Ion Therapy: A Novel Strategy for Acute Myocardial Infarction.
Ontology highlight
ABSTRACT:
SUBMITTER: Yi M
PROVIDER: S-EPMC6325593 | biostudies-literature | 2019 Jan
REPOSITORIES: biostudies-literature
Publications
Ion Therapy: A Novel Strategy for Acute Myocardial Infarction.
Yi Min M Li Hekai H Wang Xiaoya X Yan Jianyun J Gao Long L He Yinyan Y Zhong Xinglong X Cai Yanbin Y Feng Weijing W Wen Zhanpeng Z Wu Chengtie C Ou Caiwen C Chang Jiang J Chen Minsheng M
Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20181108 1
Although numerous therapies are widely applied clinically and stem cells and/or biomaterial based in situ implantations have achieved some effects, few of these have observed robust myocardial regeneration. The beneficial effects on cardiac function and structure are largely acting through paracrine signaling, which preserve the border-zone around the infarction, reduce apoptosis, blunt adverse remodeling, and promote angiogenesis. Ionic extracts from biomaterials have been proven to stimulate p ...[more]
Similar Datasets
Project description:BackgroundOxygen (O2) is widely used in people with acute myocardial infarction (AMI). Previous systematic reviews concluded that there was insufficient evidence to know whether oxygen reduced, increased or had no effect on heart ischaemia or infarct size. Our first Cochrane review in 2010 also concluded there was insufficient evidence to know whether oxygen should be used. Since 2010, the lack of evidence to support this widely used intervention has attracted considerable attention, prompting further trials of oxygen therapy in myocardial infarction patients. It is thus important to update this Cochrane review.ObjectivesTo assess the effects of routine use of inhaled oxygen for acute myocardial infarction (AMI).Search methodsWe searched the following bibliographic databases on 6 June 2015: the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, MEDLINE (OVID), Embase (OVID), CINAHL (EBSCO) and Web of Science (Thomson Reuters). LILACS (Latin American and Caribbean Health Sciences Literature) was last searched in September 2016. We also contacted experts to identify eligible studies. We applied no language restrictions.Selection criteriaRandomised controlled trials in people with suspected or proven AMI (ST-segment elevation myocardial infarction (STEMI) or non-STEMI) within 24 hours after onset, in which the intervention was inhaled oxygen (at normal pressure) compared to air, regardless of co-therapies provided to participants in both arms of the trial.Data collection and analysisTwo authors independently reviewed the titles and abstracts of identified studies to see if they met the inclusion criteria and independently undertook the data extraction. We assessed the quality of studies and the risk of bias according to guidance in the Cochrane Handbook for Systematic Reviews of Interventions. The primary outcome was death. The measure of effect used was the risk ratio (RR) with a 95% confidence interval (CI). We used the GRADE approach to evaluate the quality of the evidence and the GRADE profiler (GRADEpro) to import data from Review Manager 5 and create 'Summary of findings' tables.Main resultsThe updated search yielded one new trial, for a total of five included studies involving 1173 participants, 32 of whom died. The pooled risk ratio (RR) of all-cause mortality in the intention-to-treat analysis was 0.99 (95% CI 0.50 to 1.95; 4 studies, N = 1123; I2 = 46%; quality of evidence: very low) and 1.02 (95% CI 0.52 to 1.98; 4 studies, N = 871; I2 = 49%; quality of evidence: very low) when only analysing participants with confirmed AMI. One trial measured pain directly, and two others measured it by opiate usage. The trial showed no effect, with a pooled RR of 0.97 for the use of opiates (95% CI 0.78 to 1.20; 2 studies, N = 250). The result on mortality and pain are inconclusive. There is no clear effect for oxygen on infarct size (the evidence is inconsistent and low quality).Authors' conclusionsThere is no evidence from randomised controlled trials to support the routine use of inhaled oxygen in people with AMI, and we cannot rule out a harmful effect. Given the uncertainty surrounding the effect of oxygen therapy on all-cause mortality and on other outcomes critical for clinical decision, well-conducted, high quality randomised controlled trials are urgently required to inform guidelines in order to give definitive recommendations about the routine use of oxygen in AMI.
