sacubitril and Myocardial-Infarction

infarction (AMI) can be reduced by the use of sacubitril/valsartan. However, the therapeutic effects of sacubitril/valsartan in clinical settings are inconsistent. In this paper, the related research on the application of sacubitril/valsartan in AMI was comprehensively searched, in order to explore the clinical efficacy and safety of early application of sacubitril/valsartan after AMI.. English databases, including American National Library of Medicine, Medline, and Embase, and Chinese databases, including Chinese Biomedical Literature Database, Chinese National Knowledge Infrastructure (CNKI), Wanfang, and VIP, were searched using a combination of the following search terms: AMI, acute ST-segment elevation myocardial infarction (STEMI), acute non-ST-segment elevation myocardial infarction (NSTEMI), sacubitril/valsartan sodium tablets, and angiotensin receptor enkephalinase inhibitors. The experimental group was given Sacubitril/Valsartan sodium tablets, while the control group was given angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB). Cochrane Handbook 5.0 risk assessment table were used for quality assessment and bias risk assessment.. A total of 5 articles were included in the meta-analysis. The total incidence of adverse cardiovascular events in the sacubitril/valsartan group was significantly lower than that in the control group {relative risk (RR) =0.61 [95% confidence interval (CI): 0.46, 0.82], significance testing Z=3.36, and P=0.0008}. The difference between the rehospitalization rate of the sacubitril/valsartan group and control group was statistically significant [RR =0.67 (95% CI: 0.47, 0.95), significance testing Z=2.23, and P=0.03]. The difference in low blood pressure between the sacubitril/valsartan group and the control group was statistically significant [RR =1.28 (95% CI: 1.18, 1.40), significance testing Z=5.58, and P<0.00001]. The difference in left ventricular ejection fraction (LVEF) between the sacubitril/valsartan group and control group was statistically significant [mean difference (MD) =3.09 (95% CI: 1.69, 4.49), significance testing Z=4.33, and P<0.0001].. Sacubitril/valsartan was found to inhibit ventricular remodeling after AMI, improve cardiac function, and reduce the incidence of adverse cardiovascular events after myocardial infarction, the rehospitalization rate, and the mortality rate.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Biphenyl Compounds; Heart Failure; Humans; Myocardial Infarction; Stroke Volume; Tetrazoles; United States; Valsartan; Ventricular Function, Left

Despite advances in cardiac care, patients remain at a high risk of death and the development of heart failure (HF) following myocardial infarction (MI). These risks are highest in patients with reduced ejection fraction (EF) or signs of HF immediately after MI. Drugs to mitigate these risks have been identified through the systematic evaluation of therapies with proven efficacy in patients with HF and reduced EF (HFrEF).. Although landmark studies in patients with HFrEF consistently exclude patients with recent MI, dedicated post-MI trials of these drugs have led to multiple therapies with proven benefit in these patients. However, not all therapies with proven efficacy in patients with chronic HF have been shown to provide benefit in the post-MI population, as recently evidenced by the discrepant results between chronic HF and post-MI trials of sacubitril-valsartan. Similarly, multiple trials of early and aggressive use of therapies effective in chronic heart failure immediately post-MI failed to demonstrate benefit or were associated with harm, emphasizing the vulnerability of the post-MI population.. Trials of patients at high risk of HF following MI have emphasized the differences between the post-MI and HFrEF populations and the necessity for dedicated trials in the post-MI population. This review summarizes trials studying the use of these therapies for at-risk patients following MI from therapies used in patients with HFrEF and exploring new potential therapies for this high-risk population.

Topics: Aminobutyrates; Biphenyl Compounds; Heart Failure; Humans; Myocardial Infarction; Stroke Volume; Tetrazoles; Valsartan; Ventricular Dysfunction, Left

