Publications by authors named "Johannes Reinhold"

The aim of this study is to review the predictive value of visit-to-visit variability in glycaemic or lipid tests for forecasting major adverse cardiovascular events (MACE) in diabetes mellitus. Data from existing studies suggests that such variability is an independent predictor of adverse outcomes in this patient cohort. This understanding is then applied to the development of PowerAI-Diabetes, a Chinese-specific artificial intelligence-enhanced predictive model for predicting the risks of major adverse cardiovascular events and diabetic complications.

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Background And Aims: A randomized trial has previously demonstrated that neointimal modification with a scoring balloon improves the anti-restenotic effect of drug-coated balloon (DCB) in patients with drug-eluting stent restenosis. There are very limited data about the safety and efficacy of using scoring balloons as part of lesion preparation in patients with STEMI, especially in patients with de novo disease treated with DCB-only angioplasty.

Methods: We undertook an analysis of the SPARTAN Norwich Registry to address this question.

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Background: There are no data regarding the outcomes of patients with stent thrombosis (ST) being treated with drug-coated balloon (DCB) angioplasty. Our aim was to compare the outcomes of patients with ST treated with DCB vs. a drug eluting stent (DES).

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Aims: There is uncertainty about the definition of iron deficiency (ID) and the association between ID and prognosis in patients with advanced heart failure. We evaluated three definitions of ID in patients referred for heart transplantation.

Methods And Results: Consecutive patients assessed for heart transplantation at a single UK centre between January 2010 and May 2022 were included.

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Background: Primary percutaneous coronary intervention (pPCI) with drug-eluting stents (DES) has emerged as the standard of care, but stent-related events have persisted. Drug-coated balloon (DCB)-only angioplasty is an emerging technology, although it is not fully evaluated compared with DES in the context of pPCI.

Objectives: The aim of this study was to investigate the safety of DCB-only angioplasty compared with second-generation DES in pPCI.

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(1) Background: Iron deficiency (ID) is an important adverse prognostic marker in patients with heart failure (HF); however, it is unclear whether intravenous iron replacement reduces cardiovascular mortality in this patient group. Here, we estimate the effect of intravenous iron replacement therapy on hard clinical outcomes following the publication of IRONMAN, the largest trial in this field. (2) Methods: In this systematic review and meta-analysis, prospectively registered with PROSPERO and reported according to PRISMA guidelines, we searched PubMed and Embase for randomized controlled trials investigating intravenous iron replacement in patients with HF and co-existing ID.

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Article Synopsis
  • The study compares the effectiveness of drug-coated balloons (DCBs) versus second-generation drug-eluting stents (DESs) in treating new cases of unprotected left main stem (LMS) disease.
  • The research involved 148 patients and found no significant differences in all-cause mortality (19.5% for DCB vs. 15.9% for DES) or cardiac mortality between the two treatment options.
  • The results indicate that DCBs are a safe alternative for treating LMS disease, with outcomes similar to DES after a median follow-up of 33 months.
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Objectives: To evaluate the effectiveness of interventions to improve shared decision making (SDM) in cardiology with particular focus on patient-centred outcomes such as decisional conflict.

Methods: We searched Embase (OVID), the Cochrane library, PubMed and Web of Science electronic databases from inception to January 2021 for randomised controlled trials that investigated the effects of interventions to increase SDM in cardiology. The primary outcomes were decisional conflict, decisional anxiety, decisional satisfaction or decisional regret; a secondary outcome was knowledge gained by the patients.

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Background: Inhibiting SDH (succinate dehydrogenase), with the competitive inhibitor malonate, has shown promise in ameliorating ischemia/reperfusion injury. However, key for translation to the clinic is understanding the mechanism of malonate entry into cells to enable inhibition of SDH, its mitochondrial target, as malonate itself poorly permeates cellular membranes. The possibility of malonate selectively entering the at-risk heart tissue on reperfusion, however, remains unexplored.

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Cardiomyocytes rely on specialised metabolism to meet the high energy demand of the heart. During heart development, metabolism matures and shifts from the predominant utilisation of glycolysis and glutamine oxidation towards lactate and fatty acid oxidation. Iron deficiency (ID) leads to cellular metabolism perturbations.

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Aims: Recent randomised controlled trials (RCTs) have shown a significant prognostic benefit of sodium-glucose cotransporter 2 (SGLT2) inhibitors in the cardiovascular (CV) profile of patients with diabetes. This systematic review and meta-analysis aim to provide a concise evaluation of all the available evidence for the use of these agents in patients with heart failure (HF) regardless of their baseline diabetes status.

