AGT and RH blood group polymorphisms affect blood pressure and lipids in Afro-Caribbeans.

Population blood pressure variation is most likely due to multiple genes. This is likely the reason why monogenic testing with the angiotensinogen (AGT) gene polymorphisms on chromosome 1 (1q42-43), especially M235T, has met with negative results, especially in those of African descent. The RH blood group system, also on chromosome 1 (1 p36.2-34), has likewise been associated with blood pressure variation in African-Americans and with the rise in blood pressure with age in whites. Using a random sample of the population, we investigated the combined effects of single and combined variation of the AGTN M235T and RH genotypes on blood pressure, lipids, and lipoprotein concentrations in Afro-Caribbeans aged 18-60 years from the island nation of Dominica. In monogenic analysis, AGT M235T was not associated with blood pressure. However, it was associated with HDL (MM 42+/-23, MT 44+/-12, TT 52+/-14 (P=0.002)). RH genotype was significantly associated with systolic blood pressure (P=0.006) and Apo-A (P=0.003). These effects remained after adjustment for age, gender, weight, and BMI. In the polygenetic analysis, AGT M235T and RH were significantly associated with systolic blood pressure (P=0.037; interaction effects, P=0.068). The association of the AGT M235T with blood pressure across RH blood group haplotypes was then tested. Of the five RH haplotypes available for analysis, the AGT M235T was significantly associated with blood pressure within the "D" haplotype (P=0.01). The RH blood group and gender were significantly associated with systolic blood pressure and Apo-A levels (P=0.005 and 0.012, respectively). All interactions were independent of age and weight. In conclusion, we demonstrate a significant association of AGT M235T with blood pressure and cholesterol metabolism in an Afro-Caribbean population in the "genetic context" of the RH blood group system. Further investigation of these interactions may help understand the effects of genetic factors on cardiovascular risk in African-derived and other populations.

Allelic variation in the promoter region of the LDL receptor gene: analysis of an African-specific variant in the FP2 cis-acting regulatory element.

DNA samples of 2303 individuals from nine different population groups were screened for variant -175g-->t in the promoter region of the low-density lipoprotein receptor (LDLR) gene. The -175g-->t variant detected at carrier frequencies of 3-10% in different African population groups was absent in the Caucasian and Asian (Chinese) individuals studied. In contrast to previous findings in Black South Africans where this polymorphism predominated in patients with familial hypercholesterolaemia (FH), it occurred at a significantly lower frequency in hypercholesterolaemics from the recently admixed Coloured population of South Africa compared with population-matched controls (P<0.0001). Haplotype and mutation analysis excluded the likelihood that this finding is due to association with a specific disease-related mutation in FH patients, although reversal of the positive association with FH observed in the Black population may, at least in part, be due to admixture linkage disequilibrium. Transient transfection studies in HepG2 cells demonstrated that the -175t allele is associated with a non-significant decrease ( approximately 7%) of LDLR transcription in the absence of sterols. The data presented in this study raise the possibility that the -175g-->t polymorphism may have subtle effects that become clinically important within certain genetic and/or environmental contexts.

Omapatrilat versus lisinopril: efficacy and neurohormonal profile in salt-sensitive hypertensive patients.

