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Cardiac troponin I after carotid endarterectomy in different cardiac risk patients
George Galyfos1, Costas Tsioufis2, Dimitris Theodorou1
1First Department of Propaedeutic Surgery, University of Athens Medical School, Hippocration Hospital, Athens, Greece.
Insights
Carotid endarterectomy (CEA) can cause asymptomatic cardiac troponin I (cTnI) elevation, particularly in low and medium cardiac risk patients. High-risk patients showed no increased cardiac damage post-CEA.
Area of Science:
- Cardiovascular Surgery
- Cardiac Risk Assessment
- Biomarkers in Cardiology
Background:
- Assessing postoperative cardiac damage after carotid endarterectomy (CEA) is crucial.
- Cardiac troponin I (cTnI) elevation is a key indicator of myocardial injury.
- Stratifying patients by cardiac risk is essential for understanding perioperative outcomes.
Purpose of the Study:
- To compare postoperative cardiac damage, indicated by cTnI elevation, across different cardiac risk groups undergoing CEA.
- To evaluate the predictive value of the Vascular Study Group of New England Cardiac Risk Index (VSG-CRI) in CEA patients.
Main Methods:
- Prospective study involving 324 patients undergoing CEA.
- Stratification into low, medium, and high cardiac risk groups using VSG-CRI criteria.
- Serial cTnI measurements pre-surgery and on postoperative days 1, 3, and 7.
Main Results:
- No mortality or symptomatic myocardial infarction was observed.
- Low-risk (16/140) and medium-risk (28/160) patients showed elevated cTnI postoperatively.
- High-risk patients (n=24) did not exhibit increased postoperative cardiac damage, with lower cTnI levels compared to low/medium risk groups.
Conclusions:
- CEA is associated with a high incidence of asymptomatic cTnI elevation, linked to later cardiac events.
- High-risk patients, as defined by VSG-CRI, did not experience greater cardiac damage post-CEA compared to lower-risk groups.
- The VSG-CRI may not accurately predict cardiac risk for minor troponin elevations after CEA.
Background:
We compared postoperative cardiac damage, defined as cardiac troponin I (cTnI) elevation, in low, medium, and high cardiac risk patients, after carotid endarterectomy (CEA).
Methods:
The Vascular Study Group of New England Cardiac Risk Index (VSG-CRI) criteria for stratifying patients considered for vascular surgery into low, medium, and high cardiac risk groups were used prospectively. For all patients (n = 324), cTnI value assessments were made before surgery and on postoperative days 1, 3, and 7. Postoperative cTnI values ranging from .05 to .5 ng/mL were classified as myocardial ischemia; values more than .5 ng/mL were classified as myocardial infarction. Cardiac damage was defined as either myocardial ischemia or infarction.
Results:
Mortality was .003%, stroke rate was null, and symptomatic myocardial infarction was null as well. Low-risk patients (16 of 140) and medium-risk patients (28 of 160) increased their troponin levels on days 1 and 3 postoperatively. However, none of the high-risk patients (n = 24) showed any postoperative cardiac damage. Low and medium cardiac risk patients showed higher troponin values on each separate day, in comparison with high cardiac risk patients.
Conclusions:
CEA is followed by a high incidence of asymptomatic cTnI increase that is associated with late cardiac events. However, high cardiac risk patients as defined by the VSG-CRI criteria do not seem to suffer higher cardiac damage after CEA compared with low and medium cardiac risk patients.
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