Dietary intake of n-3, n-6 fatty acids and fish: relationship with hostility in young adults--the CARDIA study.

BACKGROUND: Hostility has been shown to predict both the development and manifestation of coronary disease. Examining the inter-relation of dietary intake of fish and of polyunsaturated (n-3 and n-6) essential fatty acids with hostility may provide additional insights into the cardioprotective effect of dietary fish and polyunsaturated fatty acids. OBJECTIVE: To examine the association of dietary n-3, n-6 fatty acids and fish with level of hostility in a sample of 3581 urban white and black young adults. DESIGN: Cross-sectional observational study as part of an ongoing cohort study. A dietary assessment in 1992-1993 and measurement of hostility and other covariates in 1990-1991 were used in the analysis. RESULTS: The multivariate odds ratios of scoring in the upper quartile of hostility (adjusting for age, sex, race, field center, educational attainment, marital status, body mass index, smoking, alcohol consumption and physical activity) associated with one standard deviation increase in docosahexaenoic acid (DHA, 22:6) intake was 0.90 (95% CI=0.82-0.98; P=0.02). Consumption of any fish rich in n-3 fatty acids, compared to no consumption, was also independently associated with lower odds of high hostility (OR=0.82; 95% CI=0.69-0.97; P=0.02). CONCLUSIONS: These results suggest that high dietary intake of DHA and consumption of fish rich in n-3 fatty acids may be related to lower likelihood of high hostility in young adulthood. The association between dietary n-3 fatty acids and hostile personality merits further research.

Psychologic factors as precursors to hypertension.

The possibility that certain psychologic factors lead to hypertension has been considered by many investigators over the past 60 years, but prospective studies with suitable methods to evaluate this hypothesis were not available for analysis until the 1990s. There are now five large longitudinal studies demonstrating a relation between symptoms of anxiety or depression and subsequent hypertension incidence. Anger expression, long considered a major psychologic factor in hypertension, has been studied less extensively, and the findings to date are less consistent. While some evidence supports the biological plausibility of psychologic factors as risk factors for hypertension, biobehavioral mechanisms explaining the relationship have not been adequately explored. The results of these recent studies may lead to new intervention trials specifically selecting hypertensive patients with anxiety or depression for treatment with stress reduction or other appropriate psychologic therapies. Such studies would further contribute to the evaluation of anxiety and depression as risk factors for hypertension.

Platelet activation in depression and effects of sertraline treatment: An open-label study.

OBJECTIVE: The authors' goal was to determine whether sertraline attenuates the increased platelet activation seen among depressed patients. METHOD: They tested 21 otherwise healthy patients with untreated major depressive episode who were 25-52 years old and 21 age- and sex-matched comparison subjects. Patients received 6 weeks of sertraline treatment, and 17 returned for retesting. RESULTS: At baseline, the depressed patients had greater platelet secretion than the comparison subjects in response to collagen. Depressed patients with a family history of coronary disease had nonsignificantly greater wound-induced fibrinogen receptor binding than the other subjects. Platelet secretion in response to collagen was significantly reduced after treatment with sertraline. CONCLUSIONS: Sertraline diminished the increased platelet secretion found among depressed patients, although the findings are limited by a lack of a placebo control group.

Do depression symptoms predict early hypertension incidence in young adults in the CARDIA study? Coronary Artery Risk Development in Young Adults.

BACKGROUND: Hypertension has been linked to several psychological factors, including depression, but the relation between hypertension incidence and depressive symptoms has not been adequately examined. OBJECTIVE: To determine if depressive symptoms independently predict hypertension incidence. DESIGN AND SETTING: A prospective, multicenter, epidemiological cohort of young adults (aged 23-35 years at study entry) from the general community without hypertension followed up for 5 years. SUBJECTS: A sample of 3343 adults from 4 urban areas stratified for race (black and white) from the CARDIA (Coronary Artery Risk Development in Young Adults) study. MAIN OUTCOME MEASURE: Hypertension incidence, which was defined as blood pressure higher than 160/95 mm Hg (assessed on a single occasion) or the use of prescribed antihypertensive medication. RESULTS: Participants with high scores (> or = 16) on the Center for Epidemiological Studies Depression (CES-D) Scale were at significant risk for hypertension incidence compared with those with low CES-D scores (< or =7; odds ratio, 2.10; 95% confidence interval, 1.22-3.61) after adjustment for other hypertension risk factors (eg, age, resting systolic blood pressure at the 5-year examination, physical activity, daily alcohol use, parental history of hypertension, education, presence of diabetes mellitus or heart disease, sex, and race) in fixed logistic models. Those with intermediate depressive symptoms (CES-D scores 8-15) were also at significant risk (adjusted odds ratio, 1.78; 95% confidence interval, 1.06-2.98). These associations were significant in blacks alone but were not found in whites, who had a lower hypertension incidence (29 [2%] of 1806) than blacks (89 [6%] of 1537). CONCLUSIONS: Depressive symptoms were predictive of later hypertension incidence in young adults, and young blacks with depressive symptoms were at high risk of developing hypertension.

