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Insights
Lower blood beta-endorphin levels in coronary heart disease (CHD) patients with metabolic syndrome (MS) correlate with cardiovascular risks. Dalargin therapy improved these markers, increasing beta-endorphin and HDL cholesterol while reducing inflammation and metabolic dysfunction.
Area of Science:
- Cardiology
- Endocrinology
- Immunology
Background:
- Coronary heart disease (CHD) patients with metabolic syndrome (MS) exhibit altered blood beta-endorphin levels.
- These alterations are potentially linked to cardiovascular risk factors, including inflammation and metabolic dysregulation.
Purpose of the Study:
- To investigate the relationship between blood beta-endorphin levels and cardiovascular risk factors in CHD patients with MS.
- To evaluate the efficacy of dalargin therapy in correcting these imbalances.
Main Methods:
- A randomized study involving 123 CHD patients with MS, comparing standard therapy to standard therapy plus dalargin.
- Biochemical and immunological markers were assessed before and after a 3-month treatment period.
Main Results:
- A significant inverse correlation was observed between beta-endorphin and leptin, insulin, cortisol, TNF-a, IL-6, oxidized LDL, and triglycerides.
- Dalargin therapy significantly increased beta-endorphin and HDL cholesterol levels.
- Dalargin therapy markedly reduced leptin, insulin, cortisol, TNF-a, IL-6, LDL, and triglyceride levels compared to standard therapy.
Conclusions:
- Decreased beta-endorphin in CHD with MS is associated with increased atherogenicity, hyperinsulinemia, hypercortisolemia, and inflammation.
- Dalargin supplementation enhances beta-endorphin levels, exerts anti-atherogenic effects, and reduces inflammatory and metabolic risk factors.
Abstract:
The study is aimed at elucidating the relationship between the blood b-endorphin level in patients with coronary heart disease (CHD) with metabolic syndrome (MS) and cardiovascular risk factors and evaluating the possibility to correct them by dalargin therapy. The study included 123 patients (61 men and 62 women) at the mean age 57.6±5,2 years randomized into 2 groups. The patients of group 1 (n=63) were given the standard treatment, those of group 2 (n=60) additionally received 2 mg/day of dalargin for 10 days (3 courses during 3 months). The group of comparison (n=84) contained 84 CHD patients without MS. Biochemical and immunological characteristics were measured by immuno enzyme and immunochemiluminescent assays before and 3 months after treatment. The study revealed inverse correlation between b-endorphin levels and those of leptin, insulin, cortisol, TNF-a, IL-6, oxidized LDLP, triglycerides (TG), and HDLP cholesterol. Standard therapy resulted in a 6.5% reduction of insulin level, 9,4% , 6,1%, and 17,4% reduction of TNF-a , IL-6, TG levels respectively; it increased the HDLP cholesterol level by 10,3% (p<0,05 for all values) but did not change other parameters of interest. Dalargin therapy caused a 32,6% and 17,4%, rise in the b-endorphin and HDLP cholesterol levels but decreased leptin, insulin, cortisol, TNF-a, IL-6, LDLP, and tG levels by 36,1%, 22,4%, 23,9%, 55%, 56,3%, 14% and 27,2% respectively (p<0,001). It is concluded that the decrease of the blood b-endorphin level in the patients with coronary heart disease and metabolic syndrome is associated with enhanced blood atherogenicity, hyperinsulinemia, hypercortisolemia, activation of pro-inflammatory cytokines and lipid peroxidation. Supplementation of conventional therapy with dalargin results in the increased b-endorphin level, enhanced anti-atherogenic effect, reduced activity of pro-inflammatory cytokines and lipid peroxidation, reduction of leptin, insulin and cortisol levels.
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