ABSTRACT
Coronary heart disease is a major health problem and one of the most important leading causes of adult deaths although it starts since childhood. Genetic predisposition of coronary heart diseases have been well established, so children of parents or grandparents with premature coronary heart diseases are more susceptible to develop the disease than others. Those with positive family history of premature coronary heart disease are more susceptible to lipid and lipoprotein abnormalities. Lipoprotein [a] is a strong predictor for premature coronary heart disease, together with total cholesterol, high density lipoprotein cholesterol and low density lipoprotein cholesterol. Lipoprotein [a] is genetically determined and if it is elevated in a child, it predicts premature coronary heart disease. The effect of a high lipoprotein [a] increases if associated with high serum low density lipoprotein cholesterol or low serum high density lipoprotein cholesterol. This study was done on two groups of children: The First Group: Included 50 children [age ranging from 5-15 years] of parents with a history of premature coronary heart disease or cerberovascular disease diagnosed clinically and through investigations. The Second Group: Included 25 children [age ranging from 5-15 years] of parents without coronary heart disease or cerberovascular disease. All these children were examined clinically and the following parameters were done and recorded: Anthropometric measurements [Height [Ht], Weight [Wt], Skin fold]. Body mass index [BMI]. Blood pressure [SBP, DBP]. Fasting blood glucose [FBG]. Uric acid level [UA]. C-reactive protein [CRP]. Lipid profile: Cholesterol [TC], Triglyerides [TG], High density lipoprotein [HDL], Low density lipoprotein [LDL], Lipoprotein [a] [LP[a]]. Anti hepatitis A virus [HAV] and anti Helicobacter pylori [H.P] antibodies. The Study Showed that: There was no significant difference between cases and controls in age, HT, WT, BMI, skin fold, SBP and DBP. There was no significant difference between cases and controls in TG. FBG and UA. There was a significant increase in cases than controls in TC and LDL. Also there was a high significant increases in cases than controls in LP[a], while there was a high significant increase in controls than cases in HDL. There was no significant difference between cases and controls in sex, HAV, HP or CRP. There was insignificant correlation between LP[a] and age, BMI, skin fold, SBP, BDP, LDL, FBG and UA. There was a significant correlation between LP[a] and TC. Also there was a high significant correlation between LP[a] and TG, HDL. We concluded that high serum TC is not enough for determination of the risk of atherosclerosis and CHD and that high TG alone is not a risk factor except if associated with low serum HDL and high serum LDL. We recommend screening of all children with a positive family history of premature CHD and/or hypercholesterolemia for lipids and lipoprotein abnormalities especially LP[a] which is a strong predictor for premature CHD and this enables early diagnosis and early successful management by following special dietetic measures with avoidance of excess saturated fatty acids, avoidance of obesity and smoking and practicing physical activities. Prevention and treatment of infections especially HAV and HP is encouraged. Genetic counseling and discouraging against marriage for heterozygotes for CHD and/or hypercholestrolemia as their children may be homozygotes for the disease