Association of hostility with coronary artery calcification in young adults: the CARDIA study. Coronary Artery Risk Development in Young Adults.

CONTEXT: Psychosocial factors, including personality and character traits, may play a role in the development and expression of coronary artery disease. OBJECTIVE: To evaluate whether hostility, a previously reported predictor of clinical coronary artery disease, is associated with coronary calcification, which is a marker of subclinical atherosclerosis. DESIGN: Prospective cohort study. SETTING AND PARTICIPANTS: Volunteer subsample from Chicago, Ill, and Oakland, Calif, consisting of 374 white and black men and women, aged 18 to 30 years at baseline, who participated in the Coronary Artery Risk Development in Young Adults (CARDIA) study. Cook-Medley hostility assessment data were collected at baseline from 1985 to 1986 and at year 5 examinations from 1990 to 1992. After the 10-year examinations in the 1995-1996 year, electron-beam computed tomographic scans were performed. MAIN OUTCOME MEASURES: Presence of any detectable coronary artery calcification (coronary calcium score >0), and coronary artery calcium scores of 20 or higher. RESULTS: In logistic regression analysis adjusting for age, sex, race, and field center comparing those with hostility scores above and below the median of the distribution of the present sample, the odds ratio of having any coronary calcification was 2.57 (95% confidence interval, 1.31-5.22), and the odds ratio of having a calcium score of 20 or higher was 9.56 (95% confidence interval, 2.29-65.9) for calcium scores of 20 or higher. The associations with any coronary artery calcification persisted after adjusting for demographic, lifestyle, and physiological variables. Results using a cynical distrust subscale were somewhat weaker than for those using the global hostility score. Power was inadequate to perform sex- or race-specific analyses. CONCLUSION: These results suggest that a high hostility level may predispose young adults to coronary artery calcification. JAMA. 2000;283:2546-2551

Increased prevalence of smaller and denser LDL particles in Asian Indians.

There is increasing evidence to believe that Asian Indians are at an increased risk of coronary heart disease (CHD), which cannot be attributed to the common risk factors. Individuals with small, dense LDL phenotype are also known to be at increased risk of CHD. Our objective was to examine whether the prevalence of smaller and denser LDL particles is increased in Asian Indians. Thirty-nine Asian Indians (22 men and 17 women), aged 25 to 45 years, were matched with 39 whites for age and gender. Cholesterol profiles of lipoprotein classes and LDL subclasses were measured using the Vertical Auto Profile-II (VAP-II) and LDL-VAP-II methods, respectively. Six LDL subclasses (LDL1 to LDL6) have been identified using the LDL-VAP-II, with LDL1 and LDL6, respectively, being the most and least buoyant subclasses. The prevalence of small, dense LDL type (subjects with major LDL subclass 5 or 6) was significantly higher in Asian Indians compared with white subjects (44% versus 21%; P<0.05). The relative position of the major LDL density peak (LDL-Rf) on 0 to 1 scale in LDL-VAP-II density gradient was also significantly decreased in Asian Indians (0.462+/-0.076 versus 0. 505+/-0.086; P<0.02), suggesting an increased LDL density. Furthermore, this increased prevalence of small, dense LDL type appears to be due to the increased triglycerides (TG) (r for LDL-Rf versus TG=0.681, P<0.001), with fasting insulin being one of the important determinants of TG (r for TG versus fasting insulin=0.572, P<0.001). In addition, fasting insulin was significantly increased in Asian Indians with small, dense LDL type compared with other Asian Indians, suggesting a significant role of insulin resistance in increasing the prevalence of small, dense LDL type. We conclude that the increased prevalence of small, dense LDL observed in Asian Indians might contribute to their increased CHD risk.