Omapatrilat, a vasopeptidase inhibitor, simultaneously inhibits neutral endopeptidase and ACE. The efficacy and hormonal profile of omapatrilat and lisinopril were compared in salt-sensitive hypertensive patients. On enrollment, antihypertensive medications were withdrawn, and patients received a single-blind placebo. On day 15, salt-sensitivity determinations were made. Salt-sensitive hypertensive patients returned within 5 to 10 days for baseline evaluations of ambulatory diastolic blood pressure, ambulatory systolic blood pressure, and atrial natriuretic peptide. Salt-sensitive hypertensive patients were randomized to receive double-blind omapatrilat (n=28) or lisinopril (n=33) at initial doses of 10 mg for 1 week, increasing to 40 and 20 mg, respectively, for an additional 3 weeks. Ambulatory blood pressure and urinary atrial natriuretic peptide were assessed at study termination. Both omapatrilat and lisinopril significantly reduced mean 24-hour ambulatory diastolic and systolic blood pressures; however, omapatrilat produced significantly greater reductions in mean 24-hour ambulatory diastolic blood pressure (P=0.008), ambulatory systolic blood pressure (P=0.004), and ambulatory mean arterial pressure (P=0.005) compared with values from lisinopril. Both drugs potently inhibited ACE over 24 hours. Omapatrilat significantly (P<0.001) increased urinary excretion of atrial natriuretic peptide over 0- to 24-hour (3.8-fold) and 12- to 24-hour (2-fold) intervals; lisinopril produced no change. Omapatrilat significantly (P<0.001) increased urinary excretion of cGMP over the 0- to 24- and 4- to 8-hour intervals compared with that from lisinopril. Neither drug had a diuretic, natriuretic, or kaliuretic effect. In conclusion, in salt-sensitive hypertensive patients, omapatrilat demonstrated the hormonal profile of a vasopeptidase inhibitor and lowered ambulatory diastolic and systolic blood pressures more than lisinopril.

Predictors of target organ damage in hypertensive blacks and whites.

The purpose of this study was to evaluate the association of the insulin resistance syndrome with both blood pressure and target organ damage in blacks and whites with essential hypertension. Eighty-two black and 63 white French Canadian patients were studied. None had diabetes, and antihypertensive medications had been discontinued for >/=1 week. Measurements included 24-hour blood pressure monitoring, fasting plasma lipids, insulin sensitivity determined with the Bergman minimal model, echocardiogram, microalbumin excretion, and inulin and lithium clearances. Compared with the white French Canadians, black patients had an attenuated nighttime reduction in blood pressure (P<0.02), increased cardiac dimensions (P<0.001), greater microalbumin excretion (P<0.05), increased inulin clearance (indicative of glomerular hyperfiltration; P<0.001), and decreased lithium clearance (indicative of increased sodium reabsorption in the proximal tubule; P<0.001). Blood pressure levels were not related to insulin resistance; although in blacks, the nighttime reduction in systolic blood pressure was inversely related to fasting plasma insulin (r=-0.18, P<0.04). In a stepwise multivariate analysis (including blood pressure levels and components of the insulin resistance syndrome as independent variables), race was the strongest predictor of left ventricular mass (r=0.53, P<0.000), relative wall thickness (r=0.49, P<0.000), and both inulin (r=0.53, P<0.000) and lithium (r=0.41, P<0.000) clearances. Nighttime systolic blood pressure was also a significant determinant of concentric left ventricular hypertrophy (r=0.37, P<0.000). In blacks, microalbumin excretion was related to insulin resistance. These observations are consistent with the hypothesis that there is a genetic contribution to cardiac hypertrophy, glomerular hyperfiltration, and sodium retention in blacks with essential hypertension.

Arterial pressure, left ventricular mass, and aldosterone in essential hypertension.

