Cardiovascular Disease In Adult Life Research Articles

Low birthweight and renal disease in Australian aborigines

Barker has proposed that low birthweight predisposes to type 2 diabetes, hypertension, dyslipidaemia, and cardiovascular disease in adult life. 1 Barker DJP Martyn CN The maternal and infant origins of cardiovascular disease. J Epidemiol Community Health. 1992; 46: 8-11 Crossref PubMed Scopus (259) Google Scholar An epidemic of these diseases, as well as renal failure, has developed among Aborigines in Australia's Northern Territory, against a background of persistent low birthweights and progressive weight gain in adult life. We investigated whether low birthweight predisposes to renal disease in one community in which renal failure incidence has reached 2700 per million and is doubling every 4 years. 2 Hoy WE Renal disease in Australian Aborigines. Med J Aust. 1996; 165: 309-312 PubMed Google Scholar

Preventive Effect of Long-Term GH Therapy on Cardiovascular Risk Factors in Patients with GH Deficiency

GH has some influence on cardiovascular risk factors. The effects of long-term GH replacement therapy on hemostatic and lipid parameters were examined in pediatric patients with GH deficiency. Hemostatic markers (fibrinogen, D-dimer, TAT, tPA-PAI, and PIC) and lipid parameters (total cholesterol, HDL-cholesterol, LDL-cholesterol, and Lp (a)) were evaluated in 30 pediatric patients before and during GH therapy. They were treated with recombinant GH (0.5 I.U. /kg/week) for 2.4±0.5 years. Eight patients had complete GH deficiency (aged 10.6±3.3 years; 5 males and 3 females), including 4 with craniopharyngioma (13.7±5.4 years; 2 males and 2 females), and 22 had partial GH deficiency (10.6±3.3 years; 11 males and 11 females). Statistical analysis was done with the Mann-Whitney nonparametric rank sum test. Plasma D-dimer (p<0.01) and fibrinogen (p<0.01) decreased after 2.4±0.5 years of GH treatment. There were no significant changes in total cholesterol, triglycerides, or HDL-and LDL-cholesterol, but there was an increase in lipoprotein (a) (p<0.02) and insulin (p<0.02). The free T3 (p<0.0003) and TSH (p<0.003) levels decreased, but there was no effect on free T4or the body mass index. Decreased hemostatic activity is a beneficial effect of GH on cardiovascular risk factors. Ceasing GH therapy by 20 years of age on completion of growth might lead to the onset of cardiovascular disease in adult life, so continuing GH therapy beyond this age may be necessary.

Ambulatory blood pressure in pregnancy and fetal growth

Retarded growth in utero has been linked with high blood pressure and other risk factors for cardiovascular disease in adult life. However, the influence on fetal growth of the maternal blood pressure during pregnancy is not well defined. In a prospective study, we examined the relation between maternal ambulatory blood pressure during pregnancy and indices of fetal growth. We studied 209 healthy nulliparous pregnant women referred to an inner-city district general hospital (86% of 244 consecutively referred women who met the study criteria). 24 h ambulatory blood-pressure recordings were obtained in early (median 18 weeks [IQR 17-18]) mid (28 weeks [28]), and late (36 weeks [36]) gestation. Eight infants delivered before 32 weeks' gestation were excluded from the analysis. A 5 mm Hg (1 SD) increase in mean 24 h diastolic blood pressure at 28 weeks' gestation was associated with a 68 g (95% Cl 3-132) decrease in birthweight; a similar change in diastolic pressure at 36 weeks' gestation was associated with a 76 g (24-129) decrease in birthweight. These associations were independent of potential confounders (maternal age, height, weight, cigarette smoking, alcohol intake, ethnic origin, pregnancy hypertension syndromes, and preterm birth). Maternal mean 24 h diastolic blood pressure at 28 weeks' gestation was also inversely associated with the infant's ponderal index at birth in multivariate analysis (p = 0.06). Higher maternal ambulatory blood pressure at 28 weeks' and 36 weeks' gestation also predicted lower head circumference, although these associations were dependent on birthweight. Associations between ambulatory systolic blood pressure and indices of fetal growth were weak and inconsistent and ambulatory blood pressure at 18 weeks' gestation did not predict fetal growth. There is a continuous inverse association between fetal growth and maternal blood pressure, throughout the range seen in normal pregnancy. Maternal blood pressure may be an important confounding factor in the reported associations between fetal growth retardation and adult hypertension and cardiovascular disease.

Early Diagnosis of Coarctation of the Aorta in Children: A Continuing Dilemma

Because late repair of coarctation of the aorta (COA) is associated with premature cardiovascular disease in adult life, early detection and treatment is important. To determine the timing of referral to see whether early detection of COA has improved in the past decade, to evaluate the pattern of and reasons for medical center referral, and to assess the clinical signs relating to the diagnosis of COA. The records of 50 consecutive patients older than 1 year who had surgical repair of COA from 1980 to 1990 were reviewed. The age of referral, pattern of referral, and presence of standard clinical signs of COA were analyzed, and data were compared with those from the previous decade. The mean and median ages at referral were 8.4 and 5.8 years, respectively. Pediatricians accounted for 64% of the referrals. A specific diagnosis of COA was made in 2 (4%) of 50 patients before referral to a pediatric cardiologist. The most consistent clinical findings were a cardiac murmur and a systolic blood pressure gradient between the arms and legs of greater than 10 mm Hg, which were both present in all patients. Lower-extremity pulses were decreased in 37 (74%) and absent in 9 (18%). Forty-seven children (94%) had upper-extremity hypertension (> 95th percentile for age); 25 (50%) had systolic blood pressure higher than 140 mm Hg. COA would have been missed in 82% of children if absent lower-extremity pulses were required as a diagnostic feature. These findings were similar to those reported by our institution in the previous decade, suggesting that early detection has not improved. The timing of, reasons for, and sources of referral for COA in this study, compared with data from the previous decade, indicate no improvement in early detection of COA by pediatricians. Screening all children for COA by routinely measuring upper- and lower-extremity blood pressures during at least one physical examination after the newborn period is mandatory.