Increased serotonin receptor density and platelet GPIIb/IIIa activation among smokers.

This study sought to determine whether depressive symptoms and/or platelet serotonin receptor (5HT2A) density are associated with increased platelet activation (PA) found among smokers. Flow cytometric detection of PA was used to study 36 smokers and 16 nonsmokers, aged 18 to 48 years. Subjects were tested at baseline and after either smoking 2 cigarettes (smokers) or a similar resting interval (nonsmokers). Assessment of PA included both platelet secretion and fibrinogen receptor (GPIIb/IIIa) binding. Platelet 5HT2A receptor binding and saturation were tested using [3H]LSD, and depressive symptoms were measured using the Beck Depression Inventory. Platelet 5HT2A receptor density was increased among smokers versus nonsmokers (82.7+/-67.7 versus 40.0+/-20.2 fmol/mg protein; P<0.005), and there was a dose-dependent relationship between receptor density and packs/d among smokers. Baseline wound-induced GPIIb/IIIa binding at 1 minute and GPIIb/IIIa binding in response to collagen stimulation in vitro was increased among smokers (P<0.05); there were no changes in PA among smokers after smoking, and platelet secretion was not elevated among smokers. Depressive symptoms were associated with 5HT2A receptor density among nonsmokers (P<0.005), but no such relationship was evident among smokers; PA was unrelated to 5HT2A receptor density in either group. The findings indicate that smoking is associated with increased platelet serotonin receptor density and with increased GPIIb/IIIa receptor binding, although these 2 factors are not related to each other or to depressive symptoms among smokers. Serotonergic dysfunction may be an important factor in the development of cardiovascular disease among smokers.

Hostility is associated with increased platelet activation in coronary heart disease.

OBJECTIVE: To determine whether Potential for Hostility is related to platelet activation (PA) among patients with coronary heart disease (CHD) and healthy controls. Increased PA has been associated with adverse secondary events after myocardial infarction or coronary angioplasty. METHODS: We tested 32 CHD patients and 23 healthy men and women, aged 45 to 73 years, for PA by using whole blood flow cytometry. PA was measured in blood exiting a bleeding time wound (wound-induced platelet activation) and also in venous blood stimulated in vitro with collagen. Monoclonal antibodies were used to test for fibrinogen receptor activation and fibrinogen receptor binding. All subjects refrained from taking aspirin for at least 14 days before testing; CHD patients stopped nitrates and calcium channel blockers for 24 hours, while continuing to take lipid-lowering medications. Potential for Hostility was assessed, using the Type A Structured Interview. RESULTS: Among the CHD patients only, all four of the wound-induced fibrinogen receptor activation indicators (activation and binding) were related to hostility; the relationships were significant for receptor activation at 2 minutes, and for receptor binding at 1 minute (r values = .46, p values = .02). Subjects on lipid-lowering medications had lower PA for most measures. Healthy subjects had higher wound-induced fibrinogen receptor activation at 2 minutes and fibrinogen receptor activation in vitro than the CHD patients (p = .04), but after statistical adjustment for lipid-lowering medications, there were no significant differences between the patients and controls. CONCLUSIONS: PA was related to hostility among CHD patients, consistent with previous studies indicating a relationship between PA and psychological factors among CHD patients. However, PA was not increased in nonsmoking, nondepressed CHD patients relative to controls.

Increased platelet activation and fibrinogen in Asian Indians. Potential implications for coronary risk.

