scholarly journals HEART REMODELING, TREATMENT OF MYOCARDIAL INFARCTION WITH DIABETES MELLITUS 2ND TYPE AND HEART FAILURE

2020 ◽  
Vol 73 (6) ◽  
pp. 1284-1289
Author(s):  
Maxim M. Potyazhenko ◽  
Nadia O. Lyulka ◽  
Yulia A. Ostapchuk

Scientific 42 articles were analyzed, which for analysis were taken from scientometric databases: Web of Science, Scopus, PubMed, Medline, on topics related to: heart remodeling, treatment of myocardial infarction with type 2 diabetes mellitus and heart failure. Analysis of current medical studies and the data obtained indicate both availability in the usage of new HF biological markers – suppressor of tumorigenesis 2 (ST2), and the efficiency in the use of antagonists of miniralocorticoid receptors and sodium-glucose linked transporter-2 inhibitors, which is complicated by HF and type 2 diabetes by slowing down the processes of LV myocardial remodeling, which promotes control of blood pressure and fluid volume and causes a decrease and gradual regression of HF regardless of its origin.

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yu Hoshika ◽  
Yoshiaki Kubota ◽  
Kosuke Mozawa ◽  
Shuhei Tara ◽  
Yukichi Tokita ◽  
...  

Background: Plasma volume status (PVS), a parameter of the discrepancy between actual plasma volume (PV) and ideal PV, has been evaluated recently as a prognostic marker of patients with heart failure. This subgroup analysis of the EMBODY trial was designed to determine whether the sodium-glucose cotransporter 2 (SGLT2) inhibitor affect the improvement of heart failure and PVS in patients after acute myocardial infarction (AMI) with congestive heart failure (CHF). Methods: The EMBODY trial was a prospective, multicenter, randomized, double-blind, placebo-controlled trial to identify the effect of the SGLT2 inhibitor on cardiac sympathetic hyperactivity in patients with AMI and type 2 diabetes mellitus (T2DM) in Japan. A total of one hundred and five patients were randomized (1:1) to receive once-daily 10 mg empagliflozin or placebo 2 weeks after the onset of AMI. In this subanalysis, we investigated the time-course of PVS on baseline, weeks 4, 12 and 24. Results: Overall, 96 patients were included in the subgroup analysis set (64.3±10.9 years, male 80.2%, and 46 in the empagliflozin group and 50 in the placebo group). The empagliflozin group showed significant decreases in body weight, systolic blood pressure, and PVS compared with the placebo group at 24 weeks (-2.2 vs. +0.1 kg, P=0.0007; -6.6 vs. +3.5 mmHg, P=0.003; and -5.1 vs. -0.3%, P=0.0006; respectively). Decreased of PVS, defined as change of PVS < -4.5 % was associated with received empagliflozin (odds ratio, 2.61; 95% confidence interval, 1.11 - 6.15; P=0.028). On the other hand, NT-Pro BNP levels significantly decreased in the empagliflozin group and placebo group (1028.7 to 370.3 pg/ml, P=0.0001 and 1270.6 to 673.7 pg/ml, P=0.006, respectively). Conclusion: Empagliflozin reduced not only body weight but also PVS. These results suggested that early SGLT2 inhibitor administration in patients with AMI, CHF and T2DM could be effective to reduce body weight and PVS.


2019 ◽  
Vol 20 (4) ◽  
pp. 63-70
Author(s):  
K. Yu. Glavatskikh ◽  
I. Yu. Lukyanova ◽  
V. I. Shalnev ◽  
I. Yu. Pchelin

The article presents data on the frequency and structure of comorbid pathology in patients with inferior wall myocardial infarction with right ventricular involvement. Its relationship with the clinical course of myocardial infarction in the acute period was studied. It was shown that patients with inferior wall myocardial infarction with right ventricular involvement have a high comorbid load. It was revealed that a more severe course of the acute period of myocardial infarction in these patients was associated with chronic cerebrovascular ischemia, fatty liver, chronic heart failure I–IIa stages, type 2 diabetes mellitus and obesity.  


