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Notwithstanding a decrease in the incidence and mortality of cardiovascular diseases during the last decades, notable disparities in health outcomes depending on a patient´s socioeconomic position persist and are most visible in acute myocardial infarction and ischemic heart disease. Education is a pivotal indicator of the socioeconomic position. Effects of the social determinants of health on the incidence, prevalence and mortality of cardiovascular diseases were previously effectually investigated and shown to be inversely associated but evidence on non-fatal health outcomes such as heart failure, ability to return to work or rehospitalizations still remain insufficiently examined. We provide a literature review dealing with the impact that formal education has on non-fatal health outcomes including major adverse cardiovascular events, clinical outcomes, depression, use of cardiac rehabilitation, quality of life, self-perceived health and social participation after a myocardial infarction from a global and comprehensive perspective., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Introduction: Acute myocardial infarction (AMI) is a major public health issue in Germany with considerable regional differences in morbidity and mortality. Possible reasons for regional differences include a higher prevalence of cardiovascular risk factors, infrastructural deficits, different levels of healthcare quality or social determinants. We aim to study associations of social determinants and of rural infrastructure with the quality of medical care (eg, time to reperfusion or medication adherence) and on the long-term outcome after myocardial infarction., Methods and Analysis: We will employ a prospective cohort study design. Patients who are admitted with AMI will be invited to participate. We aim to recruit a total of 1000 participants over the course of 5 years. Information on outpatient care prior to AMI, acute healthcare of AMI, healthcare-related environmental factors and social determinants will be collected. Baseline data will be assessed in interviews and from the electronic data system of the hospital. Follow-up will be conducted after an observation period of 1 year via patient interviews. The outcomes of interest are cardiac and all-cause mortality, changes in quality of life, changes in health status of heart failure, major adverse cardiovascular events and participation in rehabilitation programmes., Ethics and Dissemination: Ethical approval was obtained from the Ethics Committee of Brandenburg Medical School (reference: E-01-20200923). Research findings will be disseminated and shared in different ways and include presenting at international and national conferences, publishing in peer-reviewed journals and facilitating dissemination workshops within local communities with patients and healthcare professionals., Trials Registration Number: DRKS00024463., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Introduction: Evidence on the association of socioeconomic deprivation with occurrence of acute myocardial infarction (AMI) is available from international studies and urban settings in western Germany. This study aimed to assess this association based on small geographical areas in a rural setting in eastern Germany., Methods: This study used routine data of all patients with AMI who were treated in the Hospital Brandenburg in the city of Brandenburg, Germany, between May 2019 and May 2020. Hospitalisation rates of AMI were calculated for postal code regions that were located within the catchment area of the Hospital Brandenburg. Poisson regression was used to compare hospitalisation rates in areas with medium socioeconomic deprivation to areas with high deprivation, controlling for age group, sex and period (before or during COVID-19 pandemic). Publicly available social, infrastructure and healthcare-related features were mapped to characterise the study region., Results: In total, 265 cases of AMI were registered in the study area, which comprised 116,126 inhabitants. The city of Brandenburg was characterised by the highest level of socioeconomic deprivation, while neighbouring areas showed a rural settlement structure and medium levels of deprivation. The number of general practitioners per 10 000 inhabitants did not differ between both areas. The adjusted rate ratio comparing hospitalisations due to AMI in areas with medium socioeconomic deprivation to areas with high socioeconomic deprivation was 0.71 (95%CI 0.56-0.91, p=0.01)., Conclusion: This study adds evidence about the association of socioeconomic deprivation and AMI occurrence from a rural area in eastern Germany. Further research about the relationship of socioeconomic deprivation and cardiovascular health is needed from heterogeneous contexts.

Background: The implantation of cardioverter defibrillators (ICDs) is an established therapy in the prevention of sudden cardiac death in patients with systolic dysfunction after myocardial infarction. To avoid immediate implantation of an ICD, wearable cardioverter defibrillator vests (WCD) can be used to protect patients against malignant rhythm disorders, while at the same time drug-based heart failure therapy has to be initiated. This drug therapy can improve left ventricular ejection fraction and primary prophylactic cardioverter defibrillator implantation may not be necessary. However, the recent Vest Prevention of Early Sudden Death Trial (VEST) questioned the regular use of the WCD in this setting., Case Presentation: A 47-year-old Caucasian man with severely impaired left ventricular function early after myocardial infarction was prescribed a WCD as primary prophylaxis to prevent sudden cardiac death. Seven days after the patient was supplied with a WCD, the patient suffered from an electrical storm with recurrent ventricular tachycardia (VT), which was successfully terminated 17 times by the WCD. On coronary angiography, the formerly infarct-related right coronary artery had TIMI (Thrombolysis in Myocardial Ischemia Trial) III flow, and a remaining stenosis in the left anterior descending artery (LAD) was stented, which did not stop recurrent VT. In the electrophysiology (EP) study, a focus was mapped in the left inferior ventricle, which was ablated. This stopped the VT. A second radio-frequency (RF) ablation in the same area was necessary after 14 days. Finally, a permanent cardioverter defibrillator was implanted., Conclusion: We report the case of a patient who survived recurrent episodes of VT early after myocardial infarction by effective defibrillation with a WCD. The WCD is a useful device to bridge time until a final decision for implantation of a defibrillator.

