The increased prevalence of cardiovascular disease risk factors in sub-Saharan Africa has increased the incidence of cardiovascular disease in this region but whether psychological distress contributes to this observed increased risk remains largely unclear.
The aim of this study was to investigate the association between cardiovascular function and psychological distress in urbanised black South African men (n = 101) and women (n = 99).
Resting cardiovascular variables were obtained by making use of the Finometer device and 24-hour ambulatory blood pressure (BP) measurements with the Cardiotens apparatus. Psychological questionnaires assessed the perception of health (General Health questionnaire) and depression status (DSM-IV criteria). The resting ECG (NORAV PC-1200) was used to determine left ventricular hypertrophy (LVH) by making use of the Cornell product. Confounders included age, obesity, alcohol intake, smoking and physical activity.
The hypertensive groups were overweight, with lower vascular compliance and higher LVH (only men) compared to the normotensive groups. In hypertensive men, perception of health (somatic symptoms) was positively associated with blood pressure, while in hypertensive women it was associated with heart rate. Major depression was associated with LVH in hypertensive men and mean arterial pressure in hypertensive women. LVH and depression showed odds ratios of 1.02 (95% CI: 0.997–1.05) and 1.15 (95% CI: 1.01–1.32), respectively, in predicting hypertension in women.
Psychological distress was associated with higher blood pressure in hypertensive African men but also with the development of left ventricular hypertrophy in hypertensive African men and women.
depression; perception of health; cardiovascular function; urbanised Africans; hypertension
There is strong evidence of an association between chronic kidney disease (CKD) and cardiovascular disease. To date, however, proof that a reduction in glomerular filtration rate (GFR) is a causative factor in cardiovascular disease is lacking. Kidney donors comprise a highly screened population without risk factors such as diabetes and inflammation, which invariably confound the association between CKD and cardiovascular disease. There is strong evidence that increased arterial stiffness and left ventricular hypertrophy and fibrosis, rather than atherosclerotic disease, mediate the adverse cardiovascular effects of CKD. The expanding practice of live kidney donation provides a unique opportunity to study the cardiovascular effects of an isolated reduction in GFR in a prospective fashion. At the same time, the proposed study will address ongoing safety concerns that persist because most longitudinal outcome studies have been undertaken at single centers and compared donor cohorts with an inappropriately selected control group.
The reduction in GFR accompanying uninephrectomy causes (1) a pressure-independent increase in aortic stiffness (aortic pulse wave velocity) and (2) an increase in peripheral and central blood pressure.
This is a prospective, multicenter, longitudinal, parallel group study of 440 living kidney donors and 440 healthy controls. All controls will be eligible for living kidney donation using current UK transplant criteria. Investigations will be performed at baseline and repeated at 12 months in the first instance. These include measurement of arterial stiffness using applanation tonometry to determine pulse wave velocity and pulse wave analysis, office blood pressure, 24-hour ambulatory blood pressure monitoring, and a series of biomarkers for cardiovascular and bone mineral disease.
These data will prove valuable by characterizing the direction of causality between cardiovascular and renal disease. This should help inform whether targeting reduced GFR alongside more traditional cardiovascular risk factors is warranted. In addition, this study will contribute important safety data on living kidney donors by providing a longitudinal assessment of well-validated surrogate markers of cardiovascular disease, namely, blood pressure and arterial stiffness. If any adverse effects are detected, these may be potentially reversed with the early introduction of targeted therapy. This should ensure that kidney donors do not come to long-term harm and thereby preserve the ongoing expansion of the living donor transplant program (NCT01769924).
The inverse association between socioeconomic status and cardiovascular disease is well documented. We examined whether the impact of health counselling on cardiovascular risk factors in middle-aged men differed according to socioeconomic status.