We aimed to investigate whether sacubitril-valsartan could further improve the prognosis, cardiac function, and left ventricular (LV) remodelling in patients following acute myocardial infarction (AMI).. We searched the PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure (CNKI) from inception to 10 May 2021 to identify potential articles. Randomized controlled trials (RCTs) meeting the inclusion criteria were included and analysed. Thirteen RCTs, covering 1358 patients, were analysed. Compared with angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB), sacubitril-valsartan did not significantly reduced the cardiovascular mortality [risk ratio (RR) 0.65, 95% confidence interval (CI) 0.22 to 1.93, P = 0.434] and the rate of myocardial reinfarction (RR 0.65, 95% CI 0.29 to 1.46, P = 0.295) of patients following AMI, but the rate of hospitalization for heart failure (HF) (RR 0.48, 95% CI 0.35 to 0.66, P < 0.001) and the change of LV ejection fraction (LVEF) [weighted mean difference (WMD) 5.49, 95% CI 3.62 to 7.36, P < 0.001] were obviously improved. The N-terminal pro-brain natriuretic peptide (NT-ProBNP) level (WMD -310.23, 95% CI -385.89 to -234.57, P < 0.001) and the LV end-diastolic dimension (LVEDD) (WMD -3.16, 95% CI -4.59 to -1.73, P < 0.001) were also significantly lower in sacubitril-valsartan group than in ACEI/ARB group. Regarding safety, sacubitril-valsartan did not increase the risk of hypotension, hyperkalaemia, angioedema, and cough.. This meta-analysis suggests that early administration of sacubitril-valsartan may be superior to conventional ACEI/ARB to decrease the risk of hospitalization for HF, improve the cardiac function, and reverse the LV remodelling in patients following AMI.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Biphenyl Compounds; Humans; Myocardial Infarction; Stroke Volume; Valsartan

In patient with symptomatic heart failure sacubitril valsartan has been found to reduces the risk of hospitalization and death from cardiovascular causes more effectively then angiotensin converting enzymes inhibitor trail comparing the effect of these drugs in acute myocardial infarction is lacking.. We randomly assigned patient with acute myocardial infarction complicated with reduced LVEF, or pulmonary congestion to recieve sacubitril 97mg-valsartan 103mg and ramipril 5mg twice daily the primary outcome was death from cardiovascular causes or incident heart failure, outpatient symptomatic heart failure or heart failure leading to hospitalization whichever occure first.. Total 566 patient was taken in randomization 283 receive sacubitril-valsartan and 283 receive ramipril over a median of 22 months total outcome occure in 138 patient in sacubitril-valsartan group and in137 patient with ramipril group(hazard ratio 0.90: 95%confidence interval death from cardiovascular causes or hospitalization for heart failure occure i 10.9% patient reciveing sacubitril-valsartan and in 11.8%patient with ramipril group death from cardiovascular causes is 5.9 and 6.7% respectively death from anyother causes is 7.5 and 8.5 % respectively in both sacubitril-valsartan and ramipril group.. Sacubitril-valsartan was not associated with significantly lower incidence of death from cardiovascular causes or incidents heart failure then ramipril in patients with acute myocardial infarction.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Antihypertensive Agents; Biphenyl Compounds; Drug Combinations; Heart Failure; Humans; Myocardial Infarction; Neprilysin; Ramipril; Receptors, Angiotensin; Stroke Volume; Tetrazoles; Treatment Outcome; Valsartan

The win ratio can incorporate different types of outcomes and enhance statistical power, making it a useful method for analysing composite outcomes in cardiovascular trials. The application of this approach to the PARADISE-MI trial provides an additional perspective into understanding the effects of sacubitril/valsartan in patients with acute myocardial infarction.. We conducted a post-hoc analysis of the PARADISE-MI trial, which randomly assigned patients with acute myocardial infarction complicated by a reduced left ventricular ejection fraction, pulmonary congestion, or both to receive either sacubitril/valsartan (97 mg of sacubitril and 103 mg of valsartan twice daily) or ramipril (5 mg twice daily) in addition to guideline-recommended therapy. The principal composite outcome was analysed in the hierarchical order of death due to cardiovascular causes, first hospitalization for heart failure, and first outpatient episode of symptomatic heart failure. We included events confirmed by the clinical events classification (CEC) committee as well as events identified by investigators that did not meet study definitions. Results were analysed by the unmatched win-ratio method. A win ratio that exceeds 1.00 reflects a better outcome. A total of 5661 patients underwent randomization; 2830 were assigned to receive sacubitril/valsartan and 2831 to receive ramipril. The hierarchical analysis of the principal composite outcome demonstrated a larger number of wins (1 265 767 [15.7%]) than losses (1 079 502 [13.4%]) in the sacubitril/valsartan group (win ratio of 1.17, 95% confidence interval [CI] 1.03-1.33; p = 0.015). Sensitivity analyses using alternative definitions of the composite outcome showed results similar to those of the principal analysis, except for analysis restricted to events that met CEC definitions (win ratio of 1.11, 95% CI 0.96-1.30; p = 0.16).. In this post-hoc analysis of the PARADISE-MI trial using the win ratio and including investigator-identified events not having CEC confirmation, sacubitril/valsartan was superior to ramipril among high-risk survivors of acute myocardial infarction.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Biphenyl Compounds; Drug Combinations; Heart Failure; Humans; Myocardial Infarction; Neprilysin; Ramipril; Stroke Volume; Tetrazoles; Valsartan; Ventricular Function, Left

