ABSTRACT
AIM: to elucidate own and parental predictors of low levels of high density lipoprotein cholesterol (HDL-C) in blood of children of persons with early coronary heart disease (ECHD) (onset less or equal 55 years, men, or less or equal 60 years, women). METHODS: We examined 305 families: probands with ECAD (n=289, 69.2% men), their spouses (n=213, 17.8% men) and native children of probands (n=399, 56.1% men) aged 5-38 years. Low level of HDL-C in children aged 5-17 years we defined as less or equal 25 percentile (the Lipid Research Clinics, 1981), in children aged 18-38 years - <1.03 (men) and <1.29 (women) mmol/l. Predictors of low HDL-C were selected by logistical regression with adjustment for sex and age. RESULTS: Low HDL-C was revealed in 48/152 (31.6%) children aged 5-17 years. Its independent predictors were own higher triglycerides (TG) and low HDL-C of spouse. Odds ratio (OR) of top (>0.94 mmol/l) vs two bottom ( less or equal 0.94 mmol/l) tertiles of TG 2.68 (95% confidence interval [CI] 1.03-6.94; =0.043); low HDL-C of spouse 2.33 (95% CI 1.03-5.26; =0.041). Low HDL-C was revealed in 91/247 (36.8%) offsprings aged 18-38 years. Its independent predictors were higher waist circumferences (WC, OR top [>85 cm] vs bottom [ less or equal 73 cm] tertile 5.43, 95% CI 2.39-12.3; =0.000) and TG (OR 1.45, 95% CI 1.01-2.09; =0.047) of these children, atherogenic dyslipidemia of proband (OR 2.44, 95% CI 1.34-4.44; =0.0036); metabolic syndrome (OR 4.14, 95% CI 1.96-8.75; =0.0002) and lower heart rate (OR top [>72 bpm] vs two bottom [ less or equal 72 bpm] tertiles 0.41, 95% CI 0.17-0.97; =0.043) of consort-parent. CONCLUSIONS: In this group of different age children with parental ECHD independent predictors of low HDL-C were mostly own (TG) and parental metabolic factors.
Subject(s)
Cholesterol, HDL , Coronary Disease , Child , Coronary Disease/genetics , Dyslipidemias , Female , Humans , Male , Metabolic Syndrome , Middle Aged , Risk Factors , Waist CircumferenceABSTRACT
We have analyzed by different immunological methods the proteolytic degradation of cardiac troponin I (cTnI) in human necrotic tissue and in serum. cTnI is susceptible to proteolysis, and its degradation leads to the appearance of a wide diversity of proteolytic peptides with different stabilities. N- and C-terminal regions were rapidly cleaved by proteases, whereas the fragment located between residues 30 and 110 demonstrated substantially higher stability, possibly because of its protection by TnC. We conclude that antibodies selected for cTnI sandwich immunoassays should preferentially recognize epitopes located in the region resistant to proteolysis. Such an approach can be helpful for a much needed standardization of cTnI immunoassays and can improve the sensitivity and reproducibility of cTnI assays.
