Browsing by Author "Narayani, J"

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    Enhanced P-selectin expression on platelet-a marker of platelet activation, in young patients with angiographically proven coronary artery disease
    (MOLECULAR AND CELLULAR BIOCHEMISTRY, 2016) George, R; Bhatt, A; Narayani, J; Thulaseedharan, JV; Sivadasanpillai, H; Tharakan, JA
    P-selectin (CD62p) exposure is an established marker for platelet activation. P-selectin exposure can trigger variety of thrombotic and inflammatory reactions. In patients with coronary artery disease (CAD), platelets are activated, and hence, there is increased P-selectin exposure. The role of P-selectin exposure in patients on treatment with statins and anti-platelets is conflicting. A case-control study was performed to determine P-selectin exposure in consecutively recruited 142 patients (age aecurrency sign 55 years) with angiographically proven CAD on treatment and 92 asymptomatic controls. P-selectin exposure was determined by flow cytometry. Data on conventional risk factors were obtained along with estimation of levels of thrombotic [fibrinogen, lipoprotein (a), tissue plasminogen activator, plasminogen activator inhibitor-1, homocysteine and von Willebrand factor] and anti-thrombotic factors (antithrombin III). The P-selectin exposure was compared among patient groups who had different modes of presentation of CAD and categories of CAD disease severity. The patients were followed up for a period of 26 months. The results indicate that P-selectin exposure was significantly elevated in patients (mean +/- SD 9.24 +/- 11.81) compared to controls (mean +/- SD 1.48 +/- 2.85) with p < 0.0001. Similarly, conventional risk factors were significantly elevated in patients. P-selectin exposure showed significant negative correlation with antithrombin III levels. P-selectin exposure was higher in patients who presented with acute coronary syndromes than those who presented with effort angina. Cardiovascular event rate was 6 % on follow-up. The study establishes that thrombotic-inflammatory pathways enhancing P-selectin exposure unrelated to treatment might be activated in patients, while the event rate remained lowered, and hence, treatment strategies should be inclusive to control these factors.
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    Formation of protein carbonyls during myocardial reperfusion by coronary angioplasty
    (JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION, 2003) Narayani, J; Krishna, S; Gopalakrishnan, BK
    The quantitation of myocardial reperfusion injury in patients often creates problems due to lack of specific markers. Although malondialdehyde provides an index of oxidative damage, we have little information regarding effects on membrane structure and function. Therefore we investigated the effect of ischemia/reperfusion on the kinetics of protein modification along with lipid peroxidation during coronary angioplasty. Venous blood,samples were collected before angioplasty and at various intervals after primary stage of balloon deflation from humans to quantitate the above parameters. A significant transient rise in the concentration of protein carbonyls in serum (p < 0.001) was observed soon after successful reperfusion which parallels with that of lipid peroxides. This increase of protein carbonyls is an actual reflection of the increased rate of amino acid modification in membrane proteins. These structural modifications can alter lipid-protein interactions resulting in disturbed membrane functions. This study suggests that protein modification and lipid peroxidation play significant role in the pathogenesis of myocardial reperfusion injury. Further this assessment of structural modification in proteins provides an important reliable technique to detect and quantitate the exact nature and extent of myocardial injury.