New insights from the MESA study: increased high-sensitivity troponins as a cardiovascular risk factor

Abstract

The most recent high-sensitivity assays for troponins I and T (hs-TnI and hs-TnT) have made it possible to detect blood concentrations up to 10 times lower than previous assays, making troponins detectable even in asymptomatic subjects without manifest cardiovascular disease. For this reason, hs-Tn, initially introduced as markers of myocardial damage in an acute setting, have also become possible markers of subclinical myocardial damage in baseline conditions. In fact, recent evidence suggests that hs-TnT and hs-TnI predict the risk of future cardiovascular events also in the context of primary prevention, and offer incremental information when added to current risk stratification models. The different association highlighted with different outcome measures, such as coronary heart disease, atherosclerotic cardiovascular disease, heart failure, and death from all causes, seems to indicate that the risk observed in asymptomatic subjects with high levels of hs-Tn is an expression of subclinical damage secondary to multiple pathophysiological mechanisms, and not only to atherothrombosis. However, the ability of hs-TnT and hs-TnI (until now used interchangeably), to provide differential predictive information, and not redundant with respect to more traditional factors, remains to be definitively clarified, both for the purpose of predicting specific outcomes and for the implementation of specific preventive strategies. To date, evidences available allow us to hypothesize their role more as markers than as risk factors.

The Role of Fine Particles (PM 2.5) in the Genesis of Atherosclerosis and Myocardial Damage: Emphasis on Clinical and Epidemiological Data, and Pathophysiological Mechanisms

“…In general, high-sensitivity cardiac troponins are not only valuable biomarkers of the acute myocardial infarction, they also allow detecting myocardial injury in other pathological and physiological conditions that have a negative effect on cardiomyocytes [104,118,[129][130][131][132][133][134]. The mechanisms of the increase of cardiac troponins in blood serum under the exposure of a human body to PM 2.5 are not definitely known.…”

Approach to risk stratification of atherosclerotic cardiovascular disease

“…28 Although more research is needed to investigate whether hsTn provides unique information that is not otherwise captured by an individual's traditional risk factors, it remains useful as a risk marker and patients with detectable or elevated hsTn levels can be considered for earlier and more aggressive preventive interventions. 29 C-reactive protein: Inflammatory cells play a pathogenic role in the formation of early "fatty streaks," the progression to advanced atherosclerotic lesions, and the development of unstable plaques. [30][31][32][33] One of the most ubiquitous markers of inflammation is CRP, an acute-phase reactant that is predominantly made by hepatocytes in response to inflammation, infection, malignancies, or tissue damage.…”

Approche de la stratification du risque de maladies cardiovasculaires athéroscléreuses

“…Des études ont fait valoir des améliorations dans la stratification du risque cardiovasculaire en ajoutant la Tn-hs au SRF 20,24-27 et à l'algorithme du risque SCORE (Systematic COronary Risk Evaluation) de la Société européenne de cardiologie 28 . Même si plus de recherches sont nécessaires pour savoir si la Tn-hs procure des renseignements qui ne sont pas autrement captés par les facteurs de risque traditionnels d'une personne, elle demeure utile comme marqueur de risque, et les patients dont les dosages de Tn-hs sont détectables ou élevés peuvent être considérés comme nécessitant des interventions préventives plus hâtives et plus intenses 29 .…”