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Circulating Endothelial Cell Count as a Diagnostic Marker for Non–ST-Elevation Acute Coronary Syndromes
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Background—
Shedding of endothelial cells from damaged endothelium into the blood occurs in a variety of vascular disorders. The purpose of this study was to evaluate the utility of circulating endothelial cell (CEC) count as a diagnostic marker of non–ST-elevation acute coronary syndromes (ACSs).
Methods and Results—
CEC counts were determined immediately (H0), 4 hours (H4), and 8 hours (H8) after admission in 60 patients with documented non–ST-elevation ACS and 40 control patients with no evidence of coronary artery disease. A total of 32 patients in the ACS group had elevated CEC counts (>3 cells/mL) in relation to early admission and single-episode chest pain. Patients from the control group had normal CEC counts. The interval between the chest pain episode and elevation was significantly shorter for CEC than troponin I. No correlation was found between the 2 markers. Interestingly, a subgroup of ACS patients with initially normal troponin I levels had high CEC counts, thus allowing early diagnosis in 30% more cases. At H0, the mean area under the receiver operating characteristic curve was significantly higher with the CEC count than with the troponin I level. At H4 and H8, the combined use of CEC and troponin was significantly better as a marker of ACS than CEC alone or troponin I alone.
Conclusions—
This study demonstrates that CEC count can be used as an early, specific, independent diagnostic marker for non–ST-elevation ACS. A combined strategy using CEC count and troponin I level could provide an effective diagnostic tool.
Ovid Technologies (Wolters Kluwer Health)
Title: Circulating Endothelial Cell Count as a Diagnostic Marker for Non–ST-Elevation Acute Coronary Syndromes
Description:
Background—
Shedding of endothelial cells from damaged endothelium into the blood occurs in a variety of vascular disorders.
The purpose of this study was to evaluate the utility of circulating endothelial cell (CEC) count as a diagnostic marker of non–ST-elevation acute coronary syndromes (ACSs).
Methods and Results—
CEC counts were determined immediately (H0), 4 hours (H4), and 8 hours (H8) after admission in 60 patients with documented non–ST-elevation ACS and 40 control patients with no evidence of coronary artery disease.
A total of 32 patients in the ACS group had elevated CEC counts (>3 cells/mL) in relation to early admission and single-episode chest pain.
Patients from the control group had normal CEC counts.
The interval between the chest pain episode and elevation was significantly shorter for CEC than troponin I.
No correlation was found between the 2 markers.
Interestingly, a subgroup of ACS patients with initially normal troponin I levels had high CEC counts, thus allowing early diagnosis in 30% more cases.
At H0, the mean area under the receiver operating characteristic curve was significantly higher with the CEC count than with the troponin I level.
At H4 and H8, the combined use of CEC and troponin was significantly better as a marker of ACS than CEC alone or troponin I alone.
Conclusions—
This study demonstrates that CEC count can be used as an early, specific, independent diagnostic marker for non–ST-elevation ACS.
A combined strategy using CEC count and troponin I level could provide an effective diagnostic tool.
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