The purpose of the present study was to evaluate the relationship of aldosterone to blood pressure and left ventricular size in black American (n=109) and white French Canadian (n=73) patients with essential hypertension. Measurements were obtained with patients off antihypertensive medications and included 24-hour blood pressure monitoring, plasma renin activity and aldosterone, and an echocardiogram. Compared with the French Canadians, the black Americans had higher body mass indexes, higher systolic blood pressures, attenuated nighttime reduction of blood pressure, and lower serum potassium concentrations (P:<0.01 for each). Left ventricular mass index, posterior wall thickness, interventricular septal thickness, and relative wall thickness were also greater (P:<0.01 for each) in the black American patients. Supine and standing plasma renin activity was lower (P:<0.01 and P:<0.05, respectively) in the black Americans, whereas supine plasma aldosterone concentrations did not differ, and standing plasma aldosterone was greater (P:<0.05) in the black Americans (9.2+/-0.7 ng/dL) than in the French Canadians (7.3+/-0.6 ng/dL). In the black Americans, supine plasma aldosterone was positively correlated with nighttime systolic (r=0.30; P:<0.01) and diastolic (r=0.39; P:<0.001) blood pressures and inversely correlated with the nocturnal decline of systolic (r=-0.29; P:<0.01) and diastolic (r=-0.37; P:<0.001) blood pressures. In the black Americans, standing plasma aldosterone was positively correlated with left ventricular mass index (r=0.36; P:<0.001), posterior wall thickness (r=0.33; P:<0.01), and interventricular septal thickness (r=0.26; P:<0.05). When the black American patients were divided into obese and nonobese groups, significant correlations between plasma aldosterone and both blood pressure and cardiac mass were observed only in the obese. In the French Canadians, overall, plasma aldosterone did not correlate with either blood pressure or any measures of heart size. However, among obese French Canadians, supine plasma aldosterone correlated with nighttime diastolic (r=0.53, P:<0.02) and systolic (r=0.44, P:<0.01) blood pressures but not with cardiac mass. These results are consistent with the hypothesis that aldosterone contributes to elevated arterial pressure in obese black American and obese white French Canadian patients with essential hypertension and to the attenuated nocturnal decline of blood pressure and left ventricular hypertrophy in obese, hypertensive black Americans.

Impact of diet on blood pressure and age-related changes in blood pressure in the US population: analysis of NHANES III.

BACKGROUND: The impact of diet on blood pressure and the age-related changes in blood pressure have been difficult to detect within one population. We designed this analysis to study the association of major dietary factors with blood pressure and with age-related changes in blood pressure in a representative sample of the US population. METHODS: Data were obtained on all individuals 20 years or older (n = 17 030) surveyed in the Third National Health and Nutrition Examination Survey (NHANES III), including demographic data, anthropometric data, dietary intake (sodium, potassium, calcium, magnesium, protein, alcohol, and total energy) based on 24-hour recall, and blood pressure. Multivariate models relating diet to blood pressure were constructed using stepwise regression, best subset regression, and multiple regression. RESULTS: Systolic blood pressure was positively associated with higher sodium, alcohol, and protein intakes (P<.05) and negatively associated with potassium intake (P =.003). Diastolic blood pressure was negatively associated with potassium and alcohol intakes (P<.001). Pulse pressure was positively associated with sodium, protein, and alcohol intakes (P<.001). A higher intake of calcium (P =.01) was associated with a lower rate of rise in systolic blood pressure with age. CONCLUSION: A diet low in sodium, alcohol, and protein is associated with lower systolic blood and pulse pressure. Potassium intake was associated with lower systolic and diastolic blood pressure, whereas alcohol intake was associated with lower diastolic blood pressure. In addition, the age-related changes in systolic blood pressure were attenuated by higher calcium and protein intakes. Magnesium was not associated with any changes in blood pressure.

Genetic determinants of hypertension: identification of candidate phenotypes.

Our long-term objective is to identify genes whose expression results in hypertension and in phenotypic changes that may contribute to hypertension. The purpose of the present study was to describe evidence for the heritability of hypertension-related phenotypes in hypertensive, hyperlipidemic black sib pairs. Outpatient anthropomorphic measurements were obtained in >200 affected sib pairs. In addition, 68 of these sib pairs were studied under controlled, standardized conditions at an inpatient clinical research center while off both antihypertensive and lipid-lowering medications. Heritability was estimated on the basis of sib-sib correlations and with an association model. Higher heritability estimates for blood pressure were observed with multiple measurements averaged over 24 hours than with measurements at a single time point, and heritability estimates for nighttime blood pressures were higher than those for daytime blood pressures. Heritability estimates for several of the phenotypes were augmented by obtaining measurements in response to a standardized stimulus, including (1) blood pressure responses to the assumption of upright posture, standardized psychological stress, and norepinephrine infusion; (2) plasma renin, aldosterone, epinephrine, and cAMP and cGMP responses to the assumption of upright posture; (3) para-aminohippurate and inulin clearances in response to norepinephrine infusion; and (4) plasma arginine vasopressin in response to NaCl infusion. High heritability estimates were also observed for various measures of body size and body fat, left ventricular size, cardiac index, stroke volume, total peripheral resistance, and serum concentrations of LDL and HDL cholesterol and leptin. These heritability estimates identify the hypertension-related phenotypes that may facilitate the identification of specific genetic determinants of hypertension in blacks with hyperlipidemia.