In patients who survive an acute myocardial infarction (AMI), angiotensin-converting enzyme inhibitors decrease the risk of subsequent major cardiovascular events. Whether angiotensin-receptor blockade and neprilysin inhibition with sacubitril/valsartan reduce major coronary events more effectively than angiotensin-converting enzyme inhibitors in high-risk patients with recent AMI remains unknown. We aimed to compare the effects of sacubitril/valsartan on coronary outcomes in patients with AMI.. We conducted a prespecified analysis of the PARADISE-MI trial (Prospective ARNI vs ACE Inhibitors Trial to Determine Superiority in Reducing Heart Failure Events After MI), which compared sacubitril/valsartan (97/103 mg twice daily) with ramipril (5 mg twice daily) for reducing heart failure events after myocardial infarction in 5661 patients with AMI complicated by left ventricular systolic dysfunction, pulmonary congestion, or both. In the present analysis, the prespecified composite coronary outcome was the first occurrence of death from coronary heart disease, nonfatal myocardial infarction, hospitalization for angina, or postrandomization coronary revascularization.. In survivors of an AMI with left ventricular systolic dysfunction and pulmonary congestion, sacubitril/valsartan-compared with ramipril-reduced the risk of a prespecified major coronary composite outcome. Dedicated studies are necessary to confirm this finding and elucidate its mechanism.. URL: https://www.. gov; Unique identifier: NCT02924727.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Angiotensins; Biphenyl Compounds; Heart Failure; Humans; Myocardial Infarction; Neprilysin; Prospective Studies; Ramipril; Receptors, Angiotensin; Stroke Volume; Tetrazoles; Valsartan; Ventricular Dysfunction, Left

Cardiac ischemia-related myocardial damage has been considered a major reason for heart failure. We aimed to investigate the role of levosimendan (LEVO) in comparison to ramipril and sacubitril/valsartan (Sac/Val) in preventing damage associated with isoproterenol (ISO) induced myocardial infarction.. Myocardial infarction was induced by injecting subcutaneous isoproterenol (5 mg/kg once for 7 consecutive days) to establish an experimental heart failure model. Simultaneously, LEVO (1 mg/kg/day), ramipril (3mg/kg/day) and Sac/Val (68 mg/kg/day) suspension were administered orally for four weeks.. We observed a significant correlation between ISO-induced ischemia with cardiac remodeling and alterations in myocardial architecture. LEVO, ramipril, and Sac/Val significantly prevented lipid peroxidation and damaged antioxidant enzymes like superoxide dismutase, catalase, glutathione and thioredoxin reductase. We also observed their ameliorative effects in myocardium's cardiac hypertrophy, evidenced by reduced heart weight to body weight ratio and transforming growth factor β related collagen deposition. LEVO, ramipril, and Sac/Val also maintained cardiac biomarkers like lactate dehydrogenase, creatine kinase-MB, brain natriuretic peptide and cardiac Troponin-I, indicating reduced myocardial damage that was further demonstrated by histopathological examination. Decreased sarcoplasmic endoplasmic reticulum Ca2+ATPase2a and sodium-calcium exchanger-1 protein depletion after LEVO, ramipril, and Sac/Val administration indicated improved Ca2+ homeostasis during myocardial contractility.. Our findings suggest that LEVO has comparable effects to ramipril, and Sac/Val in preventing myocardial damage via balancing oxidant-antioxidant system, decreased collagen deposition, reduced myocardial stress as well as improved Ca2+ homeostasis during myocardial contractility.

