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Background: Cystatin C has been proposed as a novel marker of renal function and predictor of cardiovascular risk. The aim of this study was to investigate the role of cystatin C level as a predictor of cardiovascular events in patients with coronary artery disease (CAD). Methods: Three hundred and five coronary artery patients were included in this study. Serum cystatin C levels, highsensitive C-reactive protein (hs-CRP), and oxidative stress were measured. Estimated glomerular filtration rate (eGFR) and the CAD severity score were calculated. Results: Cystatin C was correlated with the CAD severity score (r = 0.631, P < 0.0001) and was significantly elevated in the CAD severity score >50. Every 0.1 mg/l increase in cystatin C, 2 mg/l increase in hs-CRP, 0.2 mmol/l decrease in high-density lipoprotein cholesterol, 13.7 ml/min decrease in eGFR, and 1.51 μmol/l increase in homocysteine caused a 34, 12, 5, and 22% increase in the risk of having CAD, respectively. Conclusion: Cystatin C could be a useful laboratory biochemical marker in predicting the severity of CAD. Cystatin C is associated with biochemical atherosclerosis markers such as CRP and homocysteine.

Article reçu le 8 février 2012, accepté le 16 mai 2012 Résumé. L'hyperhomocystéinémie et l'hyperactivité de l'enzyme de conversion de l'angiotensine 1 (ECA1) constituent deux facteurs de risque coronariens non classiques. L'étude de la variation de ces deux paramètres chez les coronariens ainsi que l'exploration de la relation métabolique entre ces deux biomarqueurs présentent un intérêt fondamental. Dans ce cadre, 110 patients coronariens tunisiens et 80 sujets sains ont été recrutés. L'homocystéinémie était déterminée par la méthode immunologique et l'activité de l'ECA1 était mesurée par une méthode cinétique. L'étude statistique a montré une élévation statistiquement significative de ces deux marqueurs chez les patients comparés aux témoins (homocystéine : 23 ± 18 mol/L vs 9 ± 4 mol/L ; p < 0,0001), (ECA1 : 81 ± 18 UI/L vs 55 ± 18 UI/L, p < 0,0001). D'autre part, l'homocystéine et l'ECA1 varient différemment en fonction des autres facteurs de risque. Une corrélation négative statistiquement significative (r = -0,36 ; p < 0,001) est notée entre les deux paramètres ce qui reflète des interactions métaboliques et physiopathologiques complexes. Mots clés : syndrome coronarien aigu, athérosclérose, facteurs de risque, hyperhomocystéinémie, enzyme de conversion de l'angiotensine 1Abstract. Hyperhomocysteinemia and hyperactivity of the angiotensin-1 converting enzyme (ACE1) are considered two unconventional coronary risk factors. The study of the variation of these two biochemical parameters in coronary patients and metabolic investigation of the relationship between these two markers has a fundamental interest. In this context, 110 patients and 80 control subjects are recruited for our study. Homocystenemia was determined by fluorescence polarization immunoassay (FPIA). ACE1 activity was measured by kinetic method. An increased of homocysteinemia and ACE1 activity was observed in patients compared with control subjects (Hcy: 23±18 mol/L vs 9±4 mol /L; p<0.0001); (ACEI: 81±18 UI/L vs 55±18 UI/L; p<0.0001). These two markers varied differently according to the risk factors. Homocysteinemia, was negatively correlated with ACE1 activity (r = -0.36; p<0.001). The negative correlation between these two markers reflects metabolic and physiopathological interactions.

BackgroundAn imbalance between pro-oxidants and antioxidant systems has been suggested to be implicated in the physiopathology of acute myocardial infarction (AMI). We aimed to evaluate the antioxidant capacity in Tunisian patients and to assess the possible relationship between erythrocyte catalase enzyme activity and hyperhomocysteinaemia.Methods108 patients with AMI and 81 healthy subjects were enrolled in this study. Catalase erythrocyte enzyme activity was determined spectrophotometrically whereas “total antioxidant status” (TAS) concentration was measured by a commercially available method. Serum total homocysteine (tHcy) level was determined by a fluorescence polarization immunoassay (FPIA). Lipid peroxidation was measured with a fluorimetric method as “thiobarbituric acid reactive substances” (TBARS).ResultsCompared with healthy subjects, patients with AMI had significantly lower catalase activity (P<0.001), TAS concentrations (P<0.001), and significantly higher serum tHcy (P<0.001) and TBARS levels (P<0.001). Erythrocyte catalase enzyme activity was negatively correlated with serum tHcy and TBARS while serum tHcy and TBARS were in positive correlation. Furthermore, the unbalance between pro-oxidants and antioxidants seems to be more aggravated in patients with Q wave AMI compared to patients with non-Q wave AMI.ConclusionOur results suggest the involvement of hyperhomocysteinaemia in the drop of erythrocyte catalase activity related to myocardial ischemia reperfusion. Hyperhomocysteinaemia may increase the myocardial wall dysfunction under ischemia reperfusion by excessive production of reactive oxygen species which is made evident by increased lipid peroxidation.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1623509866881834

BackgroundMyocardial infarction (MI) is a major clinical problem because of its large contribution to mortality. The genetic bases of this disease have been widely studied in recent years to find a clear association with some genetic markers that increase the risk of its occurrence. In the present investigation, the correlation between MI and the C3 complement polymorphism was analyzed using a case–control study.MethodsOur study ported on one hundred seventy survived myocardial infarction patients and ninety five healthy controls. The C3 allele identification was investigated using the amplification refractory mutation system PCR to determine the C3*S and the C3*F alleles of the C3 polymorphism.ResultsFrequencies of C3*S and C3*F in patients are 0.59 and 0.41 respectively. Fisher test results showed a significant increase of C3*F allele in the sample of patients (0.41; odds ratio: 2.616; C.I [1.738-3.938]) compared to controls (0.21; odds ratio: 0.382; 95% CI [0.254-0.575]), p = 2.742 × 10-6.ConclusionA strong positive correlation was found between C3 polymorphism and MI estimating that the risk of myocardial infarction is significantly increased among patients with C3*F allele of this polymorphism.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1190484203893646

BackgroundThe correct understanding of the biochemical and metabolic interactions between coronary risk factors contribute to the exploration of cardiovascular pathophysiology and improves therapeutic care.The aim of this study was to explore the endothelin-1 (ET-1) concentration and the angiotensin converting enzyme (ACE) activity among Tunisian patients with coronary heart disease, and to investigate the metabolic relationships between these two markers,… and to assess the possible relationship between them and the different risk factors.In this present study, ET-1 concentration was determined by an analytical method (High Performance Chromatography, coupled by Mass Spectrometry), ACE activity was measured by a kinetic method for patients and healthy controls. These subjects (157 patients and 142 controls) beneficed also by a biochemical exploration (lipid, apolipoproteins and glucose profiles) to quantify cardiovascular risk.ResultsA statistically significant increase of the ET-1 concentration was found among patients compared to healthy controls (15.2 ± 5.3 nM vs 7.1 ± 2.7 nM, p < 0,00001). For the ACE activity, in spite the treatment of the majority of patients (97%) with ACE inhibitors, this activity was statistically elevated in patients compared to healthy subjects (86.7 ± 25.4 IU/L vs 42.8 ± 12.1 IU/L, p < 0.00001).Furthermore, a statistically positive correlation was identified between these two cardiac markers (r = 0.68 p < 0.00001).ConclusionThe study of the metabolic relationship between the ET-1 and ACE among coronary patients reveals other therapeutics targets.

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