The Role of Troponin in the Diagnosis and Treatment of Acute Pulmonary Embolism: Mechanisms of Elevation, Prognostic Evaluation, and Clinical Decision-Making

Abstract

Acute pulmonary embolism (APE) is a cardiovascular disease with severe consequences, wherein cardiac troponin (Tn) plays a pivotal role in diagnosis and treatment. This article reviews the various roles of Tn in managing APE. It looks at how Tn levels increase, their importance in predicting outcomes, and their use in making clinical decisions. Studies indicate that an elevation in Tn is primarily associated with right ventricular overload, ischemia, and necrosis, changes that directly reflect the extent of right ventricular dysfunction and myocardial injury. Elevated levels of Tn are significantly correlated with both short-term and long-term mortality risks in patients with APE, serving as crucial indicators for prognostic assessment and guiding therapeutic strategies. International guidelines recommend integrating Tn testing with clinical scoring and echocardiography to optimize treatment decisions in patients with APE. Despite the significant value of Tn determination in the management of APE, further research is needed to standardize its application. This paper emphasizes future research directions, including exploring the application of Tn in different patient subgroups with APE and its potential combined use with other biomarkers.

Keywords: acute pulmonary embolism; diagnosis; mechanisms; prognostic evaluation; troponin.

Figure 1. Myocardial cell calcium dynamics and troponin (Tn) release mechanism.

(a) When myocardial cells are excited, extracellular Ca2+ enters the cell and triggers the release of more Ca2+ from the sarcoplasmic reticulum, forming an influx and binding to the C subunit of Tn (TnC), leading to the interaction of actin and myosin, generating contractile force. TnC binds to calcium ions, which is crucial for the regulation of muscle contraction. (b) Calcium efflux and myocardial relaxation: During myocardial cell repolarization, Ca2+ is expelled through calcium pumps and exchange proteins, restoring the original position of the Tn I subunit, causing the separation of actin and myosin, and resulting in relaxation force. (c) Myocardial stress and calcium overload: Excessive stress or injury (such as ischemia and hypoxia) to myocardial cells leads to calcium imbalance and overload. (d) Calcium overload and myocardial cell apoptosis: Calcium overload causes mitochondrial dysfunction and inhibition of ATP synthesis, leading to myocardial cell apoptosis. The blood level of Tn reflects the extent of myocardial cell damage and the state of cardiac function. The authors of this article used FigDraw (https://www.figdraw.com/#/paint_about).

Figure 2. Mechanical stretching and stress response of cardiomyocytes due to right ventricular dilation and their molecular mechanisms.

(a) Mechanical stretching and stress response of cardiomyocytes; (b) activation of key signaling pathways within cardiomyocytes, especially integrin-mediated signal transduction pathways; (c) MAPK, JAK/STAT, and calpain-dependent pathways; and (d) release of Tn from muscle fibers. The authors of this article used FigDraw (https://www.figdraw.com/#/paint_about). MAPK, mitogen-activated protein kinase; JAK/STAT, Janus kinase/signal transducer and activator of transcription

Figure 3. Guidelines and management of acute pulmonary embolism: a cross-sectional comparison from 2014 to 2021.

The authors of this article used FigDraw (https://www.figdraw.com/#/paint_about).