Topics: Antioxidants; Calcium; Collagen; Heart Failure; Hemodynamics; Humans; Isoproterenol; Myocardial Infarction; Ramipril; Simendan; Valsartan

In real-world clinical practice, the initiation and up-titration of sacubitril/valsartan remain challenging due to symptomatic hypotension in patients with acute myocardial infarction(AMI). The purpose of this study was to investigate the efficacy of different initial timing and dosage of sacubitril/valsartan in AMI patients.. This prospective and observational cohort study enrolled AMI patients treated with percutaneous coronary intervention(PCI), and were categorized according to the initial timing and average daily doses of sacubitril/valsartan prescription. The primary endpoint was defined as a composite of cardiovascular death, recurrent AMI, coronary revascularization, heart failure(HF) hospitalization and ischaemic stroke. Secondary outcomes included the new-onset HF, and the composite endpoints in AMI patients complicated with HF at baseline.. The study population consisted of 915 AMI patients. After a median follow-up of 38 months, early use or high dosage of sacubitril/valsartan was associated with an improvement in primary endpoint as well as the incidence of new-onset HF. Early use of sacubitril/valsartan also ameliorated the primary endpoint in AMI patients with left ventricular ejection fraction(LVEF) ≤50% as well as LVEF>50%. Besides, early use of sacubitril/valsartan improved the clinical outcomes in AMI patients complicated with HF at baseline. The low dose was well tolerated and may be associated with similar outcomes compared with high dose under some circumstances(LVEF>50% or HF at baseline).. Early use or high dosage of sacubitril/valsartan medication is associated with an improvement in clinical outcome. The low dose of sacubitril/valsartan is well tolerated and may be an acceptable alternative strategy.

Topics: Angiotensin Receptor Antagonists; Biphenyl Compounds; Brain Ischemia; Drug Combinations; Heart Failure; Humans; Myocardial Infarction; Percutaneous Coronary Intervention; Prospective Studies; Stroke; Stroke Volume; Tetrazoles; Treatment Outcome; Valsartan; Ventricular Function, Left

There are few contemporary data on outcomes, costs, and treatment following a hospitalization for heart failure (hHF) in epidemiologically representative cohorts.. This study sought to describe rehospitalizations, hospitalization costs, use of guideline-directed medical therapy (GDMT) (renin-angiotensin system inhibitors, sacubitril/valsartan, beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors), and mortality after hHF.. EVOLUTION HF (Utilization of Dapagliflozin and Other Guideline Directed Medical Therapies in Heart Failure Patients: A Multinational Observational Study Based on Secondary Data) is an observational, longitudinal cohort study using data from electronic health records or claims data sources in Japan, Sweden, the United Kingdom, and the United States. Adults with a first hHF discharge between 2018 and 2022 were included. The 1-year event rates per 100 patient-years (ERs) for death and rehospitalizations (with a primary diagnosis of heart failure (HF), chronic kidney disease [CKD], myocardial infarction, stroke, or peripheral artery disease) were calculated. Hospital health care costs were cumulatively summarized. Cumulative GDMT use was assessed using Kaplan-Meier estimates.. Of 263,525 patients, 28% died within the first year post-hHF (ER: 28.4 [95% CI: 27.0-29.9]). Rehospitalizations were mainly driven by HF (ER: 13.6 [95% CI: 9.8-17.4]) and CKD (ER: 4.5 [95% CI: 3.6-5.3]), whereas the ERs for myocardial infarction, stroke, and peripheral artery disease were lower. Health care costs were predominantly driven by HF and CKD. Between 2020 and 2022, use of renin-angiotensin system inhibitors, sacubitril/valsartan, beta-blockers, and mineralocorticoid receptor antagonists changed little, whereas uptake of sodium-glucose cotransporter-2 inhibitors increased 2- to 7-fold.. Incident post-hHF rehospitalization risks and costs were high, and GDMT use changed little in the year following discharge, highlighting the need to consider earlier and greater implementation of GDMT to manage risks and reduce costs.

