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Vol 19, No 2 (2013)
Case report
Published online: 2013-07-10

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Decreased plasma concentrations of a-ketoglutarate in patients with chronic symptomatic coronary heart disease compared with healthy controls

Magdalena Stachura, Per Gustavsson, Stefan G. Pierzynowski, Jacek Wroński
Acta Angiologica 2013;19(2):82-92.

Abstract

BACKGROUND: Recent studies revealed that mitochondrial function is altered since the earliest stages of atherosclerosis development. Experimental studies results revealed that endothelial dysfunction, elevated levels of inflammatory cytokines, such as excessive reactive oxygen species production, which underlie atherosclerosis, result in significant disruptions in the Krebs cycle flux. However, there is little data about the influence of atherosclerosis on the Krebs cycle intermediates concentrations in people. The aim of the study was to evaluate a possible influence of chronic cardiac ischemia on plasma concentrations of a-ketoglutarate in people with stable symptomatic coronary heart disease.

MATERIAL AND METHODS: Blood samples were collected from 53 patients, with stable, symptomatic coronary heart disease confirmed in coronarography, who were admitted to the hospital due to persistent severe angina despite pharmacological treatment, without the elevation of cardiac enzymes blood level. The control group included 20 healthy people. Plasma concentrations of a-ketoglutarate were determined using an high-performance liquid chromatography (HPLC).

RESULTS: Patients with stable coronary heart disease had significantly lower a-ketoglutarate plasma concentrations compared to healthy controls. There were no statistically significant differences in other analyzed clinical and biochemical parameters between both groups.

CONCLUSIONS: 1. Patients with chronic myocardial ischemia have lower plasma concentrations of a-ketoglutarate comparing to healthy controls. 2. The decrease of plasma a-ketoglutarate concentrations in these patients may be a consequence of the Krebs cycle disruption due to the influence of endothelial dysfunction and inflammatory processes involved in the development of atherosclerosis, however further investigations are required.

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