Glomerular hyperfiltration in hypertensive African Americans.

The incidence of end-stage renal disease attributable to hypertension is 5-fold greater in African Americans than in whites. To determine whether glomerular hyperfiltration is an antecedent to renal failure, we compared responses of renal blood flow and glomerular filtration rate to graded infusions of norepinephrine (0. 01, 0.025, and 0.05 microg. kg(-1). min(-1) for 30 minutes each) in 29 African Americans and 33 age-matched French Canadian whites with essential hypertension. Renal blood flow and glomerular filtration rate were measured by using a constant-infusion technique of PAH and inulin, respectively. Studies were conducted on an inpatient clinical research center, and antihypertensive medications had been discontinued for at least 1 week. Based on 24-hour blood pressure monitoring, nighttime blood pressures decreased (P<0.01) in the French Canadians but not in the African Americans. Baseline renal blood flow was higher (P<0.05) in the African Americans (1310+/-127 mL. min(-1) per 1.73 m(2)) than in the French Canadians (1024+/-42 mL. min(-1) per 1.73 m(2)); baseline glomerular filtration rate was also higher (P<0.01) in the African Americans (140+/-4 versus 121+/-4 mL. min(-1) per 1.73 m(2)). In response to norepinephrine-induced blood pressure increases, renal blood flow was autoregulated and did not change in either patient group. In the African Americans, glomerular filtration rate increased (P<0.01) to 167 mL. min(-1) per 1.73 m(2) during the first norepinephrine infusion, without subsequent change. In contrast, glomerular filtration rate did not change with norepinephrine-induced increases of blood pressure in the French Canadians. In the African Americans, the elevation of baseline glomerular filtration rate, with a further increase in response to norepinephrine, may be indicative of glomerular hyperfiltration. Glomerular hyperfiltration and lack of nocturnal blood pressure decline may contribute to the higher incidence of end-stage renal disease in hypertensive African Americans.

Prevalence of cardiovascular risk factors in the Republic of Georgia.

BACKGROUND: Eastern Europe is experiencing an epidemic of deaths from cardiovascular diseases with an increase since the early 1990s approaching 50%. The ability to survey the risk factors associated with this striking rise is severely hampered by the current disarray of the area's public health system. We used a rapid survey method to describe the epidemiology of cardiovascular risk in the capital of the Republic of Georgia, Tbilisi. METHODS: A two-stage cluster design, 'rapid survey method' developed by the Chronic Disease Center was used to estimate the frequency of hypertension, a major cardiovascular risk factor. Local personnel were trained and certified in blood pressure measurement and rapid survey techniques. The training and survey were conducted over a period of 14 days at which time a preliminary report of the survey was presented to the Ministry of Health. RESULTS: A total of 321 subjects were surveyed. The frequency of high blood pressure (>140/>90 mm Hg) at the time of the examination was 58% in men and 56% in women. The major correlates for blood pressure were gender and age. In addition we found that 31% of the population had a total cholesterol > or =220 mg% and a similar number had a low high density lipoprotein < or =35 mg%. Smoking was present in 60% of men and none were taking aspirin daily to prevent premature coronary artery disease. CONCLUSIONS: The rapid survey method is feasible in the former Soviet Union and can quickly provide estimates of the risk factors associated with the epidemic of cardiovascular disease in this area.

Ambulance sphygmomanometers are frequently inaccurate.