AIMS: To determine whether Asian Indians (Indians), a group known to have high rates of coronary heart disease, have increased platelet activation and fibrinogen levels relative to white Americans of European origin (whites). METHODS AND RESULTS: Forty healthy, non-smoking Indians, aged 25-45, were matched with 40 healthy whites for age (within 3 years) and gender. Platelet activation was tested in blood exiting a bleeding time wound at 1 and 2 min post-incision (wound-induced activation), as well as in venous blood stimulated in vitro with collagen, using whole blood flow cytometry. Other risk factors, including fibrinogen levels, family history of diabetes or coronary heart disease, fasting insulin and lipid levels, and Lp(a) were also assessed. Fibrinogen levels were higher among Indians than whites, even after adjustment for gender or family history of coronary heart disease (P < 0.05). Indians had higher levels of wound-induced glycoprotein IIb/IIIa binding and platelet secretion (P-selectin expression) than whites, with the greatest differences found when comparing the upper quintile of activation for each group (Ps < 0.05). Indians with a family history of coronary heart disease (n = 15) had higher levels of platelet secretion (wound-induced and in vitro) than Indians without a family history (Ps < 0.05), while the relationship was reversed among whites. Platelet activation measures were not consistently related to other coronary risk factors, while fibrinogen was related to triglyceride and insulin levels among Indians. CONCLUSION: Indians have elevated fibrinogen and platelet activation levels relative to whites. These factors may contribute to the increased coronary risk observed in Indians.

Inverse relationship of urinary cyclic GMP to blood pressure reactivity in the CARDIA study: vasodilatory regulation of sympathetic vasoconstriction. Coronary Artery Risk Development in Young Adults.

OBJECTIVE: To determine whether urinary cyclic GMP (cGMP), which mediates the actions of the vasodilators nitric oxide and atrial natriuretic factor, is inversely related to blood pressure (BP) reactivity. In previous work, we found that urinary cGMP was inversely related to diastolic BP, but cGMP levels were higher among individuals presumed to have increased adrenergic activity, increased reactivity, and increased risk of hypertension (blacks, individuals with a family history of hypertension). METHOD: We measured 24-hour urinary cGMP levels in a substudy of 529 individuals in the Coronary Artery Risk Development in Young Adults (CARDIA) study; the sample was 23 to 35 years of age and approximately balanced for race (black/white) and gender. BP reactivity to stressors (video game, star-tracing, cold pressor) was tested 3 years earlier. Baseline BP was included as a covariate in all analyses. RESULTS: Diastolic BP reactivity to cold pressor was inversely related to cGMP excretion (p < .05); the relationship was strongest among black women with a family history of hypertension (partial r = -.33, p < .01). Systolic BP reactivity to star-tracing was also inversely related to cGMP (p < .01); the relationship for both star-tracing and video game stressors was strongest among black men (partial r values = -.25 and -.24, respectively; p values < .01). CONCLUSIONS: The results indicate that vasodilatory activity may impact the BP response to stress through modulation of adrenergic activation, particularly among blacks.

Cardiovascular reactivity to video game predicts subsequent blood pressure increases in young men: The CARDIA study.

OBJECTIVE: This study was undertaken to determine the relationship between heightened reactivity of blood pressure (BP) during stress and 5-year changes in blood pressure and hypertensive status, using the CARDIA study. METHOD: A total of 3364 participants (910 white men, 909 white women, 678 black men, and 867 black women), initially 20 to 32 years old and normotensive, were included. Cardiovascular reactivity to psychological stressors (video game and star-tracing tasks for 3 minutes, cold pressor test for 1 minute) was measured in 1987-1988. We then examined reactivity as a predictor of significant BP change (> or = 8 mm Hg, thought to represent a clinically significant increase) over the next 5 years. Logistic regression models were used to control for potential covariates. Significant BP change and the development of hypertension (BP greater than 140/90 or taking medication for hypertension) over the 5-year follow-up were examined in separate analyses. RESULTS: Increased systolic blood pressure (SBP) reactivity to the video game was associated with a significant 5-year SBP increase among the entire cohort, independent of resting SBP (p < .0001). Subsequent analyses showed that this relationship held for men but not for women. Reactivity to the star-tracing task or the cold pressor test did not predict significant BP change. Among black men only, new hypertensives (N = 36) had greater diastolic blood pressure (DBP) reactivity to the video game (p = .01). CONCLUSIONS: Although BP reactivity to all physical and mental stressors used in this study did not consistently predict 5-year change in BP in this young cohort, the results indicate that reactivity to a video game stressor predicts 5-year change in BP and early hypertension among young adult men. These findings are consistent with other studies showing the usefulness of stressors producing a primarily beta-adrenergic response in predicting BP change and hypertension. The results may be limited by the shortened initial rest and recovery periods used in the CARDIA protocol.

