scholarly journals INFLUENCE OF COMPLEX TREATMENT WITH MAGNESIUM AND POTASSIUM SALTS OF GLUCONIC ACID, EPLERENONE AND RIVAROXABAN ON DYNAMICS OF INDICATORS OF ISCHEMIA AND MYOCARDIAL REMODELING IN PATIENTS WITH CHRONIC HEART FAILURE AFTER MYOCARDIAL INFARCTION

2021 ◽  
Vol 74 (9) ◽  
pp. 2087-2093
Author(s):  
Igor P. Vakaliuk ◽  
Nataliia V. Savchuk ◽  
Roksolana V. Nesterak ◽  
Haliia B. Kulynych ◽  
Ruslana S. Hryhoryshyn

The aim: To increase the treatment effectiveness of CHF patients after MI with stenting by using magnesium and potassium salts of gluconic acid, eplerenone, and rivaroxaban in complex therapy. Materials and methods: The research was performed at the premises of Ivano-Frankivsk Regional Clinical Cardiology Centre, Ukraine. 84 patients with CHF after past MI were examined. Results and conclusions: A more pronounced anti-ischemic effect has been linked to the use of combination therapy with rivaroxaban on the background of basic therapy (BT) in patients with CHF after MI, compared with the use of magnesium and potassium salts of gluconic acid or eplerenone. The use of eplerenone in the complex treatment of these patients on the background of BT has been proven to provide a pronounced reverse remodeling of the left myocardium in the postinfarction period.

2017 ◽  
Vol 313 (4) ◽  
pp. H690-H699 ◽  
Author(s):  
Shayne C. Barlow ◽  
Heather Doviak ◽  
Julia Jacobs ◽  
Lisa A. Freeburg ◽  
Paige E. Perreault ◽  
...  

Ischemia-reperfusion (IR) and myocardial infarction (MI) cause adverse left ventricular (LV) remodeling and heart failure and are facilitated by an imbalance in matrix metalloproteinase (MMP) activation and the endogenous tissue inhibitors of metalloproteinase (TIMPs). We have identified that myocardial injections of recombinant TIMP-3 (rTIMP-3; human full length) can interrupt post-MI remodeling. However, whether and to what degree intracoronary delivery of rTIMP-3 post-IR is feasible and effective remained to be established. Pigs (25 kg) underwent coronary catheterization and balloon occlusion of the left anterior descending coronary artery (LAD) for 90 min whereby at the final 4 min, rTIMP-3 (30 mg, n = 9) or saline was infused in the distal LAD. LV echocardiography was performed at 3–28 days post-IR, and LV ejection fraction (EF) and LV end-diastolic volume were measured. LV EF fell and LV end-diastolic volume increased from baseline (pre-IR) values (66 ± 1% and 40 ± 1 ml, respectively, means ± standard deviation) in both groups; however, the extent of LV dilation was reduced in the rTIMP-3 group by 40% at 28 days post-IR ( P < 0.05) and the fall in LV EF was attenuated. Despite equivalent plasma troponin levels (14 ± 3 ng/ml), computed MI size at 28 days was reduced by over 45% in the rTIMP-3 group ( P < 0.05), indicating that rTIMP-3 treatment abrogated MI expansion post-IR. Plasma NH2-terminal pro-brain natriuretic peptide levels, an index of heart failure progression, were reduced by 25% in the rTIMP-3 group compared with MI saline values ( P < 0.05). Although the imbalance between MMPs and TIMPs has been recognized as a contributory factor for post-MI remodeling, therapeutic strategies targeting this imbalance have not been forthcoming. This study is the first to demonstrate that a relevant delivery approach (intracoronary) using rTIMP can alter the course of post-MI remodeling. NEW & NOTEWORTHY Myocardial ischemia and reperfusion injury remain significant causes of morbidity and mortality whereby alterations in the balance between matrix metalloproteinase and tissue inhibitor of metalloproteinase have been identified as contributory biological mechanisms. This novel translational study advances the concept of targeted delivery of recombinant proteins to modify adverse myocardial remodeling in ischemia-reperfusion injury.


2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Leonardo Schirone ◽  
Maurizio Forte ◽  
Silvia Palmerio ◽  
Derek Yee ◽  
Cristina Nocella ◽  
...  

Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression. Here, we review the molecular pathways involved in cardiac remodeling, with particular emphasis on those associated with myocardial infarction. A better understanding of cell signaling involved in cardiac remodeling may support the development of new therapeutic strategies towards the treatment of heart failure and reduction of cardiac complications. We will also discuss data derived from gene therapy approaches for modulating key mediators of cardiac remodeling.


