Plasma tetranectin levels in patients with unstable and stable angina

It has been recently suggested that the acute exacerbation of chronic infla mmatory process accompanied by excessive atheromatous plaque-matrix breakdo wn may be the crucial link between chronic and acute coronary artery diseas e (CAD). In the light of this probability, the fibrinolytic regulator, tetr anectin (TN) was assessed in the plasma of 43 unstable angina (UA) patients , 35 stable angina (SA) patients, and 34 healthy subjects (HS) in associati on with selected inflammatory and fibrinolytic markers. Plasma TN levels in patients with UA and SA were significantly lower than t hose 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, Er < 10(-4)). The sensitivity, specificity and predictive v alue were 72.1, 97.1 and 97% respectively for UA patients, and 46, 97 and 9 4% respectively for SA patients. In the 26 (60.5%) of UA patients, which ha d 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 v s 9.67 (8.47-10.84) mg/L, p < 10(-4)). In SA patients the increased levels of C-reactive protein (CRP), fibrinogen (FG), tissue-type plasminogen activ ator (t-PA), plasminogen activator inhibitor-1 (PAI-I) 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 pro cess accompanied by the subclinical activation of reactive fibrinolysis. Th e substantial increase in the above-mentioned inflammatory and haemostatic markers, along with the significant correlation between the inflammatory ma rkers and DD, as well as between t-PA and DD or FG in UA patients, was cons istent with the acceleration of inflammatory and coagulative/fibrinolytic p rocesses. The negative correlation of TN with CRP (r(s) = -0.707, p < 10(-3 )) and FG (r(s) = -0.664, p < 10(-4)) in UA patients and, to a lesser degre e, in SA patients (r(s) = -0.563, p < 10(-3) and r(s) = -0.457; p = 0.006 r espectively) makes possible the involvement of inflammatory components in t he 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 w ith its superior performance characteristics and predictive correlation wit h UA clinical outcome in comparison with other inflammatory and fibrinolyti c variables studied, suggested its possible implication in the pathophysiol ogically-important processes associated with atheromatous plaque-matrix bre akdown and thrombus dissolution. The significant inverse relation between T N and lipoprotein (a) [Lp(a)] observed in SA (r(s) = -0.552, p = 0.001) hin ted at the common implication of these fibrinolytic regulators in the patho physiology 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 athero matous lesions and thrombosis.