Lack of relations of hostility, negative affect, and high-risk behavior with low plasma lipid levels in the Coronary Artery Risk Development in Young Adults Study.

BACKGROUND: Previous studies have suggested that low plasma cholesterol levels or cholesterol lowering may increase the risk of suicide and violent death. Increased aggression, risk-taking behavior, or depression has been associated with low cholesterol levels in some studies. METHODS: A total of 4240 subjects of the Coronary Artery Risk Development in Young Adults study, aged 23 to 35 years, were included in the study. Analyses were stratified by race (black or white) and sex. Persons in the lowest 10% of plasma total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride levels were compared with the other participants in each race/sex group, using standardized measures of hostility, anger suppression, depressive symptoms, and anxiety. The relations between 5-year change in hostility and 5-year change in lipid levels also were examined. The relations between lipid levels and high-risk behavior (e.g., violent arguments or having a gun at home) were examined in a subset of subjects. All analyses were adjusted for relevant covariates. RESULTS: In cross-sectional analyses, low total cholesterol levels were not related to any of the psychological measures in any race/sex group. Among black women only, low low-density lipoprotein cholesterol was related to greater anxiety, and low triglycerides were related to lower anger suppression (P < or = .002). Among white men only, increases in hostility during the 5-year follow-up were related to increases in triglycerides (P < .01), but changes in hostility were unrelated to changes in cholesterol levels. Among a subset of 371 subjects with initially elevated total cholesterol (> or = 5.17 mmol/L [> or = 200 mg/dL]) and a non-medicated decrease of 0.52 mmol/L (> or = 20 mg/dL) or more during 5 years, hostility decreased in a univariate analysis (P < .001). High-risk behaviors also were not associated with low lipid levels. CONCLUSION: The results do not support a consistent relation between hostility, negative affect, or high-risk behaviors with low lipid levels or lipid-lowering among young adults.

Relationship of diastolic blood pressure with cyclic GMP excretion among young adults (the CARDIA Study): influence of a family history of hypertension. Coronary Artery Risk Development in Young Adults.

BACKGROUND: Guanosine 3':5'-cyclic monophosphate (cGMP) is the second messenger of nitric oxide and atrial natriuretic factor, and mediates local vasodilatation. These vasodilatory factors are important in blood pressure regulation and possibly in the etiology of hypertension. Urinary cGMP levels among normotensive young adults have not previously been studied. SUBJECTS: A subset of normotensive participants from the CARDIA study (n = 563), aged 23-35 years, was studied. The sample was approximately balanced for sex and race (black/white). METHODS: Twenty-four-hour urinary cGMP levels were measured using an enzyme immunoassay; levels were adjusted for creatinine excretion. The blood pressure, smoking status, and risk factors for hypertension [including a family history of hypertension (FHH), the body mass index, education, alcohol intake, and sodium excretion] were also measured. RESULTS: Women excreted more cGMP than did men, and blacks excreted more cGMP than did whites (both P < 0.0001). Excretion of cGMP was also greater among smokers (P < 0.001) and those with an FHH (P = 0.05), and was related directly and independently to sodium excretion (P < 0.02). The diastolic blood pressure (DBP) was related inversely to the excretion of cGMP among individuals without an FHH (r = -0.36, P < 0.001), but not among individuals with an FHH. In multiple regression analysis, the excretion of cGMP remained related significantly to the DBP and accounted for more variance in DBP than did any other variable among those without an FHH (delta R2 = 0.08, P < 0.001). CONCLUSIONS: Urinary cGMP excretion is related inversely and independently to the DBP among those without an FHH but not among those with an FHH, suggesting that cGMP-related vasodilatation is impaired in those with an FHH. Sex differences in urinary excretion of cGMP are consistent with results from studies showing that estrogen increases the endothelial production of nitric oxide.

Smoking, nicotine dependence, and depressive symptoms in the CARDIA Study. Effects of educational status.

