OBJECTIVE: To investigate the pathogenesis of coronary slow flow (CSF), C-reactive protein (CRP) levels as indicator of inflammation and procoagulant activity were studied in patients with CSF. METHODS: Fifty-one patients (22 female, mean age; 53+/-10 years) who were admitted to our clinic with chest pain and had the diagnosis of CSF established by TIMI frame count method and coronary angiography, and 44 healthy subjects (18 female, mean age; 546 years) with normal coronary flow (NCF) were included in the study. Subjects with any infectious and systemic immune disease were excluded from the study. The CRP levels were measured from venous blood samples during admission, at 24th hour and after 3 months in all subjects. Additionally; fibrinogen, plasminogen, plasminogen activator inhibitor (PAI-1), tissue plasminogen activator (t-PA) and von Willebrand factor (vWF) levels were measured to determine the procoagulant activity. RESULTS: There was no significant difference between CRP levels of patients with CSF and healthy subjects during admission (7.26+/-4.2 ng/dl vs. 6.43+/-2.8 ng/dl, p>0.05), at 24th hour (7.84+/-1.3 ng/dl vs. 6.32+/-2.5 ng/dl, p>0.05) and after 3 months (6.37+/-2.4 ng/dl vs. 6.18+/-3.3 ng/dl, p>0.05). There were no differences between levels of CRP when compared according to the TIMI frame count, number of vessels with CSF and artery in which CSF was dominant. Additionally; procoagulant activity assessed by fibrinogen, plasminogen, PAI-1, t-PA and vWF levels was similar in both groups. CONCLUSION: Our findings on normal levels of CRP and procoagulant activity, and lack of relation with TIMI frame count made us to think that inflammatory and procoagulant activity did not play a role in the pathogenesis of CSF.
OBJECTIVE: To investigate the pathogenesis of coronary slow flow (CSF), C-reactive protein (CRP) levels as indicator of inflammation and procoagulant activity were studied in patients with CSF. METHODS: Fifty-one patients (22 female, mean age; 53+/-10 years) who were admitted to our clinic with chest pain and had the diagnosis of CSF established by TIMI frame count method and coronary angiography, and 44 healthy subjects (18 female, mean age; 546 years) with normal coronary flow (NCF) were included in the study. Subjects with any infectious and systemic immune disease were excluded from the study. The CRP levels were measured from venous blood samples during admission, at 24th hour and after 3 months in all subjects. Additionally; fibrinogen, plasminogen, plasminogen activator inhibitor (PAI-1), tissue plasminogen activator (t-PA) and von Willebrand factor (vWF) levels were measured to determine the procoagulant activity. RESULTS: There was no significant difference between CRP levels of patients with CSF and healthy subjects during admission (7.26+/-4.2 ng/dl vs. 6.43+/-2.8 ng/dl, p>0.05), at 24th hour (7.84+/-1.3 ng/dl vs. 6.32+/-2.5 ng/dl, p>0.05) and after 3 months (6.37+/-2.4 ng/dl vs. 6.18+/-3.3 ng/dl, p>0.05). There were no differences between levels of CRP when compared according to the TIMI frame count, number of vessels with CSF and artery in which CSF was dominant. Additionally; procoagulant activity assessed by fibrinogen, plasminogen, PAI-1, t-PA and vWF levels was similar in both groups. CONCLUSION: Our findings on normal levels of CRP and procoagulant activity, and lack of relation with TIMI frame count made us to think that inflammatory and procoagulant activity did not play a role in the pathogenesis of CSF.