2018 ◽  
pp. 46-55
Author(s):  
M. I. Shved ◽  
O. A. Prokopovych ◽  
S. N. Heryak ◽  
V. Y. Dobrianska

Inclusion of bioflavonoid quercetin in complex therapy of patientswith acute myocardial infarction provided improvement of hemodynamic parameters and liver function contributed in significant reduction of complications of myocardial infarction. The usage of RNA drug was significantly assotiated with improvement of immune status, reduced symptoms of necrosis-resorptive and immuno-inflammatory syndrome in patients with AMI and liver disfunction.


2015 ◽  
Vol 6 (1) ◽  
pp. 12-15
Author(s):  
M. B Baysultanova ◽  
A. A Elgarov ◽  
L. V Betuganova ◽  
M. A Elgarov ◽  
M. A Kalmykova

Complex therapy effectiveness in patients with myocardial infarction and chronic heart failure is established; authors monitoring positive influence on medical psychological and social aspects of rehabilitation in post infarction patients is shown, using as monitoring core individual and complex medical psychological educational program.


2017 ◽  
Vol 23 (1) ◽  
Author(s):  
N. V. Savchuk ◽  
I. P. Vakaliuk

The objective of the research was to increase the efficiency of treatment of patients with chronic heart failure (CHF) and post-infarction cardiosclerosis by adding potassium and magnesium salts of gluconic acid, eplerenone and rivaroxaban to the background therapy taking into account the indices of growth differentiation factor 15 (GDF-15), aldosterone and galectin-3. Materials and methods of the research. Emmunoenzymometric determination of the galectin-3, GDF-15 and aldosterone levels concentration in blood serum was conducted to achieve the stated objective. 42 patients with CHF and post-infarction cardiosclerosis after coronary artery stenting in the acute period of myocardial infarction (MI) were examined. The patients were randomized into four groups according to the peculiarities of treatment. Group I included patients with CHF and post-infarction cardiosclerosis treated with the background therapy (BT). Group II consisted of patients with CHF who were treated with BT and addition of potassium and magnesium salts of gluconic acid. Group III included patients with CHF who were prescribed eplerenone secondary to BT. Group IV consisted of patients who were treated with BT and rivaroxaban. Results. The proposed treatment regimens were proved to be effective in reduction of GDF-15, aldosterone and galectin-3 indices in 12 months of treatment. Conducted therapy with the use of rivaroxaban secondary to BT led to more intensive decrease in GDF-15 concentration in comparison with the use of potassium and magnesium salts of gluconic acid or eplerenone on the background of BT. This index constituted (2110.21±107.4) pg/ml before the treatment in these patients and significantly decreased to (1286.75±109.6) pg/ml being significantly before the therapy. The performed treatment with the use of eplerenone secondary to BT was proved to be more effective for normalization of aldosterone and galectin-3 levels in blood serum compared to other studied treatment regimens. The average value of aldosterone changed in the treatment process by 67.24%. Thus, the average level of this index constituted (139.8±7.63) pg/ml before the treatment and was equal to (45.8±5.52) pg/ml at the end of the treatment course. The average value of galectin-3 in patients with CHF and post-infarction cardiosclerosis was noted to be (34.69±1.67) ng/ml before the treatment. It constituted (22.53±0.98) ng/ml after the end of treatment being significantly lower compared to the value before the treatment. The average value of this index changed in the course of twelve-month treatment by 35.05%. Lower risk of sudden cardiac arrest (SCA), acute coronary syndrome (ACS) and stroke was observed in the patients with CHF and post-infarction cardiosclerosis with the use of rivaroxaban secondary to BT.Conclusions. Thus, the use of rivaroxaban combination therapy secondary to BT led to more intensive decrease in GDF-15 concentration in comparison with the use of potassium and magnesium salts of gluconic acid or eplerenone. Conducted therapy with the use of eplerenone on the background of BT was more effective for the normalization of galectin-3 and aldosterone levels in the blood compared to other studied treatment regimens.


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.