| S-EPMC6463792 | biostudies-literature
Project description:Cardioprotection refers to a strategy aimed at enhancing survival pathways in the injured yet salvageable myocardium following ischemia-reperfusion. Low-density lipoprotein receptor-related protein 1 (LRP1) is a multifunctional receptor that can be targeted following reperfusion, to induce a cardioprotective signaling through the activation of the reperfusion injury salvage kinase (RISK) pathway. The data from preclinical studies with non-selective and selective LRP1 agonists are promising, showing a large therapeutic window for intervention to reduce infarct size after ischemia-reperfusion. A pilot clinical trial with plasma derived α1-antitrypsin (AAT), a naturally occurring LRP1 agonist, supports the translational value of LRP1 as a novel therapeutic target for cardioprotection. A phase I study with a selective LRP1 agonist has been completed showing no toxicity. These findings may open the way to early phase clinical studies with pharmacologic LRP1 activation in patients with acute myocardial infarction (AMI).
| S-EPMC6387161 | biostudies-literature
Project description:BackgroundPreclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.Methods and resultsOverall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.ConclusionsThe presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.
| S-EPMC4599491 | biostudies-literature
Project description:Cell transplantation therapy is considered a novel and promising strategy in regenerative medicine. Recent studies point out that paracrine effects and inflammation induced by transplanted cells are key factors for the improvement of myocardial function. The present study aims at differentiating paracrine effects from inflammatory reactions after cell transplantation. Therefore, in vitro induced apoptotic bodies were transplanted after myocardial infarction in a rat model. Eight weeks after transplantation, the functional results showed no improvement in left ventricular function. Histological analysis revealed no significant differences in the amount of infiltrated cells and collagen content did not differ among the four groups, which sustains the functional data. Surprisingly, angiogenesis increased in groups with apoptotic bodies derived from HUVEC and endothelial progenitor cells, but not from fibroblasts. A complex genetic analysis of apoptotic bodies indicated that miRNAs could be responsible for these changes. In conclusion, our study demonstrates both that neoangiogenesis alone is not sufficient to improve function and that inflammation is critical for scar remodeling and improvement of the heart function after cell therapy. Given what we have learned about microRNAs, we hypthesized that the molecular mechanisms of angiogenesis induction could involve apoptotic bodies exerting paracrine angiogenic effects. Using GeneChip miRNA 3.0 Array, microRNAs were analysed in apoptotic bodies from endothelial progenitor cells (EPCs), human umbilical veno-endothelial cells (HUVECs), and fibroblasts. From human EPCs, human dermal fibroblasts, and HUVECs, apoptotic bodies were isolated after treatment with cycloheximide in hypoxia for 24 hours.
2015-12-31 | E-GEOD-48218 | biostudies-arrayexpress
Project description:BackgroundMost deaths from coronary artery disease (CAD) are due to acute myocardial infarction (AMI). There is an urgent need for early AMI detection, particularly in patients with stable CAD. 5-methylcytosine (5mC) regulatory genes have been demonstrated to involve in the progression and prognosis of cardiovascular diseases, while little research examined 5mC regulators in CAD to AMI progression.MethodTwo datasets (GSE59867 and GSE62646) were downloaded from Gene Expression Omnibus (GEO) database, and 21 m5C regulators were extracted from previous literature. Dysregulated 5mC regulators were screened out by "limma." The least absolute shrinkage and selection operator (LASSO) and support vector machine recursive feature elimination (SVM-RFE) algorithm were employed to identify hub 5mC regulators in CAD to AMI progression, and 43 clinical samples (Quantitative real-time PCR) were performed for expression validation. Then a logistic model was built to construct 5mC regulator signatures, and a series of bioinformatics algorithms were performed for model validation. Besides, 5mC-associated molecular clusters were studied via unsupervised clustering analysis, and correlation analysis between immunocyte and 5mC regulators in each cluster was conducted.ResultsNine hub 5mC regulators were identified. A robust model was constructed, and its prominent classification accuracy was verified via ROC curve analysis (area under the curve [AUC] = 0.936 in the training cohort and AUC = 0.888 in the external validation cohort). Besides, the clinical effect of the model was validated by decision curve analysis. Then, 5mC modification clusters in AMI patients were identified, along with the immunocyte infiltration levels of each cluster. The correlation analysis found the strongest correlations were TET3-Mast cell in cluster-1 and TET3-MDSC in cluster-2.ConclusionNine hub 5mC regulators (DNMT3B, MBD3, UHRF1, UHRF2, NTHL1, SMUG1, ZBTB33, TET1, and TET3) formed a diagnostic model, and concomitant results unraveled the critical impact of 5mC regulators, providing interesting epigenetics findings in AMI population vs. stable CAD.
