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.
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.