Purpose: To develop and validate a fast cardiac magnetic resonance imaging T1 mapping technique with high spatial resolution based on a radial inversion-recovery (IR) spoiled gradient-echo acquisition., Materials and Methods: Approval for the study was granted by the local institutional review board, and all subjects gave written informed consent. An electrocardiographically triggered radial single-shot IR (TRASSI) sequence was developed in conjunction with a custom-written fitting algorithm. The proposed imaging technique was validated in phantom measurements and then used for cardiac T1 mapping in 62 subjects with or without cardiac disease. The study population included 51 healthy subjects, three patients with arrhythmia, and eight patients with myocardial infarction. The potential heart rate dependency of the TRASSI method was tested by using linear regression analysis. Statistically significant differences between the sexes and various section orientations were analyzed with a Student t test for independent groups and a repeated-measures analysis of variance for dependent groups., Results: High-spatial-resolution T1 maps (1.17 × 1.17 mm) without motion artifacts and without heart rate dependency (slope = -0.0303, R(2) = 0.0000887, P = .899) were acquired with an acquisition time of less than 6 seconds in all subjects. The mean T1 of healthy left ventricular myocardium across all examined subjects was 1031 msec ± 33 (standard deviation). Testing for reproducibility in three individuals with 34 repetitive measurements revealed a mean standard deviation of 4.1 msec (0.412%). Subacute and chronic myocardial infarction could be detected in all eight patients. T1 disturbances due to arrhythmia proved to be minimal in three patients (standard deviation, <1.2%)., Conclusion: Fast and accurate cardiac T1 mapping is feasible within a single-shot IR experiment.

Background: We previously demonstrated that conditional overexpression of neuronal nitric oxide synthase (nNOS) inhibited L-type Ca2+ channels and decreased myocardial contractility. However, nNOS has multiple targets within the cardiac myocyte. We now hypothesize that nNOS overexpression is cardioprotective after ischemia/reperfusion because of inhibition of mitochondrial function and a reduction in reactive oxygen species generation., Methods and Results: Ischemia/reperfusion injury in wild-type mice resulted in nNOS accumulation in the mitochondria. Similarly, transgenic nNOS overexpression caused nNOS abundance in mitochondria. nNOS translocation into the mitochondria was dependent on heat shock protein 90. Ischemia/reperfusion experiments in isolated hearts showed a cardioprotective effect of nNOS overexpression. Infarct size in vivo was also significantly reduced. nNOS overexpression also caused a significant increase in mitochondrial nitrite levels accompanied by a decrease of cytochrome c oxidase activity. Accordingly, O(2) consumption in isolated heart muscle strips was decreased in nNOS-overexpressing nNOS(+)/αMHC-tTA(+) mice already under resting conditions. Additionally, we found that the reactive oxygen species concentration was significantly decreased in hearts of nNOS-overexpressing nNOS(+)/αMHC-tTA(+) mice compared with noninduced nNOS(+)/αMHC-tTA(+) animals., Conclusion: We demonstrated that conditional transgenic overexpression of nNOS resulted in myocardial protection after ischemia/reperfusion injury. Besides a reduction in reactive oxygen species generation, this might be caused by nitrite-mediated inhibition of mitochondrial function, which reduced myocardial oxygen consumption already under baseline conditions.