| S-EPMC9816341 | biostudies-literature
Project description:(1) Background: While an artificial intelligence (AI)-based, cardiologist-level, deep-learning model for detecting acute myocardial infarction (AMI), based on a 12-lead electrocardiogram (ECG), has been established to have extraordinary capabilities, its real-world performance and clinical applications are currently unknown. (2) Methods and Results: To set up an artificial intelligence-based alarm strategy (AI-S) for detecting AMI, we assembled a strategy development cohort including 25,002 visits from August 2019 to April 2020 and a prospective validation cohort including 14,296 visits from May to August 2020 at an emergency department. The components of AI-S consisted of chest pain symptoms, a 12-lead ECG, and high-sensitivity troponin I. The primary endpoint was to assess the performance of AI-S in the prospective validation cohort by evaluating F-measure, precision, and recall. The secondary endpoint was to evaluate the impact on door-to-balloon (DtoB) time before and after AI-S implementation in STEMI patients treated with primary percutaneous coronary intervention (PPCI). Patients with STEMI were alerted precisely by AI-S (F-measure = 0.932, precision of 93.2%, recall of 93.2%). Strikingly, in comparison with pre-AI-S (N = 57) and post-AI-S (N = 32) implantation in STEMI protocol, the median ECG-to-cardiac catheterization laboratory activation (EtoCCLA) time was significantly reduced from 6.0 (IQR, 5.0-8.0 min) to 4.0 min (IQR, 3.0-5.0 min) (p < 0.01). The median DtoB time was shortened from 69 (IQR, 61.0-82.0 min) to 61 min (IQR, 56.8-73.2 min) (p = 0.037). (3) Conclusions: AI-S offers front-line physicians a timely and reliable diagnostic decision-support system, thereby significantly reducing EtoCCLA and DtoB time, and facilitating the PPCI process. Nevertheless, large-scale, multi-institute, prospective, or randomized control studies are necessary to further confirm its real-world performance.
| S-EPMC8623357 | biostudies-literature
Project description:BackgroundOral antiplatelet therapy is the cornerstone of treatment for acute myocardial infaction (AMI). However, detailed usage data on oral antiplatelet therapy are lacking.MethodsUsing data from a nationally representative sample of patients with AMI, the detailed usage of oral antiplatelet therapy was analyzed in 40,202 consecutive eligible patients.ResultsThe proportions of patients with AMI taking loading doses of aspirin and P2Y12 inhibitors were relatively low (62.2% and 63.6%, respectively), whereas approximately 90% of patients received maintenance doses of aspirin, P2Y12 inhibitors, and dual antiplatelet therapy. The proportions of patients taking loading doses of aspirin and P2Y12 inhibitors gradually decreased with age. Male sex, an educational level of at least college, an interval from onset to treatment of < 24 h, and primary PCI use were associated with a higher proportion of patients taking a loading dose of antiplatelet therapy, whereas those receiving conservative treatment had a lower rate of antiplatelet use (all P < 0.05). The proportion of patients taking loading doses of aspirin was highest in the western region, and that of patients taking loading doses of P2Y12 inhibitors was highest in the eastern region (P < 0.05). In addition, 76.7% of patients with ST-elevation MI and 91% of patients with non-ST-elevation MI received 300-mg loading dose of clopidogrel.ConclusionsThe proportion of patients with AMI receiving loading doses of aspirin and P2Y12 inhibitors during hospitalization was relatively low, and this rate was affected by many factors, such as age, sex, educational level, region of residence, and the interval from onset to treatment. The underutilization of guideline-based P2Y12 inhibitors was also problematic. Hence, quality improvement initiatives are needed to enhance adherence to guidelines to improve consistent use of oral antiplatelet therapy. Trial registration The Chinese Acute Myocardial Infarction Registry; Trial registration number: ChiCTR-ONC-12002636; Registered 31 October 2012; http://www.chictr.org.cn/showproj.aspx?proj=6916.