The present study was designed to determine whether depressive symptoms are independently associated with smoking and nicotine dependence among cigarette smokers, using 1990-1991 data from the Coronary Artery Risk Development in Young Adults (CARDIA) Study. A total of 3,933 participants (788 black men, 1,090 black women, 974 white men, and 1,081 white women) aged 23-35 years were included. Analyses were stratified by race and sex. Depressive symptoms were measured by means of the Center for Epidemiologic Studies Depression (CES-D) Scale. Nicotine dependence was defined as smoking one's first cigarette of the day within 30 minutes of awakening. Analysis of covariance was used to control for potential covariates (age, body mass index, alcohol consumption, and education). In unadjusted comparisons, smokers had more depressive symptoms than never smokers in all groups except white men; this relation showed little change after adjustment for age, body mass index, and alcohol consumption. However, after adjustment for education in addition to the above variables, these differences became attenuated and were significant only among white women (adjusted CES-D score difference = 1.9, p < 0.02). When analyses were further stratified by nicotine dependence, dependent smokers had higher CES-D scores than never smokers in all groups. The differences again became attenuated when education was added to the model, and were significant only among black women (adjusted CES-D score difference = 2.3, p < 0.01). These results indicate that although smoking in general and nicotine-dependent smoking in particular are related to symptoms of depression, controlling for educational level attenuates these relations.

Platelet activation and restenosis after coronary stenting: flow cytometric detection of wound-induced platelet activation.

BACKGROUND: Platelet activation has been implicated in restenosis after percutaneous transluminal coronary angioplasty (PTCA), but previous studies may have been confounded by factors such as elastic recoil and arterial remodelling. Restenosis after coronary stenting is unlikely to be affected by these factors. METHODS: Forty-nine patients who had stenting for acute or impending closure after PTCA were included in the study. Patients with restenosis (> or = 50% stenosis by angiography) and without restenosis were selected using a case-control design. Restenosis was determined by the caliper method. Patients were tested for platelet activation 1-4 years after their procedure while taking their usual medications (including aspirin). Reliability testing was conducted with 11 healthy subjects. Platelet activation was measured in blood leaving a bleeding-time wound (wound-induced platelet activation), using flow cytometry. Blood was collected from the wound site 1 and 2 min after the incision. Monoclonal antibodies were used to test for activation of glycoprotein (GP) IIb/IIIa (PAC-1), GPIIb/IIIa ligand binding (anti-ligand-induced binding site 1: anti-LIBS-1), and P-selectin expression (AC1.2). RESULTS: Short-term intersample reliability was very good to excellent for anti-LIBS-1 and AC1.2 (intraclass correlation coefficients 0.79-0.96), but only fair for PAC-1. Patients with restenosis (n = 25) had greater activation in all measures than patients without restenosis (n = 24); the difference was significant for GPIIb/IIIa ligand binding at 1 min (P = 0.03). The correlation between GPIIb/IIIa ligand binding at 1 min and percent stenosis at follow-up was also significant (P = 0.03). Patients taking nitrates had lower activation; after eliminating these patients, GPIIb/IIIa ligand binding was greater among patients with restenosis at both 1 and 2 min (P = 0.04 for both). CONCLUSIONS: The results suggest that increased GPIIb/IIIa ligand binding may be associated with restenosis after coronary stenting. The results also suggest that the wound-induced platelet activation method is a reliable and valid measure of platelet activity.

Lack of independent relationships between left ventricular mass and cardiovascular reactivity to physical and psychological stress in the Coronary Artery Risk Development in Young Adults (CARDIA) Study.

The objective of this study was to determine whether exaggerated blood pressure (BP) reactivity to stress and psychosocial characteristics are related to left ventricular mass (LVM) in a large cohort of young adults. Analyses were conducted with 3,742 participants of the CARDIA study (945 white men, 1,024 white women, 781 black men, and 992 black women), evaluated in 1990 to 1091 with echocardiographic measurement of LVM. Analyses were stratified by gender and race. The relationships of LVM/height2.7 and cardiovascular reactivity to physical and psychological stressors (treadmill exercise, cold pressor, video game, and star-tracing tasks), were examined in both univariate and multivariate analyses adjusting for baseline BP, weight, and other relevant biobehavioral variables. The relationships between LVM and several psychosocial characteristics (hostility, anger suppression, anxiety, depressive symptoms, and education) were also assessed. Systolic blood pressure (SBP) reactivity to exercise was significantly related to LVM in black and white men; LVM was 10% greater among white men with exaggerated (upper quintile) peak exercise SBP than among other white men. SBP reactivity to the cold pressor test was related to LVM in all race/gender groups, although the relationship remained significant only among white men and women in the multivariate analysis. Diastolic blood pressure (DBP) reactivity to the video game was related to LVM only among black men in adjusted analyses. After adjusting for resting BP, weight, and other covariates in linear multiple regression models, SBP reactivity to exercise explained only 3% of the variance in LVM among white men. Otherwise, reactivity to other stressors or psychosocial variables accounted for no more than 1% of the variance in LVM. It was concluded that among a cohort of young adults, blood pressure reactivity to physical and mental stressors did not add substantially to the prediction of LVM when resting BP, weight, and other covariates were taken into account.