OBJECTIVE: To determine the accuracy and reliability of sphygmomanometers used in a metropolitan emergency medical services (EMS) system. METHODS: As a cross-sectional, convenience sample, 150 sphygmomanometers used by EMS personnel in Milwaukee County, Wisconsin, were evaluated. Each sphygmomanometer was checked for accuracy by connecting the manometer to a new, standard mercury manometer using a "Y" connector. Pressure was checked at readings of 60, 90, 120, and 200 mm Hg. The integrity of the device (leaking) was checked by inflating the cuff around a can to 300 mm Hg and measuring the pressure lost in 1 minute. Devices were determined to be inaccurate if the average of the absolute differences at each pressure deviated by more than 3 mm Hg. The device was determined to be unreliable (leaked) if it lost pressure greater than 15 mm Hg in 1 minute. RESULTS: Twenty-eight percent (41/149) of the devices were inaccurate at 90 mm Hg and 25% (37/149) were inaccurate overall. The overall and 90 mm Hg average deviations were +/- 6.6 and +/- 6.0 mm Hg, respectively. Sixty-three percent (94/150) of the devices were unreliable (leaked). When considering both accuracy and reliability at 90 mm Hg, a total of 73% (109/150) of the devices failed one or both of the criteria. CONCLUSION: This study suggests that an accurate blood pressure measurement may not be reliably obtained with 73% of the sphygmomanometers currently used in the county's EMS system.

Stress hypertension: the "wrong" genes in the "wrong" environment.

Jim Henry demonstrated an animal's society can induce an increase in blood pressure and its cardiovascular sequale. He recognized that the stress required to elevate blood pressure was a function of the genetically determined behavioral traits of the mice used. He termed some strains aggressive, others peaceable. Being highly inbred (indeed isogenic strains) it was intriguing to find that the behavior of these genetically identical individuals could differ markedly once placed in a society that decreased territory. A dominant or "king" mouse emerged. Other non-dominant males were aggressive and striving to be king. Adrenal medullary systems were activated and renins high. Others huddled in one cage and appeared to have given up. Jim called them depressed. Their adrenal cortex was hyperplastic suggesting pituitary adrenal axis activation as in depression, their renin was low and corticosterone high. In rats, careful selection of a strain genetically aggressive had to be combined with titration of societal stress to reliably induce hypertension. Its likely that humans retain some, if not all, of these variations, i.e. some respond to stress with an increase in blood pressure and others do not, some respond via the sympathetic pathway and others by adrenal cortical activation. The suggestion that African American's high blood pressures is due to stress is relevant to the Henry paradigm and the known genetic influences on sodium retention in blacks. The integration of this paradigm with the genetically increased sensitivity to the blood pressure raising effects of dietary sodium in blacks is proposed and discussed.

Blood pressure variation in blacks: genetic factors.

Persons of African descent living in the Western hemisphere, including African Americans, have the highest prevalence of hypertension in the world. Debate continues as to whether it is their African ancestry or the Western environment that is more important in increasing the prevalence of hypertension in the African Diaspora above that of indigenous Africans as well as of fellow inhabitants in the Western hemisphere. Current data support that hypertension in African Americans, like that in other population groups, arises from the interaction of environmental factors with a susceptible physiology that is determined in part by genetic factors. Dietary sodium chloride (NaCl) is an important environmental factor, and the inability to prevent blood pressure from increasing to hypertensive levels in response to the comparatively high NaCl content of Western diets characterizes the majority of hypertensive African Americans. Studies discussed herein suggest a strong genetic component for the physiology of "salt sensitivity." Phenotypes that are indicative of this sensitivity are more common in African Americans than in Americans of European descent and in hypertensive African Americans compared with normotensive African Americans. Further studies are needed to more clearly define these genetic markers that determine salt sensitivity.

A curriculum for the training and certification of blood pressure measurement for health care providers.

