trimethylamine/infarkt

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Relation of Circulating Trimethylamine N-Oxide With Coronary Atherosclerotic Burden in Patients With ST-segment Elevation Myocardial Infarction.

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The gut microbial metabolite trimethylamine N-oxide (TMAO) promotes atherosclerosis and cardiovascular diseases. TMAO levels are associated with the coronary atherosclerotic burden in patients with stable coronary artery disease. However, the relation between TMAO levels and the coronary

Trimethylamine N-oxide and cardiovascular outcomes in patients with chronic heart failure after myocardial infarction.

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Accumulating evidence has demonstrated that intestinal microbiota-dependent trimethylamine N-oxide (TMAO) is involved in the pathogenesis of various cardiovascular diseases. The present study was designed to investigate the prognostic value of TMAO in patients with chronic heart

Association of trimethylamine N-oxide with coronary atherosclerotic burden in patients with non-ST-segment elevation myocardial infarction

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Background: Recently, trimethylamine N-oxide (TMAO) unexplained gut microbe has been proposed as a promising risk factor for atherosclerotic cardiovascular disease (CVD) pathogenesis and adverse events. The relationship of TMAO with

Plasma Trimethylamine N-Oxide as a Novel Biomarker for Plaque Rupture in Patients With ST-Segment-Elevation Myocardial Infarction.

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Trimethylamine N-oxide (TMAO) is reported to promote the pathogenesis of atherosclerosis and be associated with cardiovascular events risk. It is unknown whether plasma TMAO is associated with plaque morphology in patients with acute myocardial infarction. We investigated the

Trimethylamine N-oxide and Risk Stratification after Acute Myocardial Infarction.

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BACKGROUND Risk stratification in acute myocardial infarction (MI) remains a clinical challenge. Trimethylamine N-oxide (TMAO), a gut-derived metabolite, was investigated for its ability to assist in risk stratification for acute MI hospitalizations. METHODS TMAO was analyzed in 1079 acute MI

Reductions in gut microbiota‑derived metabolite trimethylamine N‑oxide in the circulation may ameliorate myocardial infarction‑induced heart failure in rats, possibly by inhibiting interleukin‑8 secretion.

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Myocardial infarction (MI) is a common cause of chronic heart failure (HF). Increasing evidence has revealed that trimethylamine N‑oxide (TMAO), a gut‑microbiota‑derived metabolite, contributes to the pathogenesis of cardiovascular disease by promoting inflammation. Elevated levels of circulating

Gut Microbiota-Dependent Trimethylamine N-oxide and Cardiovascular Outcomes in Patients With Prior Myocardial Infarction: A Nested Case Control Study From the PEGASUS-TIMI 54 Trial.

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Background Trimethylamine N-oxide (TMAO) may have prothrombotic properties. We examined the association of TMAO quartiles with major adverse cardiovascular events (MACE) and the effect of TMAO on the efficacy of ticagrelor. Methods and Results PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in

Effects of gut microbial metabolite trimethylamine N-oxide (TMAO) on platelets and endothelial cells

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Thrombotic events result from different pathologies and are the underlying causes of severe diseases like stroke or myocardial infarction. Recent basic research now revealed a link between food uptake, food conversion and gut metabolism. Gut microbial production of trimethylamine N-oxide (TMAO) from

Probiotics Supplementation on Cardiac Remodeling Following Myocardial Infarction: a Single-Center Double-Blind Clinical Study

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Adverse cardiac remodeling after myocardial infarction (MI) can lead to the syndrome of heart failure (HF). Recently, changes in gut microbiota composition (dysbiosis) have appeared as a novel candidate that may be linked to the development of CR and HF. The aim of this trial was to evaluate the

Impairment of the erythrocyte membrane fluidity in survivors of acute myocardial infarction. A prospective study.

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Erythrocytes have to constantly adapt themselves to the varying circulatory system shear stress forces and capillaries diameter. Membrane lipid and protein content have an important role in determining the erythrocyte shape and are main determinants of the membrane solid and fluid behaviour which

Luhong Granules Prevent Ventricular Remodelling after Myocardial Infarction by Reducing the Metabolites TMAO and LPS of the Intestinal Flora.

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Ventricular remodelling is a common pathological change at all stages of heart disease. Luhong granules are widely used in patients with chronic ventricular remodelling after myocardial infarction and can alleviate chest tightness, shortness of breath, and other symptoms. However, its

Relationship between elevated plasma trimethylamine N-oxide levels and increased stroke injury.

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To investigate whether elevated plasma trimethylamine N-oxide (TMAO) levels are associated with initial stroke severity and infarct volume.This cross-sectional study included 377 patients with acute ischemic stroke and 50 healthy controls. Plasma TMAO

Trimethyllysine, a trimethylamine N-oxide precursor, provides near- and long-term prognostic value in patients presenting with acute coronary syndromes.

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Trimethyllysine (TML) serves as a nutrient precursor of the gut microbiota-derived metabolite trimethylamine N-oxide (TMAO) and is associated with incident cardiovascular (CV) events in stable subjects. We examined the relationship between plasma TML levels and incident CV events in

Trimethylamine N-Oxide and Cardiovascular Outcomes in Patients with End-stage Kidney Disease Receiving Maintenance Hemodialysis.

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BACKGROUND AND OBJECTIVES

Trimethylamine N-oxide (TMAO), a compound derived from byproducts of intestinal bacteria, has been shown to accelerate atherosclerosis in rodents. To date, there are conflicting data regarding the association of serum TMAO with cardiovascular

Associations among serum trimethylamine-N-oxide (TMAO) levels, kidney function and infarcted coronary artery number in patients undergoing cardiovascular surgery: a cross-sectional study.

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BACKGROUND Trimethylamine-N-oxide (TMAO) is a metabolite of phosphatidylcholine generated by gut microbiota and liver enzymes, and has recently been recognized as contributing to atherosclerosis. Elevated serum TMAO levels have been shown to increase the risk of cardiovascular disease (sudden death,

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