Abstract
The aim of this study was to assess the relations between inflammation, immune response, and coronary angiographic findings in patients with unstable angina pectoris (UAP).
Recent studies suggest a role for inflammation in the pathophysiology of UAP. Although activation of neutrophils, monocytes and lymphocytes has been shown in UAP, no studies have correlated the activation findings with clinical and angiographic features of patients with UAP.
Seventy-three patients undergoing coronary angiography were classified according to their ischaemic syndrome; stable angina pectoris (SAP) (n=25) and UAP (n=48). Patients with UAP were classified using the Braunwald classification; UAP class I (n=15), UAP class II (n=15), and UAP class III (n=18). Patients with UAP were also classified into a progression to myocardial infarction (MI(+)) group (n=15) and a non-progression to myocardial infarction (MI(-)) group (n=33). Venous blood samples were taken from all patients. Cell surface receptors (CD4, CD8, CD3, CD14, CD45, CD56+16, and HLA-DR) were detected by flow cytometry using monoclonal antibodies tagged with fluorescent markers and serum levels of C-reactive protein (CRP) were measured.
The serum levels of CRP and the percentages of HLA-DR, CD14, and CD16+56 were higher in UAP than SAP. The serum levels of CRP and percentages of HLA-DR, CD14, and CD16+56 were higher in UAP class II than UAP class I. The serum levels of CRP and percentages of HLA-DR, CD14, and CD16+56 were higher in UAP class III than UAP class II and UAP class I. The serum levels of CRP and percentages of CD16+56 were higher in the MI(+) group than the MI(-) group. The CRP levels in serum and the percentages of cell surface antigens had no correlation with extent of coronary artery disease (no differences among one, two or three vessels) but Type C lesion had significantly higher percentages of HLA-DR, CD14, CD16+56 and the serum levels of CRP than Type A and Type B lesions.
This investigation shows that inflammatory and immunologial components may be detectable in UAP and were correlated with the clinical severity, progression to myocardial infarction, and lesion morphology, but were not correlated with the extent of coronary artery disease.
