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Original ArticleOpen Access
D-Dimer Plasma Levels in NSTE-ACS Patient
Charoensri N 
,
Pornratanarangsi S
,
Pornratanarangsi S Background: Acute Coronary Syndrome (ACS) occurs when a vulnerable plaque ruptures and induces platelet aggregation
and coagulation process at the rupture. Thrombogenesis is the final process that forms a clot in the coronary lumen causing
myocardial injury. Plasma D-dimer, a primary degradation product and circulating marker of fibrin turnover, serves as a
direct marker of ongoing fibrinolysis in site of coronary artery occlusion.
Objective: To determine the correlation between plasma D-dimer levels and severity of coronary artery obstruction based on
angiographic data that is composed of the number of coronary arteries affected and the percentage of maximum stenosis of
coronary artery lumen in non-ST elevation ACS (NSTE-ACS) patients.
Material and Method: NSTE-ACS patients who admitted in Siriraj hospital during June 2009 and March 2010 were enrolled.
Conditions that increased plasma D-dimer other than NSTE-ACS were excluded. Demographic characteristics were assessed
by a standardized questionnaire. Plasma D-dimer was measured and coronary angiography was performed to evaluate
severity of coronary artery stenosis.
Results: Total of 74 NSTE-ACS patients were enrolled (29 in unstable angina and 45 in non-ST elevation myocardial
infarction). Mean age of these patients (54.1% in female and 45.9% in male) were 66 years. D-Dimer was significantly
increased with the number of coronary arteries affected (p = 0.03). In non-significant and single coronary artery disease
(CAD) patients, median D-dimer was 406 (178-2,788) mcg/L. In multivessel CAD, median D-dimer was 941 (131-7,110)
mcg/L. D-dimer levels had a trend to be increased with percentage of maximum stenosis of coronary artery lumen;
atheromatosis, (p = 0.30). In mild and moderate atheromatosis (coronary artery stenosis < 70%), median D-dimer was 479
(182-5,902) mcg/L while median D-dimer was 789 (131-7,110) mcg/L in severe atheromatosis (coronary artery stenosis
> 70%). Moreover, plasma D-dimer levels correlated with complication of NSTE-ACS (Congestive heart failure; p < 0.001,
arrhythmia; p = 0.007 and death; p = 0.009) and was increased in patients who underwent treatment with CABG more often
than those who received PCI and medication treatment alone. D-dimer also correlated with serum creatinine (r = 0.517, p <
0.001), creatinine clearance (r = -0.463, p < 0.001), troponin-T level (r = 0.381, p < 0.001) and left ventricular ejection
fraction (r = -0.368, p = 0.002).
Conclusion: D-dimer is useful coagulation marker use to evaluate extent of coronary affected and may predict in-hospital CV
complication. However, other conditions that increased plasma D-dimer also excluded.
Keywords: D-dimer, Acute coronary syndrome
and coagulation process at the rupture. Thrombogenesis is the final process that forms a clot in the coronary lumen causing
myocardial injury. Plasma D-dimer, a primary degradation product and circulating marker of fibrin turnover, serves as a
direct marker of ongoing fibrinolysis in site of coronary artery occlusion.
Objective: To determine the correlation between plasma D-dimer levels and severity of coronary artery obstruction based on
angiographic data that is composed of the number of coronary arteries affected and the percentage of maximum stenosis of
coronary artery lumen in non-ST elevation ACS (NSTE-ACS) patients.
Material and Method: NSTE-ACS patients who admitted in Siriraj hospital during June 2009 and March 2010 were enrolled.
Conditions that increased plasma D-dimer other than NSTE-ACS were excluded. Demographic characteristics were assessed
by a standardized questionnaire. Plasma D-dimer was measured and coronary angiography was performed to evaluate
severity of coronary artery stenosis.
Results: Total of 74 NSTE-ACS patients were enrolled (29 in unstable angina and 45 in non-ST elevation myocardial
infarction). Mean age of these patients (54.1% in female and 45.9% in male) were 66 years. D-Dimer was significantly
increased with the number of coronary arteries affected (p = 0.03). In non-significant and single coronary artery disease
(CAD) patients, median D-dimer was 406 (178-2,788) mcg/L. In multivessel CAD, median D-dimer was 941 (131-7,110)
mcg/L. D-dimer levels had a trend to be increased with percentage of maximum stenosis of coronary artery lumen;
atheromatosis, (p = 0.30). In mild and moderate atheromatosis (coronary artery stenosis < 70%), median D-dimer was 479
(182-5,902) mcg/L while median D-dimer was 789 (131-7,110) mcg/L in severe atheromatosis (coronary artery stenosis
> 70%). Moreover, plasma D-dimer levels correlated with complication of NSTE-ACS (Congestive heart failure; p < 0.001,
arrhythmia; p = 0.007 and death; p = 0.009) and was increased in patients who underwent treatment with CABG more often
than those who received PCI and medication treatment alone. D-dimer also correlated with serum creatinine (r = 0.517, p <
0.001), creatinine clearance (r = -0.463, p < 0.001), troponin-T level (r = 0.381, p < 0.001) and left ventricular ejection
fraction (r = -0.368, p = 0.002).
Conclusion: D-dimer is useful coagulation marker use to evaluate extent of coronary affected and may predict in-hospital CV
complication. However, other conditions that increased plasma D-dimer also excluded.
Keywords: D-dimer, Acute coronary syndrome
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