Author(s):  
S. I. Estrin ◽  
T. V. Kravchenko ◽  
A. O. Kovalchuk

Introduction. Heart failure as a result of ischemic myocardial remodeling is one of the most severe diseases with poor prognosis. Drug therapy alone with surgical or percutaneous revascularization of damaged myocardium often fails to achieve optimum effect in the treatment of the mentioned syndrome. Cell cardiomyoplasty using autologous bone marrow derived mesenchymal stem cells (BM-MSCs) has already proved to be promising alternative to both these treatment methods, as it’s aimed directly at restoration of normally functioning myocard. The aim. To study the effects of different techniques of cardiomyoplasty with BM-MSCs on morphometrical and functional indices of post-infarctional left ventricular remodeling in experiment. Materials and methods. An experimental model of myocardial infarction in laboratory rats was used for the research. The survived animals were equally divided into 5 groups; the animals of 3 groups underwent BM-MSC transplantation. A certain technique of cardiomyoplasty was used in each of the 3 groups: direct injection into necrotic myocardium, intravenous injection and injection inside left ventricular cavity (which imitates intracoronalintroduction). Other 2 groups were comparison groups where the animals did not achieve BM-MSCs after infarction. There was also control group with intact animals with normal values of all the studied indices. The following invasive and noninvasive measurements of functional heart indices have been done in all research groups: left ventricular weight and its relation to body weight, end-systolic and end-diastolic left ventricular internal dimensions, fractional shortening, ejection fraction, stroke volume, heart rate, systemic arterial pressure and left ventricular inner pressure, both systolic and diastolic. The follow-up period was 1 and 3 months after the experiment. Finally, all animals were euthanized and autopsied, and the results of macroscopic examination of their hearts have been matched with aforecited functional indices in each group. Results and discussion. The analysis of all measured parameters and their comparison between groups have revealed that BM-MSC transplantation (irrespective of technique) conduces to reliably significant retention of functioning myocardium volume, reliably significant improvement of contractility parameters, particularly, reduced end-systolic and end-diastolic internal dimensions, increased ejection fraction, fractional shortening and stroke volume; it also contributes to maximal inalterability of such hemodynamic parameters as heart rate, systemic arterial pressure, left ventricular inner pressure. In addition, in all 3 groups of cell therapy the indices of contractility and pump function of the left ventricle were very close to normal rates. But the optimal results have been obtained in the group of direct intramyocardial injections. Conclusion. Cell cardiomyoplasty with BM-MSCs tends to prevent ischemic myocardial remodeling and, as a result, to improve myocardial contractility and neutralize manifestations of severe heart failure in short-term follow-up of 1 and 3 months.


2004 ◽  
Vol 50 (2) ◽  
pp. 265-278 ◽  
Author(s):  
Saeed A Jortani ◽  
Sumanth D Prabhu ◽  
Roland Valdes

Abstract Background: Heart failure (HF) is a devastating disease with increasing prevalence in elderly populations. One-half of all patients die within 5 years of diagnosis. The annual cost of treating patients with HF in the US is more than $20 billion, which is estimated to be greater than that of myocardial infarction and all cancers combined. Given the complex pathophysiology and varied manifestations of HF, interest has intensified in developing biological markers to predict susceptibility and aid in the early diagnosis and management of this disease. Methods: We searched Medline via Ovid for studies published during the period 1966–2003 regarding various biomarkers suggested for HF. Our review focused on developing strategies for discovering and using new biomarkers, particularly those potentially linked to pathophysiologic mechanisms. We also point out strategic advantages, limitations, and methods available for measuring each of the currently proposed markers. Results: Biomarkers reviewed include those released from the heart during normal homeostasis (natriuretic peptides), those produced elsewhere that act on the heart (endogenous cardiotonic steroids and other hormones), and those released in response to tissue damage (inflammatory cytokines). The concept of using a combination of multiple markers based on diagnosis, prognosis, and acute vs chronic disease is also discussed. In view of recent advances in our understanding of molecular biochemical derangements observed during cardiac failure, we consider the concept of myocardial remodeling and the heart as part of an endocrine system as strategies. Conclusion: Strategically, biomarkers linked to mechanisms involved in the etiology of HF, such as dysregulation of ion transport, seem best suited for serving as early biological markers to predict and diagnose disease, select therapy, or assess progression.


2022 ◽  
Vol 8 ◽  
Author(s):  
Chan Wu ◽  
Binghong Liu ◽  
Ruiying Wang ◽  
Gang Li

Myocardial infarction (MI) is the most frequent end-point of cardiovascular pathology, leading to higher mortality worldwide. Due to the particularity of the heart tissue, patients who experience ischemic infarction of the heart, still suffered irreversible damage to the heart even if the vascular reflow by treatment, and severe ones can lead to heart failure or even death. In recent years, several studies have shown that microRNAs (miRNAs), playing a regulatory role in damaged hearts, bring light for patients to alleviate MI. In this review, we summarized the effect of miRNAs on MI with some mechanisms, such as apoptosis, autophagy, proliferation, inflammatory; the regulation of miRNAs on cardiac structural changes after MI, including angiogenesis, myocardial remodeling, fibrosis; the application of miRNAs in stem cell therapy and clinical diagnosis; other non-coding RNAs related to miRNAs in MI during the past 5 years.


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