We used data from a community based study assessing the risk for cardiovascular disease among middle-aged men in Helsinki, Finland. Traditional cardiovascular disease risk factors were measured and cardiovascular disease risk was assessed by a modified risk tool used in the North Karelia project (CVD Risk Score). Those men with increased risk for cardiovascular disease at their baseline visit in 2006 received lifestyle counselling. After two years these high-risk men were invited to a follow-up visit. The same measurements and risk assessments were repeated.
Based on the CVD Risk Score there were significant differences between the groups at baseline (p = 0.001) and at follow-up (p<0.001) with the highest scores in the lowest educational group. There were no significant differences in traditional cardiovascular risk factors according to educational attainment between groups either at baseline or at follow-up. Baseline lifestyle characteristics differed between the groups regarding use of soft fat (p = 0.019). All groups responded positively to lifestyle counselling.
The present study showed that lifestyle counselling is feasible in high-risk middle-aged men and lifestyle intervention works in all educational groups. Interestingly the traditional risk factors did not show improvement, but the risk score improved. From a practical point of view our findings stress the importance of using risk score calculators in health counselling instead of looking at individual cardiovascular disease risk factors.
OBJECTIVE: To examine the association between birth weight and non-fatal adult cardiovascular disease while controlling for potential confounders such as socioeconomic group and adult lifestyle. DESIGN: Retrospective self report of birth weight in an ongoing longitudinal cohort of nurses followed up by postal questionnaire every two years. SETTING: Nurses' health study, a cohort of 121700 women followed up since 1976. MAIN OUTCOME MEASURES: Non-fatal cardiovascular disease, including myocardial infarction, coronary revascularisation, and stroke. RESULTS: Among the 70297 women free of cardiovascular disease at baseline who reported birth weight in the 1992 questionnaire there were 1309 first cases of non-fatal cardiovascular disease. Increasing birth weight was associated with decreasing risk of non-fatal cardiovascular disease. There were 1216 first cases of non-fatal cardiovascular disease among women who were singletons and had been born full term; their relative risks adjusted for several cardiovascular risk factors were 1.49 (95% confidence interval 1.05 to 2.10) for birth weight < 2268 g (< 5 lb 0 oz); 1.25 (0.98 to 1.61) for birth weight 2268-2495 g (5 lb 0 oz to 5 lb 8 oz); 1.12 (0.98 to 1.27) for birth weight > 2495-3175 g (> 5 lb 8 oz to 7 lb 0 oz); 1.00 (referent) for birth weight > 3175-3856 g (> 7 lb 0 oz to 8 lb 8 oz); 0.96 (0.80 to 1.15) for birth weight > 3856-4536 g (> 8 lb 8 oz to 10 lb 0 oz); and 0.68 (0.46 to 1.00) for birth weight > 4536 g (> 10 lb 0 oz) (P value for trend = 0.0004). The inverse trend was apparent for both coronary heart disease and stroke. CONCLUSIONS: These data provide strong evidence of an association between birth weight and adult coronary heart disease and stroke.
► Associations of exposures with mortality may be confounded by existing ill health. ► We used a son's height as an instrument for parents’ height to avoid confounding. ► Parents of taller sons had lower cardiovascular and respiratory disease mortality. ► Parents of taller sons had higher mortality from cancer. ► Previous studies of height are not substantially confounded by existing ill health.
Height is associated with mortality from many diseases, but it remains unclear whether the association is causal or due to confounding by social factors, genetic pleiotropy,1 or existing ill-health. The authors investigated whether the association of height with mortality is causal by using a son's height as an instrumental variable (IV) for parents’ height among the parents of a cohort of 1,036,963 Swedish men born between 1951 and 1980 who had their height measured at military conscription, aged around 18, between 1969 and 2001. In a two-sample IV analysis adjusting for son's age at examination and secular trends in height, as well as parental age, and socioeconomic position, the hazard ratio (HR) for all-cause paternal mortality per standard deviation (SD, 6.49 cm) of height was 0.96 (95% confidence interval (CI): 0.95, 0.96). The results of IV analyses of mortality from all causes, cardiovascular disease (CVD), respiratory disease, cancer, external causes and suicide were comparable to those obtained using son's height as a simple proxy for own height and to conventional analyses of own height in the present data and elsewhere, suggesting that such conventional analyses are not substantially confounded by existing ill-health.