Blood pressure measurement in clinical practice is almost never performed according to accepted guidelines. This is likely to be a result of inadequate training. We describe a standardized training program for teaching blood pressure measurement to health care students, practitioners and clinical investigators as well as lay personnel. The goal is to have the student understand the rationale and be able to perform accurate blood pressure measurements. Students must master the knowledge of proper blood pressure measurement technique, document their accuracy on standardized video tests and demonstrate their performance of proper technique. In addition the program reviews key historical and physiological aspects of blood pressure measurement and the cardiovascular complications of high blood pressure. The operation and maintenance of sphygmomanometers and the stethoscope, and monitoring for biases in blood pressure measurements in clinical practice, are also covered. The curriculum time requires a minimum of 7 h and biannual recertification is recommended. With training of instructors, the program can be easily replicated and should be considered in any setting in which blood pressure measurement is taught.

Chromogranin A in human hypertension. Influence of heredity.

Multiple heritable traits are associated with essential (genetic) hypertension in humans. Because chromogranin A is increased in both human and rodent genetic hypertension, we examined the influence of heredity and blood pressure on chromogranin A in humans. In estimates derived from among- and within-pair variance in monozygotic versus dizygotic twins, plasma chromogranin A displayed significant (F15,18 = 2.93, P = .016) genetic variance (sigma 2 g), and its broad-sense heritability was high (h2B = 0.983). Plasma chromogranin A was increased in essential hypertension (99.9 +/- 6.7 versus 62.8 +/- 4.7 ng/mL, P < .001) but was influenced little by genetic risk for (family history of) hypertension (in normotensive or hypertensive subjects), by race, or by several antihypertensive therapies (angiotensin-converting enzyme inhibitor, diuretic, or beta-adrenergic antagonist). In normotensive subjects at genetic risk for essential hypertension, neither basal nor sympathoadrenal stress-evoked chromogranin A differed from values found in subjects not at risk. In established essential hypertension, plasma chromogranin A responses to adrenal medullary (insulin-evoked hypoglycemia) or sympathetic neuronal (dynamic exercise) activation were exaggerated, whereas responses to sympathoadrenal suppression (ganglionic blockade) were diminished, suggesting increased vesicular stores of chromogranin A and an adrenergic origin of the augmented chromogranin A expression in this disorder. We conclude that plasma chromogranin A displays substantial heritability and is increased in established essential hypertension. Its elevation in established hypertension is associated with evidence of increased vesicular stores of the protein and with adrenergic hyperactivity but is influenced little by customary antihypertensive therapies. However, the chromogranin A elevation is not evident early in the course of genetic hypertension.

Relative role of genes and environment on BP: twin studies in Madras, India.

This study was conducted to test the feasibility of the twin research model in a developing country with diverse cultures and to understand the relative influence of genetic and environmental factors on BP variation among South Indians. This was a cross-sectional twin study of volunteers using a two-by-two factorial design for the analysis of quantitative traits. The factors were twin type (monozygotic and dizygotic) and sex (male and female). The study was conducted in Madras. Twenty-four pairs of twins were contacted for participation in the project. Of the 24 pairs we contacted, 91% (20) actually participated in our study. Among 20 sets we studied, 10 (50%) are males and 10 (50%) are females with an average age of 23 years. The mean SBP of this volunteer twin population was 115.18 +/- 1.27 mmHg and DBP was 68.53 +/- 1.41 mmHg. Analysis of dietary habits (vegetarian/nonvegetarian) showed that BP was greater (118.26 +/- 2.29/71.88 +/- 2.34 mmHg) in vegetarian twins than nonvegetarians (112.28 +/- 1.42/66.2 +/- 1.90 mmHg). Also a positive correlation between urinary excretion of calcium and BP was observed. The present study demonstrates that epidemiological research in a developing country like India is feasible and economical, using the twin research methodology. As observed in other populations, the major source of BP variation in the population appears to be predominantly under genetic control.

Systolic blood pressure levels in black populations in sub-Sahara Africa, the West Indies, and the United States: a meta-analysis.

