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Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
Published on: February 10, 2013
Can dobutamine stress echocardiography induce cardiac troponin elevation?
Alex Blatt1, Gil Moravsky, Semion Pilipodi
1The Department of Cardiology The Department of Anesthesiology Clinical Biochemistry Laboratory, Assaf-Harofeh Medical Center, Zerifin, Sackler School of Medicine, Tel-Aviv University, Ramat-Aviv, Israel.
Insights
Dobutamine stress echo (DSE) does not elevate cardiac troponin I (cTnI) levels, even with significant wall motion abnormalities. Therefore, cTnI is not a useful marker for assessing ischemia during DSE.
Area of Science:
- Cardiology
- Clinical Biochemistry
Background:
- Cardiac troponin (cTn) elevation typically indicates myocardial damage.
- Extreme physical exertion can cause elevated cTn and wall motion abnormalities (WMAs).
- The potential for dobutamine stress echo (DSE) to induce cTn elevation requires investigation.
Purpose of the Study:
- To determine if dobutamine stress echo (DSE) can cause cardiac troponin I (cTnI) elevation in patients undergoing the procedure.
- To compare clinical and echocardiographic features between patients with and without cTnI elevation post-DSE.
Main Methods:
- Prospective enrollment of stable adult patients referred for DSE.
- Standardized DSE protocol with blood sampling for cTnI at baseline and 18-24 hours post-test.
- Comparison of patient characteristics and DSE findings based on cTnI levels.
Main Results:
- Fifty-seven patients were included; 45.4% showed no ischemia on DSE.
- Among patients with ischemia, varying degrees (mild, moderate, severe) were observed.
- Crucially, no patients exhibited elevated cTnI levels 18-24 hours after DSE.
Conclusions:
- Dobutamine stress echo (DSE) does not lead to an elevation in cardiac troponin I (cTnI) levels.
- cTnI is not a suitable additional diagnostic marker for evaluating ischemia during DSE.
- The study suggests that WMAs on DSE do not correlate with myocardial injury as indicated by cTnI.
Background:
Elevation of cardiac troponin (cTn) is considered specific for myocardial damage. Elevated cTn and echocardiogrpahic documentation of wall motion abnormalities (WMAs) that were recorded after extreme physical effort raise the question whether dobutamine stress echo (DSE), can also induce elevation of troponin.
Methods:
we prospective enrolled stable patients (age >18 years) referred to DSE. The exam was performed under standardized conditions. Blood samples for cTnI were obtained at baseline and 18-24 hours after the test. We aimed to compare between the clinical and echocardiographic features of patients with elevated cTnI and those without cTnI elevations.
Results:
Fifty-seven consecutive patients were included. The average age was 64.4 ± 10.7, 73% of the patients were males, and nearly half of the patients were known to have ischemic heart disease. Two of the patients were excluded due to technical difficulty. No signs of ischemia were recorded in 25 (45.4%). Among the patients with established ischemia on DSE, 12 (22%) had mild ischemia, 13 (23.6%) had moderate and 5 (9%) had severe ischemia. Angiography was performed in 13 (26%) of the patients, of which 7 had PCI and one was referred to bypass surgery. None of the patients had elevated cTnI 18-24 hours after the DSE.
Conclusions:
Our results indicate that there is no elevation of cTn despite the occurrence of significant WMAs on DSE. We conclude that cTnI cannot be used as an additional diagnostic tool during pharmacological stress test performed to evaluate the presence and severity of ischemia.
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