Troponin I and <smlcap>D</smlcap>-Dimer for Discriminating Acute Pulmonary Thromboembolism from Myocardial Infarction

Abstract

Background: Acute pulmonary thromboembolism (APTE) is a life-threatening condition, often manifesting with chest pain, dyspnea, and increased cardiac biomarkers including cardiac troponin I (CTI) and <smlcap>D</smlcap>-dimer. Therefore, APTE is often misdiagnosed with classical non-ST elevation myocardial infarction (NSTEMI), resulting in unnecessary coronary interventions and a delay of therapy. Objectives: Our aim was to distinguish APTE from NSTEMI based on CTI and <smlcap>D</smlcap>-dimer levels. Methods: Complete clinical and laboratory data sets from APTE patients (n = 123) were compared with matched NSTEMI patients (n = 123) who presented with chest pain. The APTE diagnosis was confirmed by chest tomography, angiography, or radionuclide ventilation-perfusion scan, while NSTEMI was established by clinical symptoms, cardiac biomarkers, and coronary angiography. Clinical characteristics, CTI (initial and peak), and <smlcap>D</smlcap>-dimer levels at presentation were retrospectively analyzed. Results: The clinical characteristics were not different between APTE and NSTEMI patients. However, significantly lower initial CTI (0.2 ± 0.5 vs. 4.4 ± 9.5 ng/ml) and peak CTI (0.7 ± 2.7 vs. 17.1 ± 20.4 ng/ml), but higher initial <smlcap>D</smlcap>-dimer (9.8 ± 9.4 vs. 1.6 ± 3.6 ng/ml), distinguished APTE from NSTEMI. By receiver operating characteristic curve analysis, the cutoff values for initial CTI, peak CTI, and <smlcap>D</smlcap>-dimer were 0.25, 0.98, and 3.18 ng/ml, respectively. Conclusion: Patients with APTE exhibited lower initial and peak CTI but higher <smlcap>D</smlcap>-dimer levels than NSTEMI patients. Assessing cardiac biomarkers is useful for differentiating APTE from NSTEMI. Further large randomized biomarker studies are urgently needed to facilitate a better APTE diagnosis since clinical characteristics are not particularly helpful.

Diagnostic Value of Serum D-Dimer for Detection of Gallbladder Carcinoma

“…Plasma D-dimer has been widely used to diagnose pulmonary embolism, disseminated intravascular coagulation, myocardial infarction and thromboembolism. [10][11][12][13][14][15] Recent studies have shown that D-dimers are dysregulated in many different types of cancers, including gastric cancer, musculoskeletal sarcoma, lung cancer, pancreatic cancer, esophageal squamous cell carcinoma, ovarian cancer, nasopharyngeal cancer, liver cancer, lymphoma, spinal giant cell tumor, and breast cancer. 6,7,[16][17][18][19][20][21][22][23][24][25][26] Moreover, several studies have shown that elevated levels of D-dimer are significantly associated with cancer recurrence, metastasis, and worse survival outcome.…”

Understanding haemorrhagic risk following thrombolytic therapy in patients with intermediate-risk and high-risk pulmonary embolism: a hypothesis paper

“… 42 The difference in D-dimer levels (a fibrin degradation product), which are much higher in patients with PE compared with patients with MI, supports this mechanistic difference, but also emphasises the greater activation of the fibrinolytic cascade in patients with PE. 43 …”

Exosomal microRNA‑4516, microRNA‑203 and SFRP1 are potential biomarkers of acute myocardial infarction

“…Traditionally, AMI has been diagnosed based on specific electrocardiogram (ECG) presentations and elevated cardiac serum markers, including lactate dehydrogenase, cardiac Troponin I (cTnI), cardiac muscle troponin T (cTnT) and creatine kinase MB (CK-MB) ( 4 , 5 ). However, the complexity of the condition of the patient, the onset of acute pericarditis, myocarditis, heart failure, hypertension and acute pulmonary embolism can also lead to elevated levels of existing markers, which makes distinguishing AMI from these conditions difficult ( 6 , 7 ). Only ST-segment elevation MI (STEMI) can be detected by electrocardiography, while the infarcted vessels cannot be predicted the first time.…”