Average systolic blood pressure levels from epidemiological studies conducted on black populations in sub-Sahara Africa were pooled and compared with pooled systolic blood pressure levels from black populations in the northern portion of the Western hemisphere (the West Indies and the United States). Studies published in English that listed systolic blood pressure means and standard deviations and sample sizes in 40-49-year-old men and women were included. Overall, systolic blood pressure levels were higher (p less than 0.05) in blacks from the northern Western hemisphere than in blacks from sub-Sahara Africa for both men (12 mm Hg higher) and women (13 mm Hg higher). The analysis was also conducted on regions within sub-Sahara Africa and in rural and urban subgroups. Systolic blood pressure was lower (p less than 0.05) in East Africa than in the other three regions within Africa for both sexes. Overall, urban blacks within Africa had higher systolic blood pressures (p less than 0.05) than rural blacks for both sexes. In the northern Western hemisphere, rural blacks had higher systolic blood pressures (p less than 0.05) than urban blacks for both sexes. Studies should be designed with standardized methods to unravel these intraracial differences in blood pressure levels.

Genetic effects on cardiovascular responses to cold and mental activity in late adulthood.

The purpose of the present investigation was to examine the genetic contributions to cardiovascular reactivity in an adult cohort of male twins. A total of 47 monozygotic (MZ) twin pairs and 54 dizygotic (DZ) twin pairs, aged 59 to 69 years, were laboratory tested at four sites as part of the third examination of the National Heart, Lung, and Blood Institute Twin Study. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were recorded during two tasks, a mental arithmetic task involving serial subtraction and the cold pressor test. Significant cardiovascular responsivity was observed during both tasks as measured by substantial elevations in SBP, DBP, and HR from resting periods to task periods. Heritability estimates were statistically significant for SBP and DBP but not HR levels during pretask baseline periods and during both tasks. Genetic variance was maintained for blood pressure reactivity to the mental arithmetic task after adjustments for baseline and performance. No genetic variance for SBP or DBP reactivity to the cold pressor test was evident.

The association of skin color with blood pressure in US blacks with low socioeconomic status.

To determine the association of skin color, measured by a reflectometer, with blood pressure in US blacks, we studied a community sample of 457 blacks from three US cities. Persons taking antihypertensive medications were excluded. Both systolic and diastolic blood pressure were higher in darker persons and increased by 2 mm Hg for every 1-SD increase in skin darkness. However, the association was dependent on socioeconomic status, whether measured by education or an index consisting of education, occupation, and ethnicity, being present only in person with lower levels of either indicator. Using multiple linear regression, both systolic and diastolic blood pressure remained significantly associated with darker skin color in the lower levels of socioeconomic status, independent of age, body mass index, and concentrations of blood glucose, serum urea nitrogen, serum uric acid, and urinary sodium and potassium. The association of skin color with blood pressure only in low socioeconomic strata may be due to the lesser ability of such groups to deal with the psychosocial stress associated with darker skin color. However, these findings also are consistent with an interaction between an environmental factor associated with low socioeconomic status and a susceptible gene that has a higher prevalence in persons with darker skin color.

Concordance of ischemic heart disease in the NHLBI twin study after 14-18 years of follow-up.

Morbidity and mortality were assessed in the NHLBI twin study at the end of 1987. Deaths were greater in DZ twins (58/520, 11.2%) than MZ twins (38/508, 7.5%). Ischemic heart disease concordances were 2.3 times higher in MZ pairs and 2.8 times higher in DZ pairs than expected based on the prevalence of ischemic heart disease in the cohort. Family history scores for heart disease, calculated 14-18 years earlier at entry to the study, were significantly higher in DZ pairs where one or both members later developed ischemic heart disease and in corcordant MZ pairs than in twin-pairs without any subsequent heart disease. Concordance rates were not significantly different between MZ and DZ pairs. The results agree with previous suggestions that selection at enlistment into the armed services over 40 years ago, as well as later volunteering for the NHLBI twin study, resulted in a decline in the number of concordant MZ pairs.