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Failure of thrombin generation markers to triage patients presenting with chest pain
M E McKenzie1, A Pothula, P A Gurbel
1The Sinai Center for Thrombosis Research, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Insights
Thrombin generation markers did not effectively triage emergency department patients with chest pain. Surprisingly low levels were observed in acute myocardial infarction patients, warranting further investigation.
Area of Science:
- Cardiology
- Hematology
- Emergency Medicine
Background:
- Thrombin generation (TG) is implicated in acute coronary syndromes like acute myocardial infarction (AMI).
- The diagnostic value of TG for triaging chest pain patients is uncertain.
Purpose of the Study:
- To investigate if plasma markers of thrombin generation can triage patients presenting with chest pain.
- To compare TG markers in patients with non-cardiac chest pain, unstable angina (UA), congestive heart failure (CHF), and AMI against healthy controls.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure soluble plasma levels of prothrombin fragment 1+2 (F(1+2)) and thrombin/antithrombin III complexes (TAT).
- Measurements were taken in 80 chest pain patients and 20 healthy controls presenting to the Emergency Department.
Main Results:
- No differences in F(1+2) or TAT were found between non-cardiac chest pain patients and controls.
- TAT levels were elevated in UA patients compared to controls (6.05 ± 1.15 vs. 3.34 ± 0.20 ng/ml, p=0.033).
- Contrary to expectations, TAT levels in AMI patients were lower than in UA and CHF patients. F(1+2) levels were significantly lower in AMI patients than in controls (0.84 ± 0.10 vs. 1.22 ± 0.11 ng/ml, p=0.026).
Conclusions:
- Plasma F(1+2) and TAT levels at presentation failed to effectively triage chest pain patients.
- The unexpectedly low TG marker levels in AMI patients require further investigation before therapy initiation.
Abstract:
Thrombin generation (TG) is an important pathogenic factor in acute coronary syndromes including acute myocardial infarction (AMI). Since the diagnostic utility of TG remains uncertain we sought to determine whether markers of TG may triage patients presenting to the Emergency Department with chest pain. Soluble plasma levels of prothrombin fragment 1+2 (F(1+2)), and thrombin/antithrombin III complexes (TAT) were determined by ELISA in 80 patients presenting with chest pain to the Emergency Department and compared with 20 controls. There were no differences in TG markers between patients with non-cardiac chest pain and healthy controls. Patients with unstable angina (UA), and congestive heart failure (CHF) did not differ from controls with respect to F(1+2), and TAT was elevated in UA patients (6.05 +/- 1.15 ng/ml, p = 0.033) when compared with controls (3.34 +/- 0.20 ng/ml). Contrary to expectations, TAT levels at presentation with AMI were well below the concentrations observed in patiens with UA and CHF. Moreover, plasma F(1+2) levels were significantly lower than in healthy controls (0.84 +/- 0.10 ng/ml versus 1.22 +/- 0.11, p = 0.026). At the time of presentation to the Emergency Department, F(1+2) and TAT failed to suitably triage patients with chest pain. The surprisingly low levels of TG markers in AMI patients before applying intensive therapy and reperfusion strategies deserves further investigation.