2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Yunlong Lu ◽  
Zhen Wang ◽  
Marios K. Georgakis ◽  
Hefeng Lin ◽  
Liangrong Zheng

Background Observational studies have indicated that depression is associated with coronary artery disease (CAD) and myocardial infarction. Nevertheless, causal associations between depression and cardiovascular diseases remain controversial. Hence, we conducted a Mendelian randomization and mediation analysis to evaluate the associations of depression‐related genetic variants with CAD and myocardial infarction. Methods and Results Summary statistics from genome‐wide association studies of depression (807 553 individuals), and CAD (60 801 cases, including 43 676 with myocardial infarction, and 123 504 controls) were used. We pooled Mendelian randomization estimates using a fixed‐effects inverse‐variance weighted meta‐analysis and multivariable Mendelian randomization. The mediation effects of potential cardiovascular risk factors on depression‐CAD and myocardial infarction risk were investigated by using mediation analysis. We also explored the relationship of genetic liability to depression with heart failure, atrial fibrillation, and ischemic stroke. Genetic liability to depression was associated with higher CAD (odds ratio [OR], 1.14; 95% CI, 1.06–1.24; P =1.0×10 −3 ) and myocardial infarction (OR, 1.21; 95% CI, 1.11–1.33; P =4.8×10 −5 ) risks. Results were consistent in all sensitivity analyses. Type 2 diabetes mellitus and smoking demonstrated significant mediation effects. Furthermore, our Mendelian randomization analyses revealed that the genetic liability to depression was associated with higher risks of heart failure and small vessel stroke. Conclusions Genetic liability to depression is associated with higher CAD and myocardial infarction risks, partly mediated by type 2 diabetes mellitus and smoking. The potential preventive value of depression treatment on cardiovascular diseases should be investigated in the future.


2021 ◽  
Vol 8 (4) ◽  
pp. 6-17
Author(s):  
O. K. Lebedeva ◽  
Alexey I. Ermakov ◽  
Larisa Gaikovaya ◽  
Galina A. Kukharchik

Background. The processes of inflammation and repair in the area of myocardial infarction (MI) are carried out and regulated by various populations of immune cells, including monocytes, lymphocytes, and NK-cells. The success of myocardial recovery after infarction and the risk of developing acute heart failure (AHF) depend on their adequate interaction. The presence of type 2 diabetes mellitus (T2DM), in which chronic low-gradient inflammation occurs, can affect the monocytic and lymphocytic response in MI, which may contribute to the development of AHF.Objective. to assess the features of monocytic and lymphocytic responses in patients with MI T2DM complicated by the development of AHF.Design and methods. The study included 121 patients with MI T2DM (38 of them with AHF). The control group included 59 patients without diabetes mellitus (including 13 patients with AHF). For all patients within 1 day, on days 3, 5 and 12 of MI, the total number of monocytes and lymphocytes, the monocytes-to-lymphocytes ratio (MLR), subpopulations of monocytes and T-lymphocytes with NK cells (T&NK-cells) were determined by flow cytometry.Results. In patients with T2DM, the number of monocytes of different subpopulations did not differ depending on the development of AHF. In patients without T2DM with MI, complicated by AHF, compared with patients without AHF, on day 3, the number of CD14(+)CD16(-)monocytes was higher: 1018 (824; 1144) vs 593 (557; 677) cells/μL, p <0,01, and on days 3 and 5, the number of CD16(+) T&NK-cells was lower: 122 (95; 275) cells/μL and 307 (220; 406) cells/μL, respectively (p = 0,03); (117 (61; 228) and 437 (408; 545) cells/μL, respectively, p < 0,01. On the 12th day of MI in patients with T2DM and AHF lymphocytes and CD16(+)T&NK-cells counts were lower in comparison with patients without AHF: 1856 (1245; 1975) cells/μL and 2294 (1827; 2625) cells/μL, respectively, p = 0,04; 268 (128; 315) cells/μL and 344 (226 ; 499) cells/ μL, respectively, p = 0,04.Conclusion. In patients with T2DM, the development of AHF is associated with a low number of lymphocytes in the absence of a pronounced monocytic response. In non-diabetic patients, the development of AHF is associated with an increase in CD16(-)monocytes and a lower number of CD16 (+) T&NК-cells.


2016 ◽  
Vol 22 ◽  
pp. 20-21
Author(s):  
Aditya D. Raju ◽  
Anna D. Coutinho ◽  
Weijia Wang ◽  
Sharash Shetty ◽  
Stephen S. Sander ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1142-P
Author(s):  
DOMINIC PILON ◽  
MICHAEL DURKIN ◽  
AMEUR MANCEUR ◽  
ISABELLE GHELERTER ◽  
MARIE-HÉL LAFEUILLE ◽  
...  

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