Topics: Adrenergic beta-Antagonists; Adult; Angiotensin Receptor Antagonists; Antihypertensive Agents; Glucose; Heart Failure; Hospitalization; Humans; Longitudinal Studies; Mineralocorticoid Receptor Antagonists; Myocardial Infarction; Peripheral Arterial Disease; Renal Insufficiency, Chronic; Sodium; Sodium-Glucose Transporter 2 Inhibitors; Stroke; Stroke Volume; United States; Valsartan

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Biphenyl Compounds; Drug Combinations; Heart Arrest; Heart Failure; Humans; Myocardial Infarction; Prospective Studies; Stroke Volume; Tetrazoles; Valsartan

Fabry disease (FD) is a rare, X-linked lysosomal deposition disease characterized by multi-system symptoms. The accumulation of globotriaosylceramide in various organs, such as the kidneys and heart, as well as the nervous system, has been speculated to be the mechanism involved in tissue damage, including vascular impairment with thrombotic events.. Here, we describe a 72-year-old male patient diagnosed with FD, who first presented with acute myocardial infarction, left ventricular thrombosis, and pericardial effusion, accompanied by cardiac hypertrophy.. A physical examination showed that he was hemodynamically stable and an electrocardiogram showed ventricular tachycardia (Fig. 1A). The single obvious abnormality was an ST segment depression with a preterminal negative T wave in leads I and aVL (Fig. 1B). Coronary angiography revealed regular findings (Fig. 2). Echocardiogram conducted at our hospital revealed hypertrophy, ejection fraction 40%, pericardial effusion (Fig. 3). Speckle tracking two-dimensional echocardiography strain analysis technology confirmed left ventricular thrombosis, and also revealed decreased movement of the inferior and posterior walls, the basal segment of the posterior wall was locally fibrotic (Fig. 4A and B). Further, myocardial contrast echocardiography confirmed left ventricular thrombosis (Fig. 4C). Cardiovascular magnetic resonance imaging indicated biventricular uneven hypertrophy, which was considered metabolic cardiomyopathy, with diffuse fibrosis of biventricular walls, apical thrombosis, and ischemic cardiomyopathy in the basal segment of the left ventricular lateral wall and left ventricular anterior wall (Fig. 5). Serum alpha-galactosidase concentration was 0.7 nmol/h/mgPr (normal range, 29.0-64.4 nmol/h/mgPr). Subsequent genetic testing revealed that he was hemizygous for a previously reported missense mutation (c.902G>A) inexon 6 of the GLA gene,[1] which induce p.R301Q (p.Arg301Gln), confirming a diagnosis of FD (Fig. 6).. Orally administered drugs included rivaroxaban, sacubitril valsartan, beta blockers, dapagliflozin, and mineralocorticoid receptor antagonist. Cardiac resynchronization therapy with an implanted defibrillator was implemented to prevent sudden death.. At present, he is still in follow-up and there have been no adverse events.. Our case suggests that clinicians should consider the possibility of FD in patients with acute myocardial infarction and cardiomyopathy. A detailed analysis of subtle historical clues would help promote earlier diagnosis of FD.

Topics: Aged; Aminobutyrates; Arrhythmias, Cardiac; Biphenyl Compounds; Cardiomegaly; Fabry Disease; Humans; Male; Myocardial Infarction; Pericardial Effusion; Thrombosis

The PARADISE-MI study compared standard treatment with an ACE inhibitor (ramipril) after an acute myocardial infarction with the newer sacubitril/ valsartan combination (so-called ARNI) medication in 5661 patients. Most patients had a reduced cardiac function (40% ejection fraction or less) and in about 50% of patients it was accompanied by complaints of congestion. The expected 15% reduction in primary endpoint cardiovascular death or rehospitalization or extra visits for heart failure was not met after 22 months. The study is characterized by an increased incidence of symptomatic hypotension of 28,3% in the group treated with the ARNI, compared to an incidence of 21,9% in the group treated with the ACE inhibitor. The interpretation of the trial is hampered by the mixed design of prevention and treatment trial for heart failure. A continuing careful approach is advised with ACE inhibitors as first choice in the first week(s) after myocardial infarction.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Biphenyl Compounds; Drug Combinations; Heart Failure; Humans; Myocardial Infarction; Neprilysin; Receptors, Angiotensin; Stroke Volume; Tetrazoles; Treatment Outcome