Methods And Results: PubMed, Web of Science, and Cochrane library databases were systematically searched from inception until November 20 2020.

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Background: Iron deficiency (ID) is an important predictor of adverse outcomes in patients with heart failure, however it is unclear whether ID also affects prognosis in patients with acute coronary syndrome (ACS). The aim of this systematic review and meta-analysis was to assess the prognostic value of iron deficiency in patients with ACS.

Methods: We searched PubMed, Web of Science, and the Cochrane library and included cohort studies of patients with ACS that were stratified by ID status.

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Aging is the largest risk factor for cardiovascular disease, yet the molecular mechanisms underlying vascular aging remain unclear. Mitochondrial DNA (mtDNA) damage is linked to aging, but whether mtDNA damage or mitochondrial dysfunction is present and directly promotes vascular aging is unknown. Furthermore, mechanistic studies in mice are severely hampered by long study times and lack of sensitive, repeatable and reproducible parameters of arterial aging at standardized early time points.

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Objective: Mitochondrial DNA (mtDNA) damage is present in murine and human atherosclerotic plaques. However, whether endogenous levels of mtDNA damage are sufficient to cause mitochondrial dysfunction and whether decreasing mtDNA damage and improving mitochondrial respiration affects plaque burden or composition are unclear. We examined mitochondrial respiration in human atherosclerotic plaques and whether augmenting mitochondrial respiration affects atherogenesis.

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Background: Glucagon-like peptide-1 (7-36) amide (GLP-1) protects against stunning and cumulative left ventricular dysfunction in humans. The mechanism remains uncertain but GLP-1 may act by opening mitochondrial K-ATP channels in a similar fashion to ischemic conditioning. We investigated whether blockade of K-ATP channels with glibenclamide abrogated the protective effect of GLP-1 in humans.

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Background: Although vascular smooth muscle cell (VSMC) proliferation is implicated in atherogenesis, VSMCs in advanced plaques and cultured from plaques show evidence of VSMC senescence and DNA damage. In particular, plaque VSMCs show shortening of telomeres, which can directly induce senescence. Senescence can have multiple effects on plaque development and morphology; however, the consequences of VSMC senescence or the mechanisms underlying VSMC senescence in atherosclerosis are mostly unknown.

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Oxidative damage from elevated production of reactive oxygen species (ROS) contributes to ischemia-reperfusion injury in myocardial infarction and stroke. The mechanism by which the increase in ROS occurs is not known, and it is unclear how this increase can be prevented. A wide variety of nitric oxide donors and S-nitrosating agents protect the ischemic myocardium from infarction, but the responsible mechanisms are unclear.

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The diagnosis of myocardial infarction (MI) depends on a rise and/or fall of cardiac biomarkers such as troponins in the appropriate clinical context. Conventional troponin assays lack sensitivity and precision at the low serum concentrations observed in the early hours after the onset of chest pain. New, highly sensitive troponin assays may offer improved certainty in these early hours.

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Objective: Sphingosine-1-phosphate (S1P) is a bioactive lipid, which influences migration and proliferation of endothelial cells through activation of S1P receptors and has been shown to support SDF-1 induced migration and bone marrow homing of CD34+ progenitors.

Methods And Results: Here, we show that incubation of patient-derived endothelial progenitor cells (EPCs) with S1P or its synthetic analog FTY720 improved blood flow recovery in ischemic hind limbs. Likewise, recovery of blood flow was dramatically reduced after induction of hindlimb ischemia in mice deficient for the S1P receptor 3 (S1P3).

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Transplantation of bone marrow cells as well as circulating endothelial progenitor cells (EPC) enhances neovascularization after ischemia. The chemokine receptor CXCR4 is essential for migration and homing of hematopoietic stem cells. Therefore, we investigated the role of CXCR4 and its downstream signaling cascade for the angiogenic capacity of cultured human EPC.

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Purpose: To evaluate the effect of a compulsory evidence-based medicine (EBM) seminar in critical appraisal skills and the overall acceptance of compulsory EBM seminars for Year 3 medical undergraduate students.

Methods: Small group seminars by peer teaching were conducted for up to 23 undergraduates. Knowledge and skills in EBM before and after the compulsory seminars were evaluated by 2 different sets of 20 questions.

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Background: Transplantation of endothelial progenitor cells (EPCs) improves neovascularization after ischemia, but patients with coronary artery disease (CAD) or diabetes mellitus show a reduced number of EPCs and impaired functional activity. Therefore, we investigated the effects of risk factors, such as glucose and TNF-alpha, on the number of EPCs in vitro to elucidate the underlying mechanisms.

Methods And Results: EPCs of patients or healthy subjects were isolated from peripheral blood.

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