Background and Purpose: Our recent experiments demonstrated that the Sphingosine-1-phosphate (S1P) receptor agonist FTY720 (2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol hydrochloride) improves recovery of function after myocardial ischaemia-reperfusion ex vivo. Therefore, we tested the hypothesis that pharmacological post-conditioning with FTY720 reduces infarct size after myocardial ischaemia-reperfusion in vivo., Experimental Approach: Myocardial ischaemia was induced in Wistar rats by ligation of the left coronary artery for 45 min. FTY720 (0.5 mg kg(-1)) was applied i.p. either once, before reperfusion, or twice, 24 h before myocardial ischaemia and before reperfusion. After 24 h reperfusion, we determined infarct size by triphenyltetrazolium chloride staining and granulocyte infiltration by immunohistochemistry. Tumour necrosis factor-alpha (TNF)-alpha concentration was determined by elisa. S1P receptor expression was studied by Western blot. Calcium transients were evaluated in Indo-1-loaded cardiomyocytes., Key Results: In both groups, FTY720 significantly reduced lymphocyte count in peripheral blood. FTY720 treatment attenuated granulocyte infiltration and TNF-alpha protein expression in reperfused myocardium. However, both treatment regimens were not able to reduce infarct size. FTY720 increased mortality due to induction of fatal ventricular tachyarrhythmias when administered once before reperfusion, but protected against reperfusion arrhythmias when given 24 h prior to ischaemia. Pretreatment selectively down-regulated S1P(1) receptor expression within the myocardium. S1P receptor agonists did not induce calcium deregulation in cardiomyocytes., Conclusions and Implications: FTY720 applied during reperfusion did not reduce infarct size but increased mortality during myocardial ischaemia-reperfusion due to induction of arrhythmias. Pretreatment with FTY720 before ischaemia abrogated the deleterious pro-arrhythmic effects without reducing infarct size.

Secreted protein, acidic, and rich in cysteine (SPARC) is thought to regulate cell matrix interaction during wound repair. We hypothesized that SPARC might promote migration via integrin-dependent mechanisms. The present study was designed to clarify the contribution of SPARC in the wound healing process after myocardial infarction (MI). Adult mice received a specific alpha(v) integrin inhibitor or vehicle through osmotic mini pumps. Mice of each group were either sham-operated or MI was induced. SPARC expression was investigated 2 days, 7 days, and 1 month after the surgical procedure. For migration assays, a modified Boyden chamber assay was used. A transient increase of SPARC levels was observed, starting at day 2 (2.55+/-0.21), day 7 (3.72+/-0.28), and 1 month (1.9+/-0.16) after MI. After 2 months, SPARC expression dropped back to normal levels compared to sham-operated hearts. Immunofluorescence analysis showed an increase of SPARC in the infarcted area 2 days after MI, a strong increase in the scar area 7 days after MI, and only low levels in the scar area 2 months after MI. Integrin alpha(v) inhibition abolished the up-regulation of SPARC. In vitro migration assays demonstrated that fibronectin-stimulated haptotaxis of fibroblasts was modulated by SPARC. This study provides evidence that SPARC is significantly up-regulated in the infarcted region after MI. This up-regulation is dependent on alpha(v) integrins. As SPARC is found to regulate fibroblast migration, it appears to play an important role in the injured myocardium with regard to healing and scar formation.

Influenza is a common disease in the population. Influenza vaccination is performed routinely and is usually well tolerated. Minor local or systemic side effects like fever and myalgia are described. Rarely there are more severe adverse events. Systemic vasculitis has been reported in some cases. In this case we report on a female patient with secondary vasculitis and myocardial infarction after influenza vaccination. The patient received cortisol and recovered. The literature about influenza vaccination, its side effects and recommendations about vaccination in patients with coronary artery disease is reviewed.

Acute kidney injury (AKI) occurs frequently in hospitals worldwide, but the therapeutic options are limited. Diabetes mellitus (DM) affects more and more people around the globe. The disease worsens the prognosis of AKI even further. In recent years, cell-based therapies have increasingly been applied in experimental AKI. The aim of the study was to utilize two established autophagy inducers for pharmacological preconditioning of so-called proangiogenic cells (PACs) in PAC treatment of diabetic AKI. Insulin-dependent DM was induced in male C57/Bl6N mice by intraperitoneal injections of streptozotocine. Six weeks later, animals underwent bilateral renal ischemia for 45 min, followed by intravenous injections of either native or zVAD (benzyloxycarbonyl-Val-Ala-Asp-fluoro-methylketone)- or Z-Leu-Leu-Leu-al (MG132)-pretreated syngeneic murine PACs. Mice were analyzed 48 h (short term) and 6 wk (long term) later, respectively. DM worsened postischemic AKI, and PAC preconditioning with zVAD and MG132 resulted in a further decline of excretory kidney function. Injection of native PACs reduced fibrosis in nondiabetic mice, but cell preconditioning promoted interstitial matrix accumulation significantly. Both substances aggravated endothelial-tomesenchymal transition (EndoMT) under diabetic conditions; these effects occurred either exclusively in the short (zVAD) or in the short and long term (MG132). Preconditioned cells stimulated the autophagocytic flux in intrarenal endothelial cells, and all experimental groups displayed increased endothelial abundances of senescenceassociated β-galactosidase, a marker of premature cell senescence. Pharmacological autophagy activation may not serve as an effective strategy for improving PAC competence in diabetic AKI in general. On the contrary, several outcome parameters (excretory function, fibrosis, EndoMT) may even be worsened. [ABSTRACT FROM AUTHOR]