Effects of hostility on platelet reactivity to psychological stress in coronary heart disease patients and in healthy controls.

Previous studies have demonstrated a potential relationship between psychological stress and platelet activation, which may serve as a link between stress and myocardial infarction (MI). However, the possibility that personality traits associated with coronary heart disease may affect platelet activation has not been adequately investigated. The effect of a laboratory stressor (Type A Structured Interview (SI) and speech task) on platelet activation was assessed in 14 stable post-MI patients and 15 age-matched healthy men, using a standardized method of measuring plasma beta-thromboglobulin (BTG) levels. BTG levels were increased after the stressor (average change = 2.0 ng/ml, p = .005). Increases in BTG with stress were related to higher SI ratings of Potential for Hostility (r = .53, p = .004) and Type A behavior (r = .43, p = .02) but not to Cook-Medley-rated hostility scores. Increases in norepinephrine levels and in diastolic blood pressure were nonsignificantly related to increases in BTG levels (ps < .10), whereas increases in epinephrine levels were unrelated. Despite ceasing aspirin and other platelet inhibitors for 10 days before testing, individuals taking platelet inhibitors before the study had less change in BTG with stress (p = .05). However, after statistical adjustment for this factor, SI ratings of Potential for Hostility were still strongly related to increases in BTG with stress (adjusted r = .56, p = .002). Contrary to expectations, healthy men tended to have greater change in BTG with stress than post-MI patients (p = .06). These results indicate that acute stress increases BTG levels and that hostility is related to greater platelet reactivity, independent of any long term effects of platelet inhibition.

Psychological predictors of hypertension in the Framingham Study. Is there tension in hypertension?

OBJECTIVE: To test the hypothesis that heightened anxiety, heightened anger intensity, and suppressed expression of anger increase the risk of hypertension, using the Framingham Heart Study. DESIGN: A cohort of men and women without evidence of hypertension at baseline were followed up for 18 to 20 years. Baseline measures of anxiety (tension), anger symptoms, and expression of anger (anger-in and anger-out) were taken, along with biological and behavioral predictors of hypertension (initial systolic blood pressure, heart rate, relative weight, age, hematocrit, alcohol intake, smoking, education, and glucose intolerance). PARTICIPANTS: A total of 1123 initially normotensive persons (497 men, 626 women) were included. Analyses were stratified by age (45 to 59 or > or = 60 years) and gender. MAIN OUTCOME MEASURES: Hypertension was defined as either taking medication for hypertension or blood pressures higher than 160/95 mm Hg at a biennial examination. RESULTS: In univariate analyses, middle-aged men who went on to develop hypertension had greater baseline anxiety levels than men who remained normotensive (P = .04). Older hypertensive men had fewer anger symptoms at baseline (P = .04) and were less likely to hold their anger in (P = .01) than normotensives. In multivariate Cox regression analysis including biological predictors, anxiety remained an independent predictor of hypertension in middle-aged men (P = .02). Among older men, anger symptoms and anger-in did not remain significant predictors in the multivariate analysis. Further analysis showed that only middle-aged men with very high levels of anxiety were at increased risk (relative risk, 2.19; 95% confidence interval, 1.22 to 3.94). No psychological variable predicted hypertension in middle-aged or older women in either univariate or multivariate analyses. CONCLUSIONS: The results indicate that among middle-aged men, but not women, anxiety levels are predictive of later incidence of hypertension.