| S-EPMC8204547 | biostudies-literature
Project description:Although ?-blockers reduce mortality after acute myocardial infarction (AMI), early reports linking ?-blocker use with subsequent depression have potentially limited their use in vulnerable patients. We sought to provide empirical evidence to support or refute this concern by examining the association between ?-blocker initiation and change in depressive symptoms in AMI patients.Using data from 2 US multicenter, prospective registries of AMI patients, we examined 1-, 6-, and 12-month changes in depressive symptoms after the index hospitalization among patients who were ?-blocker-naïve on admission. Depressive symptoms were assessed using the validated 8-item Patient Health Questionnaire (PHQ-8), which rates depressive symptoms from 0 to 24, with higher scores indicating more depressive symptoms. A propensity-matched repeated-measures linear regression model was used to compare change in depressive symptoms among patients who were and were not initiated on a ?-blocker after AMI.Of 3,470 AMI patients who were ?-blocker-naïve on admission, 3,190 (91.9%) were initiated on a ?-blocker and 280 (8.1%) were not. Baseline PHQ-8 scores were higher in patients not initiated on a ?-blocker (mean 5.78 ± 5.45 vs 4.88 ± 5.11, P = .005). PHQ-8 scores were progressively lower at 1, 6, and 12 months in both the ?-blocker (mean decrease at 12 months 1.16, P < .0001) and no-?-blocker groups (mean decrease 1.71, P < .0001). After propensity matching 201 untreated patients with 567 treated patients, initiation of ?-blocker therapy was not associated with a difference in mean change in PHQ-8 scores at 1, 6, or 12 months after AMI (absolute mean difference with ?-blocker initiation at 12 months of 0.08, 95% CI -0.81 to 0.96, P = .86).Initiation of ?-blocker therapy after AMI was not associated with an increase in depressive symptoms. Restricting ?-blocker use because of concerns about depression appears unwarranted and may lead to undertreatment of AMI patients.
| S-EPMC4802859 | biostudies-literature
Project description:Objective Although the importance of evidence-based optimal medical therapy (OMT) after acute myocardial infarction (AMI) has been recognized, the prescription rate of OMT is not sufficiently high in real-word clinical settings. The purpose of this study was to identify the clinical characteristics of AMI patients who did not receive OMT. Methods The present study was a retrospective study. OMT was defined as the combination of antiplatelet therapy, angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs), beta-blockers, and statins at the time of hospital discharge. Non-OMT was defined as the lack of either antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, or statins. Results A total of 457 AMI patients were included as the final study population, and 98 patients (22.4%) lacked at least 1 OMT medication. The prescription rates of antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, and statins were 98.7%, 87.5%, 90.4%, and 96.7%, respectively. In the multivariate logistic regression analysis, age [per 1-year increase: odds ratio (OR) 1.033, 95% confidence interval (CI) 1.007-1.059, p=0.014], hemodialysis (vs. no hemodialysis: OR 2.707, 95% CI 1.082-6.774, p=0.033), estimated glomerular filtration rate <30 mL/min/1.73 m2 without hemodialysis (OR 4.585, 95% CI 1.975-10.644, p<0.001), AMI caused by vasospastic angina (VSA) (vs. no VSA: OR 13.198, 95% CI 1.809-96.260, p=0.011), and asthma (vs. no asthma: OR 7.241, 95% CI 1.716-30.559, p=0.007) were significantly associated with non-OMT, whereas heart rate on admission (per 1-bpm increase: 0.987, 95% CI 0.975-0.999, p=0.033), any PCI (vs. no PCI: OR 0.156, 95% CI 0.066-0.373, p<0.001), and ST-elevation myocardial infarction (STEMI) (vs. NSTEMI: OR 0.384, 95% CI 0.218-0.675, p=0.001) were inversely associated with non-OMT. Conclusion An advanced age, VSA, bradycardia, asthma, impaired renal function, non-PCI revascularization, and non-ST-elevation myocardial infarction were significantly associated with non-OMT.
| S-EPMC7364243 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-12-12 | GSE185266 | GEO