The relative contributions of genes and shared environment to cardiovascular risk factors were studied in twins and pedigrees in 1983-1985. Sitting, standing, isometric hand grip, bicycling, and mentally stressed (serial subtraction) blood pressures were obtained from 146 male monozygous twins, 162 male dizygous twins, and 1,102 healthy adults in 67 Utah pedigrees. Fasting total plasma cholesterol, triglycerides, high density lipoprotein cholesterol (HDL), and body mass index were also measured. Heritability was estimated before and after adjusting for 12 environmental variables (measures of socioeconomic status; personality types; exercise levels; use of tobacco, alcohol, coffee, etc.) by using age-adjusted twin intraclass correlations. These heritabilities were compared with those obtained from a variance components analysis of the pedigree data separating genetic and common household effects. Sitting and standing blood pressure heritability estimates were much higher from twin than from pedigree data (39-63% in twins vs. 16-22% in pedigrees), as were those for cholesterol and triglycerides (65 and 75% from twins vs. 42 and 37% from pedigrees) and body mass index (51 vs. 21%). Estimates were similar for heritability of HDL cholesterol (51 vs. 45%). Most of the stressed blood pressure heritabilities were similar to sitting blood pressure estimates. No common household effect (except for adjusted HDL cholesterol (24%), p less than 0.01) was statistically significant for the lipids, blood pressures, or body mass index. Environmental variables correlated much better in monozygous twins and spouses than in dizygous twins, brothers, or sisters. Spouse correlations for lipids, blood pressures, and body mass index were low, with a maximum of 0.12 (p less than 0.05) for HDL cholesterol. We conclude that genes contribute much more than shared environment to the well-recognized familial correlation of blood pressures, lipids, and body mass index.
NTIMICROBIAL RESISTANCE IS A serious public threat that is exacerbated by the gradual withdrawal of the pharmaceutical industry from new antimicrobial agent development. 1 Overuse of antimicrobial agents fosters the spread of antimicrobial-resistant organisms. 2,3 Despite recent trends that demonstrate reduced outpatient use of antimicrobial agents, prescribing continues to significantly exceed prudent levels. 4-8 Approximately 50% of courses of ambulatory antimicrobial drugs are prescribed for patients with viral respiratory infections and therefore are not clinically indicated. 9-12 Behavioral facilitators of antimicrobial overuse and barriers to prudent use operate on both clinicians and patients. 13-16 Patient demand, perceived or actual, creates chal-See also pp 2315 and 2354.
Color duplex flow imaging (CDFI) permits pain- and risk-free direct imaging of the deep venous system of the lower extremities. To prospectively ascertain the accuracy and limitations of this technique, CDFI was performed in 75 lower limbs of 69 consecutive patients referred for venographic evaluation of clinically suspected lower extremity deep venous thrombosis (DVT). The CDFI study was obtained within 24 hours of the contrast venogram. Both studies were interpreted without knowledge of the patient's clinical findings or the results of the other test. Contrast venography was regarded as the standard for diagnosis of DVT. Accuracy was 99% for detection of DVT above the knee and 81% below the knee. Sonographic evaluation of the calf veins was technically adequate in 60% of limbs; accuracy was 98% in this group. In the 40% of limbs with technically limited CDFI studies of the calf, accuracy decreased to 57%. Although small nonocclusive thrombi occurred infrequently in this series of symptomatic patients, CDFI missed three of four such thrombi. It is concluded that CDFI, when not technically compromised, is sufficiently accurate to definitively diagnose symptomatic lower extremity DVT.
An overview of published observations suggests that both genetic predisposition and environment work together to produce hypertension in most persons. High blood pressure before age 55 occurs 3.8 times more often among persons with a strong positive family history of high blood pressure. Much of the total variability in blood pressure in modern populations seems attributable to genetic factors. Estimates of the proportion of the variance attributable to all genetic factors (heritability [H2]) vary from 25% in pedigree studies to 65% in twin studies for sitting diastolic blood pressure. Several biochemical traits associated with high blood pressure are highly genetic (H2, 78-84%) and may help elucidate the pathophysiology of high blood pressure. While pertinent environmental factors such as salt intake, alcohol use, and amount of exercise also correlate significantly among relatives, only 7% of the total variance of diastolic blood pressure seems attributable to all shared environmental factors in family households. Thus most familial aggregation of high blood pressure appears to be due to genes rather than shared family environment. Practical benefit may result from identifying familial predisposition in multiple siblings with high blood pressure before age 55 and lipid abnormalities (labeled "familial dyslipidemic hypertension"). About 12% of high blood pressure patients have familial dyslipidemic hypertension and also have high risk of early coronary heart disease. Hyperinsulinemia and central obesity as well as high triglycerides and low high density lipoprotein cholesterol are prominent features of familial dyslipidemic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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