Cardiac troponin is associated with cardiac outcomes in men and women with atrial fibrillation, insights from the ARISTOTLE trial

Røsjø, Helge; Hijazi, Ziad; Omland, Torbjørn; Westerbergh, Johan; Lyngbakken, Magnus Nakrem; Alexander, John H.; Gersh, Bernard J.; Granger, Christopher B.; Lópes, Renato D.; Siegbahn, Agneta; Wallentin, Lars

doi:10.1111/joim.13072

Cited by 5 publications

(2 citation statements)

References 31 publications

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“…Hence, data from several independent cohorts support a model of cardiac troponins as either directly or indirectly associated with heart failure development. This model is supported by high-sensitivity troponin concentrations being correlated with indices of structural heart disease, and most prominently left ventricular mass(42,44–46).…”

Section: Discussionmentioning

confidence: 82%

Using human genetics to understand the causes and consequences of circulating cardiac troponin I in the general population

Moksnes¹,

Røsjø²,

Richmond³

et al. 2020

Preprint

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Circulating cardiac troponin proteins are associated with structural heart disease and predict incident cardiovascular disease in the general population. However, the genetic contribution to cardiac troponin I (cTnI) concentrations and its causal effect on cardiovascular phenotypes is unclear. We combine data from the Trondelag Health Study and the Generation Scotland Scottish Family Health Study and perform a genome-wide association study of high-sensitivity cTnI concentrations with 48 115 individuals. We identified 12 genetic loci (8 novel) associated with cTnI concentrations. Associated protein-altering variants highlighted putative functional genes: CAND2, HABP2, ANO5, APOH, FHOD3, TNFAIP2, KLKB1 and LMAN1. Using two-sample Mendelian randomization we confirmed the non-causal role of cTnI in acute myocardial infarction, but could not rule out a causal role for cTnI in heart failure. Using genetically informed methods for causal inference of cTnI helps inform the role and value of measuring cTnI in the general population.

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Section: Discussionmentioning

confidence: 82%

Using human genetics to understand the causes and consequences of circulating cardiac troponin I in the general population

Moksnes¹,

Røsjø²,

Richmond³

et al. 2020

Preprint

Self Cite

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“…In anticoagulated individuals with AF, however, high-sensitivity troponin concentrations remain equally related to poor clinical outcomes regardless of sex. 35 In many stable individuals with persistent AF who did not have ischemic heart disease, elevated TnT was found. A substantial decrease in heart rate due to the study drugs was connected to a large drop in TnT level.…”

Section: Methodsmentioning

confidence: 99%

The Role of Biochemical Cardiac Markers in Atrial Fibrillation

RAFAQAT,

IJAZ

2023

J Innov Cardiac Rhythm Manage.

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Atrial fibrillation (AF) is the most common type of cardiac arrhythmia. Proteins are a component of cardiac biomarkers containing cell structures that are released into the circulation when a myocardial injury occurs. They are essential in the diagnosis, risk assessment, and treatment of patients who have chest pain, are thought to have acute coronary syndrome, or are experiencing acute heart failure exacerbations. There are numerous biochemical cardiac markers, but this article summarizes the basic role of major biochemical cardiac markers, including cardiac natriuretic peptides, cardiac troponins, C-reactive protein (CRP), creatine kinase-MB, heart - type fatty acid-binding protein, ischemia-modified albumin, lipoprotein (a), osteopontin (OPN), and soluble suppression of tumorigenicity 2 (sST2), in AF. Atrial natriuretic peptide may serve as an indicator of atrial integrity, which may help to select appropriate treatment approaches for AF. Higher levels of N-terminal pro–B-type natriuretic peptide and brain natriuretic peptide are predictive of incidental AF. Increased troponin T release may indicate better clinical results following AF ablation. Similarly, CRP increases the risk of the AF-increasing calcium (Ca) influx in atrial myocytes, but not because of atrial fibrosis. Patients with postoperative AF have lower FABP3 gene expression in the atrium. Lipoprotein (a) (Lp[a]) may play a causative role in the onset of AF and impact various cardiac tissues. Clinical trials for Lp(a)-lowering drugs should assess their impact on preventing AF. Also, OPN was highly expressed in the circulation of AF patients and further increased with the progression of AF. sST2 was a reliable predictor of new-onset AF and can improve the accuracy of the AF risk model. There is a greater chance that these cardiac biomarkers might be employed to enhance clinical risk stratification in AF.

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