Coronary heart disease in diabetes mellitus: three new risk factors and a unifying hypothesis

The standard risk factors--dyslipidaemia, hypertension and smoking--provide little help in explaining the raised cardiovascular risk in diabetes. It can be calculated that intervening for disturbances of these risk factors could do little to rectify the loss of life expectancy of around 10 years for a middle-aged diabetic man. Three new risk factors are discussed, which together may contribute to some of the excess cardiovascular risk in diabetes. Plasminogen activator inhibitor is an inhibitor of fibrinolysis which is elevated in concentration in diabetic subjects, and may increase both the incidence of thrombotic events and the risk of reinfarction after the initial infarct. Recent work also suggests that high activity of this substance may impair pharmacological fibrinolysis. Proinsulin-like molecules are elevated in concentration in diabetic patients and correlate with levels of a number of other risk factors. Whilst these correlations may represent cause and effect for plasminogen activator inhibitor, there is no evidence that changes in levels of proinsulin-like molecules influence levels of other risk factors. Microalbuminuria provides a powerful indicator of cardiovascular risk in both diabetic and non-diabetic subjects, but whilst the mechanisms for this association are unclear, they are again unlikely to be mediated through changes in levels of standard risk factors. Recent observations of an association between short stature and microalbuminuria suggest that intrauterine or early infant nutrition may represent a common antecedent, these having also been shown to predict both components of the insulin resistance syndrome and cardiovascular disease in adult life.

Fetal and pediatric origins of adult cardiovascular disease.

Adult-onset cardiovascular disease has its origin in childhood. During the past year there have been a number of articles that have dealt with the effects of fetal nutrition on the development of cardiovascular disease in adult life, identification of the child at high risk for the development of essential hypertension, the effects of passive smoking as a risk factor for coronary artery disease, and strategies for diagnosis and treatment for familial hypercholesterolemia. Two of the most important observations over the past year are that there appears to be a significant relationship between fetal and early childhood nutrition and the risk of developing many of the cardiovascular diseases seen in adult individuals and that environmental tobacco smoking, including smoke at work, results in an increased risk of developing coronary heart disease.

Fibrinogen and factor VII in male neonates

Recent studies have suggested that retarded fetal and early growth predisposes to cardiovascular disease of males in adult life. This is partly explicable by an association between the haemostatic variables fibrinogen and factor VII and the placenta/birth weight ratio. Since many characteristics influence clotting factors during life, levels of fibrinogen and clotting factor VII were measured in cord blood of male neonates. The placenta/birth weight ratio did not correlate with the birth weight for gestational age and appeared to be only a minor indicator of fetal growth. These findings make it unlikely that the level of fetal outcome ‘programmes’ male neonates via fibrinogen or factor VII to develop cardiovascular disease in adult life.

Fetal nutrition and cardiovascular disease in adult life

Babies who are small at birth or during infancy have increased rates of cardiovascular disease and non-insulin-dependent diabetes as adults. Some of these babies have low birthweights, some are small in relation to the size of their placentas, some are thin at birth, and some are short at birth and fail to gain weight in infancy. This paper shows how fetal undernutrition at different stages of gestation can be linked to these patterns of early growth. The fetuses' adaptations to undernutrition are associated with changes in the concentrations of fetal and placental hormones. Persisting changes in the levels of hormone secretion, and in the sensitivity of tissues to them, may link fetal undernutrition with abnormal structure, function, and disease in adult life.

The relation of small head circumference and thinness at birth to death from cardiovascular disease in adult life.

To determine how fetal growth is related to death from cardiovascular disease in adult life. A follow up study of men born during 1907-24 whose birth weights, head circumferences, and other body measurements were recorded at birth. Sheffield, England. 1586 Men born in the Jessop Hospital. Death from cardiovascular disease. Standardised mortality ratios for cardiovascular disease fell from 119 in men who weighed 5.5 pounds (2495 g) or less at birth to 74 in men who weighed more than 8.5 pounds (3856 g). The fall was significant for premature cardiovascular deaths up to 65 years of age (chi 2 = 5.0, p = 0.02). Standardised mortality ratios also fell with increasing head circumference (chi 2 = 4.6, p = 0.03) and increasing ponderal index (weight/length3) (chi 2 = 3.8, p = 0.05; for premature deaths chi 2 = 6.0, p = 0.01). They were not related to the duration of gestation. Among men for whom the ratio of placental weight to birth weight was in the highest fifths the standardised mortality ratio was 137. These findings show that reduced fetal growth is followed by increased mortality from cardiovascular disease. They suggest that reduction in growth begins early in gestation. They are further evidence that cardiovascular disease originates through programming of the body's structure, physiology, and metabolism by the environment during fetal life. Maternal nutrition may have an important influence on programming.

The effect of nutrition of the fetus and neonate on cardiovascular disease in adult life.

The effect of nutrition of the fetus and neonate on cardiovascular disease in adult life.