The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), a multicenter, randomized, double-blind study, tested the efficacy of cholesterol lowering in reducing risk of coronary heart disease (CHD) in 3,806 asymptomatic middle-aged men with primary hypercholesterolemia (type II hyperlipoproteinemia). The treatment group received the bile acid sequestrant cholestyramine resin and the control group received a placebo for an average of 7.4 years. Both groups followed a moderate cholesterol-lowering diet. The cholestyramine group experienced average plasma total and low- density lipoprotein cholesterol (LDL-C) reductions of 13.4% and 20.3%, respectively, which were 8.5% and 12.6% greater reductions than those obtained in the placebo group. The cholestyramine group experienced a 19% reduction in risk (p less than . 05) of the primary end point–definite CHD death and/or definite nonfatal myocardial infarction–reflecting a 24% reduction in definite CHD death and a 19% reduction in nonfatal myocardial infarction. The cumulative seven-year incidence of the primary end point was 7% in the cholestyramine group v 8.6% in the placebo group. In addition, the incidence rates for new positive exercise tests, angina, and coronary bypass surgery were reduced by 25%, 20%, and 21%, respectively, in the cholestyramine group. The risk of death from all causes was only slightly and not significantly reduced in the cholestyramine group. The magnitude of this decrease (7%) was less than for CHD end points because of a greater number of violent and accidental deaths in the cholestyramine group. The LRC-CPPT findings show that reducing total cholesterol by lowering LDL-C levels can diminish the incidence of CHD morbidity and mortality in men at high risk for CHD because of raised LDL-C levels. This clinical trial provides strong evidence for a causal role for these lipids in the pathogenesis of CHD.
△ a family history of congenital heart disease. Brothers and sisters suffering from congenital heart disease at the same time, parents and children suffering from congenital heart disease at the same time the situation was quite rare, and it is very similar to the nature of their disease. If the first child born to mothers who suffer from congenital heart disease, the possibility of a second child ill about 2%; if two consecutive fetal congenital heart disease who Jie Wei, regeneration of infants with congenital heart disease may be increased to 10%. If the mothers suffering from congenital heart disease, the second-generation risk of suffering from the first disease was 10%.
△ contact with pregnant women in early pregnancy teratogenic drugs, such as lithium, phenytoin, or steroids, can lead to fetal congenital heart disease prevalence rate of 2%.
△ early pregnancy were exposed to radioactive substances, such as X-rays, isotopes such as overexposure.
△ virus infection. Women in the first 3 months of pregnancy, especially pregnant 3 weeks -8 weeks, as were virus infection, fetal prone to cardiovascular malformations. Where rubella virus is the major cause fetal congenital heart disease culprit. In addition, influenza, mumps, Coxsackie virus, herpes virus, such as congenital heart disease in children tend to be the “perpetrators.”
△ next of kin marriages. Next of kin marriage is to make the occurrence of fetal teratogenic risk factor for congenital heart disease.
△ bad habits. Pregnant women hobby “puff” or a husband-smoking, wife “passive smoking” can enable fetal malformation or congenital heart disease occur in children. The incidence of infants with congenital heart disease, infants born to smoking mothers are twice as non-smoking mothers. Husband and wife “drunken intercourse pregnancy”, fetal chromosome abnormalities will, gave birth to babies suffering from alcoholism, disease, most associated with cardiovascular abnormalities.
Early detection of children with congenital heart disease is essential for prenatal and postnatal care. 20 weeks -28 weeks of pregnancy, the use of cardiac ultrasound scanner aspect can be clearly identified whether the fetal heart “defect.” In addition, whether the fetus can be found in ascites or edema, etc., thus speculated that the fetus is suffering from heart malformations.
2. Do not contact with pets pets of bacteria and microbes can also cause a child with congenital heart disease
Environmental factors surrounding a fetus within the uterus during early pregnancy to rubella virus infection after infection, often caused by more common patent ductus arteriosus and pulmonary stenosis followed by the Coxsackie virus (Coxsakie) can cause endocardial fibroelastosis In addition, amniotic membrane mechanical pressure around the lesion of fetal maternal nutrition, vitamin deficiency and metabolic diseases barriers to maternal use cytotoxic drugs, or a longer time may be related to radiation exposure are related Benbingfasheng .
2 5% of genetic factors in patients with congenital heart disease occurred in the same family the same or similar kinds of their disease may be due to genetic anomalies or chromosomal aberrations caused by
Three other highland areas of patent ductus arteriosus and atrial septal defect that may have a higher prevalence of congenital heart disease and hypoxia related to some gender-biased