Sacubitril/Valsartan, a dual inhibitor of the neprilysin and angiotensin receptor, exerts cardioprotective effects in heart failure. Little is known on the impact of Sacubitril/Valsartan in hypertensive patients early post myocardial infarction.. Spontaneously hypertensive rats (SHR) were pretreated by daily angiotensin receptor blocker (ARB; 30 mg/kg intraperitoneally), Sacubitril/Valsartan (ARNI; 60 mg/kg intraperitoneally) or the same dosage of physiological saline for 1 week. Then each group underwent myocardial infarction induction and received the same treatment for another week. The blood pressure and cardiac function were evaluated prior to sacrifice. We performed histological and molecular evaluation of fibrosis in vivo and in vitro.. The blood pressure was comparable between three groups both 1 week prior to and post myocardial infarction. ARNI and ARB restore the decreased ejection fraction (57.3 ± 7.6 vs. 42.9 ± 5.2%, P < 0.05; 54.3 ± 6.9 vs. 42.9 ± 5.2%, P < 0.01, respectively) and fractional shortening (31.6 ± 5.4 vs. 22.1 ± 3.1%, P < 0.05; 29.4 ± 4.5 vs. 22.1 ± 3.1%, P < 0.05, respectively) post myocardial infarction. The infarct size and collagen deposition were also significantly mitigated in ARNI and ARB groups. In addition, ARNI and ARB treatment reduced the expression of cardiac remodeling-related factors, such as Bnp, α-SMA, Vimentin, and Col1a1 (all P < 0.05 vs. MI group). Finally, ARNI and ARB decreased the expression of α-SMA in cardiac fibroblasts treated with Ang II.. In conclusion, pretreatment with ARNI maintained cardiac function and reduced myocardial fibrosis in myocardial infarction, probably prior to any anti-hypertensive effect.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Biphenyl Compounds; Drug Combinations; Fibrosis; Heart Failure; Hypertension; Myocardial Infarction; Rats; Rats, Inbred SHR; Tetrazoles; Valsartan

Sacubitril valsartan (lcz696) has been demonstrated as a substitute for angiotensin-converting enzyme inhibitors and angiotensin receptor blockers for the treatment of heart failure. This research is aimed at examining the effects of lcz696 and its target molecules on myocardial infarction (MI). A rat model of MI was induced by left anterior descending artery ligation and treated with lcz696. Lcz696 treatment significantly reduced cardiac injury and heart failure, restored the left ventricular fractional shortening and ejection fraction, and reduced oxidative stress and inflammatory responses in rat myocardium. By analyzing the heart failure-related GSE47495 dataset and performing gene ontology (GO) functional enrichment analysis, we obtained histone lysine methyltransferase SUV39H1 and secreted phosphoprotein 1 (SPP1) as two molecules implicated in the oxidative stress and inflammation processes. An elevation of SUV39H1 whereas a decline of SPP1 were detected in cardiac tissues after lcz696 treatment. Enrichments of SUV39H1 and H3K9me3 at the SPP1 promoter were identified by chromatin immunoprecipitation assay. SUV39H1 catalyzed H3K9me3 modification to suppress the expression of SPP1. Preconditioning of SUV39H1 silencing blocked the protective roles of lcz696, but SPP1 silencing alleviated the myocardial injury. In conclusion, this study demonstrates that lcz696 enhances cardiac function and alleviates MI in rats through a SUV39H1/SPP1 axis.

Topics: Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Biphenyl Compounds; Heart Failure; Histone-Lysine N-Methyltransferase; Methyltransferases; Myocardial Infarction; Neprilysin; Osteopontin; Rats; Repressor Proteins; Stroke Volume; Tetrazoles; Valsartan

The purpose of this study was to explore the effect of sacubitril-valsartan on rats with acute myocardial infarction.. Sprague-dawley rats were randomly divided into six groups. Rats in Group A and B were threaded without deligation and treated with valsartan (34 mg/kg) or sacubitril-valsartan (68 mg/kg) after operation. Rats in Group C and D were given the two drugs (34 mg/kg, 68 mg/kg) after ligation of the left anterior descending branch for 40 minutes. Rats in Group E and F were restored the blood of the coronary artery after ligation, and given the two drugs (34 mg/kg, 68 mg/kg) at the same time. N-terminal pro-brain natriuretic peptide, high sensitivity troponin T, aldosterone and Cyclic guanosine monophosphate were measured and Color Doppler echocardiography was performed. Six weeks later, the rats were killed, the hearts were weighed and stained with Masson staining.. Compared with Group A and B, the levels of N-terminal pro-brain natriuretic peptide, high sensitivity troponin T, aldosterone and Cyclic guanosine monophosphate in other groups were significantly increased (. Early application of sacubitril-valsartan has a protective effect on rats with acute myocardial infarction.

Topics: Aminobutyrates; Animals; Biphenyl Compounds; Humans; Myocardial Infarction; Myocardium; Rats; Rats, Sprague-Dawley; Valsartan