Plasma tetranectin levels in patients with unstable and stable angina

Abstract

Summary It has been recently suggested that the acute exacerbation of chronic inflammatory process accompanied by excessive atheromatous plaque-matrix breakdown may be the crucial link between chronic and acute coronary artery disease (CAD). In the light of this probability, the fibrinolytic regulator, tetranectin (TN) was assessed in the plasma of 43 unstable angina (UA) patients, 35 stable angina (SA) patients, and 34 healthy subjects (HS) in association with selected inflammatory and fibrinolytic markers. Plasma TN levels in patients with UA and SA were significantly lower than those in HS (8.18 (7.08–9.58) mg/L and 10.00 (7.22–10.96) mg/L vs 12.09 (11.78–12.37) mg/L, p −4 ). The sensitivity, specificity and predictive value were 72.1, 97.1 and 97% respectively for UA patients, and 46, 97 and 94% respectively for SA patients. In the 26 (60.5%) of UA patients, which had a complicated in-hospital course, TN levels were significantly lower than those in the 17 (39.5%) uncomplicated UA patients (7.38 (6.77–8.15) mg/L vs 9.67 (8.47–10.84) mg/L, p −4 ). In SA patients the increased levels of C-reactive protein (CRP), fibrinogen (FG), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and D-dimer (DD), in conjunction with the significant positive correlation between CRP and FG, and of both with DD, revealed the existence of a low-grade inflammatory process accompanied by the subclinical activation of reactive fibrinolysis. The substantial increase in the above-mentioned inflammatory and haemostatic markers, along with the significant correlation between the inflammatory markers and DD, as well as between t-PA and DD or FG in UA patients, was consistent with the acceleration of inflammatory and coagulative/fibrinolytic processes. The negative correlation of TN with CRP (r s = −0.707, p −3 ) and FG (r s = −0.664, p −4 ) in UA patients and, to a lesser degree, in SA patients (r s = −0.563, p −3 and r s = −0.457, p = 0.006 respectively) makes possible the involvement of inflammatory components in the regulation of TN in CAD. The negative correlation of TN with DD in SA (r s = −0.356, p = 0.036) and UA (r s = −0.319, p = 0.037) patients along with its superior performance characteristics and predictive correlation with UA clinical outcome in comparison with other inflammatory and fibrinolytic variables studied, suggested its possible implication in the pathophysiologically-important processes associated with atheromatous plaque-matrix breakdown and thrombus dissolution. The significant inverse relation between TN and lipoprotein (a) [Lp(a)] observed in SA (r s = −0.552, p = 0.001) hinted at the common implication of these fibrinolytic regulators in the pathophysiology of chronic CAD. A further investigation of the role played by TN in CAD could perhaps shed light on its significance as a marker of the development of coronary atheromatous lesions and thrombosis.