4, and -5 were significantly increased in KD patients compared with control subjects (p < 0.05). After administration of IVIG, the expression of these genes decreased considerably. Of particular note, the methylation status of the CpG sites of the caspase-4 and -5 genes demonstrated significant opposite tendencies between the KD patients and controls. Furthermore, compared with patients who responded to IVIG, refractory KD patients had a lower expression of the caspase-3 gene prior to IVIG treatment. Conclusion: Our study is the first to report the upregulation of pyroptotic caspase-1, -4, and -5 in peripheral leukocytes of KD patients. Moreover, the expression of caspase-3 may be associated with IVIG resistance in KD.


Author(s):  
Abuagla M. Dafalla ◽  
Leena A. Dafalla ◽  
ShamsEldein M. Ahmed ◽  
Yousif A. Mohammed ◽  
Adam D. Abakar ◽  
...  

Background: Cardiac diseases are one of the major causes of death worldwide with increasing incidence rate per year, particularly in developing countries such as Sudan owing to urbanization and changing lifestyle. Myocardial infarction is a consequence of the imbalance between the heart blood supply and the required heart cell; this disorder leads to necrosis of myocardium and may cause death. It could be diagnosed by at least two of the following criteria: chest pain, electrocardiography (ECG) elevation, and levels on cardiac biomarkers. This study aimed to evaluate the efficiency of N-terminal pro-B-type natriuretic peptide (NTproBNP) for the diagnosis of acute myocardial infarction (AMI).  Methods: This analytical case–control hospital-based study was conducted on a total of 70 individuals, of which 40 participants were suspected of or diagnosed with AMI, while 30 healthy subjects  were included as a control group. Three ml of venous blood were collected in lithium heparin containers. Troponin I (TnI) as a cardiac biomarker was measured by TOSOH AIA-360, while the NTproBNP level was detected using I-Chroma II. Personal and clinical data were collected directly from each participant using a predesigned questionnaire. Results: A significant increase in the TnI level (mean: 13.13 ± 18.9 ng/ml) and NTproBNP (mean: 5756.5 ± 8378.2 pg/mL) in AMI patients were detected when compared with control mean (0.02 ± 0.00 ng/ml and 57.8 ± 42.32 pg/mL, respectively). Conclusions: NTproBNP gave a high sensitivity (87.5%), specificity (100%), positive predictive value (100%), and negative predictive value (85.7%) in the diagnosis of AMI when compared with another cardiac biomarker such as TnI. Keywords: acute myocardial infarction, NTproBNP, troponin I, Medani Heart Center, Sudan


2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Tri Prasetyorini ◽  
Rizka Noviyanti ◽  
Putu Puja Permata Kasih ◽  
Diah Lestari

Acute Myocardial Infarction (AMI) is a manifestation of acute myocardial ischemia and is generally caused by the rupture of atherosclerosis and thrombus in the coronary blood vessels. Rupture causes an inflammatory process that leukocytes which acts as a marker of inflammation increases. Heart muscle damage that occurs also resulted in levels of troponin I as one of the markers of increased cardiac examination. Based on that research aims to determine the correlation between the levels of troponin I and the number of leukocytes in patients with suspected AMI.This research method is analytical observation with a data sample of 100 patients with suspected AMI diagnosis by doctors as well as examine the levels of troponin I and the number of leukocytes in dr. Abdulmadjid Chasbullah Bekasi. The correlation between the levels of troponin I and leukocyte counts were analyzed using Spearman's test. Data studied consisted of 52 people (52%) men and 48 (48%) of women. By age group, age range 46-65 years become the largest age group into patients with suspected AMI is 55 people (55%). Obtained 34 (34%) of patients with suspected AMI who had higher levels of troponin I and normal leukocyte count, and 39 (39%) of patients with suspected AMI who had troponin I levels and elevated leukocyte count. On Spearman’s test seen the correlation between levels of troponin I with the total of leukocytes in patients with suspected AMI (p = 0.000 and r = 0.50). This shows an increase in troponin I, which runs parallel with the increase in the total of leukocytes. Suggested for further research to see the difference increased levels of troponin I and the total of leukocytes between 3-5 hours and 14-18 hours after myocardial injury


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