Metabolic interactions between the hyperhomocysteinemia and angiotensin-1 converting enzyme activity in Tunisian patients with coronary heart disease

Abstract

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.

Low erythrocyte catalase enzyme activity is correlated with high serum total homocysteine levels in tunisian patients with acute myocardial infarction

“…ROS can act on angiotensin converting enzyme to increase its catalytic activity resulting in the increase in angiotensin II production, which, in turn, is a major endogenous inducer of NADPH oxidase. Oxidative stress, endothelial dysfunction and inflammation represent a key triad for the development and progression of Coronary heart disease [19,20]. …”

Pathological interactions between the endothelin-1 and the angiotensin- converting enzyme among Tunisian coronary patients

“…Unlike reversible dyslipidemia (only related to diet and lifestyle), easy to corrected by statins, mixed and genetic dyslipidemia requires a combined medication (statins + fibrates, or nicotinic acid) whereas Apo A1 (statistically higher in healthy croup) has acardio-protective effect supported by various studies. These apolipoproteins are under genetic control which showed the polygenic origin of ACS [4, 14, 16]. …”

“…ACE activity was determined by kinetic method at 340 nm, according the Chalghoum A protocol, 2012 [4], using a synthetic substrate, Furylacryloyl-phenylalanyl– glycyl-glycine (FAPGG) (Trinity Biotech,St Louis USA), with an initial measurement at t = 0 min and a final measurement at t = 5 min.…”

“…The risk factors are varied and diversified, according to the Framingham reference study; these factors are classified into modifiable factors (smoking, arterial hypertension, diabetes, obesity …) and un-modifiable factors (age, gender, heredity…). Atherosclerosis is the main etiology of this syndrome [1–4]. …”

Epilepsy Treatment and Nutritional Intervention

“…epilepsy (Azam et al, 2012), headache (Vurucu et al, 2013) but also in other organ function e.g. heart, vascular disorders, diabetes, nasal polyps (Bozkus et al, 2013;Büyükkaya et al, 2013;Chalghoum et al, 2012;Kim et al, 2013;Madmani et al, 2013). Moreover, for the first time the pathophysiological consequences of L-ferritin deficiency in a human helped to define the concept for new disease entity − halmarked by idiopatic generalized seizures and atypical restless leg syndrome − in 23 yrs old female (Cozzi et al, 2013).…”