IV, instrumental variable; HR, hazard ratio; SD, standard deviation; CI, confidence interval; CVD, cardiovascular disease; BMI, body mass index; SEP, socioeconomic position; CHD, coronary heart disease; Body height; Mortality; Confounding factor; Causality; Cohort studies
Chronic kidney disease (CKD) and its associated morbidity pose a worldwide health problem. As well as risk of endstage renal disease requiring renal replacement therapy, cardiovascular disease is the leading cause of premature death among the CKD population. Proteinuria is a marker of renal injury that can often be detected earlier than any tangible decline in glomerular filtration rate. As well as being a risk marker for decline in renal function, proteinuria is now widely accepted as an independent risk factor for cardiovascular morbidity and mortality. This review will address the prognostic implications of proteinuria in the general population as well as other specific disease states including diabetes, hypertension and heart failure. A variety of pathophysiological mechanisms that may underlie the relationship between renal and cardiovascular disease have been proposed, including insulin resistance, inflammation, and endothelial dysfunction. As proteinuria has evolved into a therapeutic target for cardiovascular risk reduction in the clinical setting we will also review therapeutic strategies that should be considered for patients with persistent proteinuria.
proteinuria; albuminuria; microalbuminuria; cardiovascular risk
BACKGROUND. Where health professionals and patients hold similar views of a problem, health outcomes may be better. AIM. The aims of this paper were to document how attenders at primary care cardiovascular screening clinics perceived their risks of coronary heart disease prior to screening; the degree of similarity between perceived level of risk and an epidemiologically derived risk score; and the relative importance assigned to individual risk factors by subjects compared with those assigned by the risk score. METHOD: These issues were investigated in 3725 middle aged men and women who accepted an invitation to attend health screening as part of the British family heart study. RESULTS. Overall, there was a tendency for subjects to be optimistic (37%) rather than pessimistic (21%) when judging their risk of coronary heart disease. Nevertheless, there were strong significant associations between perceived risk and the levels of individual risk factors, particularly personal and family medical history and body mass index. There was also a strong association with the overall risk score though a large minority (31%) held views of their risk of coronary heart disease that were quite different from those based upon the epidemiologically derived index of risk. Respondents accorded greater importance to smoking and parental death from coronary heart disease and less importance to cholesterol level and blood pressure than did the risk score. CONCLUSION. Possible explanations for the observed disagreement are over-optimism or the relative importance given to individual risk factors. The relationships between patients' perceptions of risk and the epidemiological indices likely to be espoused by health professionals are important in understanding the difficulties in communication that might arise in offering lifestyle advice after screening for cardiovascular risk.
Posttraumatic stress disorder (PTSD) is related to acute coronary syndrome (ACS; i.e., myocardial infarction or unstable angina) recurrence and poor post-ACS adherence to medical advice. Since risk perceptions are a primary motivator of adherence behaviors, we assessed the relationship of probable PTSD to ACS risk perceptions in hospitalized ACS patients (n = 420). Participants completed a brief PTSD screen 3–7 days post-ACS, and rated their 1-year ACS recurrence risk relative to other men or women their age. Most participants exhibited optimistic bias (mean recurrence risk estimate between “average” and “below average”). Further, participants who screened positive for current PTSD (n = 15) showed significantly greater optimistic bias than those who screened negative (p < 0.05), after adjustment for demographics, ACS severity, medical comorbidities, depression, and self-confidence in their ability to control their heart disease. Clinicians should be aware that psychosocial factors, and PTSD in particular, may be associated with poor adherence to medical advice due to exaggerated optimistic bias in recurrence risk perceptions.
PTSD; cardiovascular disease; acute coronary syndrome; myocardial infarction; risk perceptions; secondary prevention
Aortic stiffness is a strong predictor of cardiovascular disease endpoints. