Svetlana G. Dorofeeva, Eugenia N. Konoplya, Oksana V. Mansimova

Correction of protein and lipid spectra of erythrocyte membranes as a pathogenetic supplement to the therapy of coronary heart disease

Introduction

Correction of protein and lipid spectra of erythrocyte membranes as a pathogenetic supplement to the therapy of coronary heart disease. Study reveals Mexicor, added to traditional therapy for coronary heart disease, corrects erythrocyte membrane protein and lipid spectra, enhancing clinical course & functional indicators.

Abstract

Introduction: Coronary heart disease is currently a pressing problem in the medical and scientific community. The hemic component, which is a disruption of the ability of red blood cells to effectively exchange gases, is of great importance in ischemic myocardial damage. Oxidative stress, through functional and structural changes in red blood cells, can significantly impair the efficiency of oxygen delivery to tissues. Materials and Methods: In this clinical study, 80 patients suffering from coronary heart disease (stable angina pectoris functional class II-III) were selected. They were divided into two groups, one of which received traditional treatment, and the other – traditional treatment in combination with Mexicor. Before the start of taking the drugs and 11 days after the start of therapy, the clinical condition of the patients, bicycle ergometry indicators and the values of protein and lipid spectra of erythrocyte membranes were assessed. Results: Addition of Mexicor, a drug with antioxidant and endothelioprotective properties, to the classical approach to therapy resulted in correction of various clinical parameters by values from 11% to 58.82%; bicycle ergometry – from 20.29% to 70.31%; protein spectrum of erythrocyte membranes – from 3.08% to 75.41%; and lipid spectrum – from 8.67% to 35.83%. Moreover, most of the studied parameters statistically significantly differed from those both in the control group and the traditional treatment group. Conclusion: The combination of traditional treatment with single daily intravenous injections of 5 mL of Mexicor(ethylmethylhydroxypyridine succinate 50 mg/mL), made it possible not only to improve the clinical course and functional indicators, but also to positively influence the pathogenetic causes of ischemia development through significant, statistically reliable correction of the indicators of the protein and lipid spectrum of red blood cell membranes.

Review

This study presents an intriguing exploration into the adjunctive therapeutic benefits of Mexicor in managing coronary heart disease (CHD), with a specific focus on its impact on the integrity of erythrocyte membranes. The authors meticulously connect the established role of the hemic component and oxidative stress in ischemic damage to the potential for therapeutic intervention. By conducting a clinical study involving 80 CHD patients, they compared traditional treatment with a regimen supplemented by Mexicor. The results compellingly demonstrate that the addition of Mexicor led to statistically significant improvements across various parameters, including clinical status, functional capacity as assessed by bicycle ergometry, and, most notably, the protein and lipid spectra of erythrocyte membranes, thus supporting its proposed pathogenetic role. While the study offers promising insights, a more detailed methodological exposition would enhance its critical appraisal. The abstract mentions "traditional treatment" without specifying its components, which is crucial for reproducibility and understanding the context of Mexicor's additive effect. Similarly, information regarding blinding, specific patient demographics beyond functional class, and the precise statistical methods used would strengthen the argument. The 11-day observation period, while revealing rapid changes, is quite short for evaluating a chronic condition like CHD, prompting questions about the long-term durability and clinical significance of these improvements. Further, while percentage corrections are impressive, presenting baseline and endpoint absolute values for the membrane parameters would provide a clearer picture of the extent of correction. Despite these areas for potential elaboration, the study provides valuable preliminary evidence for Mexicor's potential beyond symptomatic relief, directly addressing cellular-level pathogenetic factors in CHD. The focus on erythrocyte membrane integrity as a therapeutic target is particularly noteworthy, offering a novel avenue for improving oxygen delivery and mitigating ischemic damage. This research clearly warrants further investigation through larger, potentially placebo-controlled trials with extended follow-up periods to confirm the sustained clinical benefits, safety profile, and to fully delineate the molecular mechanisms underpinning the observed corrections in erythrocyte membrane spectra. The findings lay a strong foundation for considering Mexicor as a beneficial supplement in the comprehensive management of CHD.

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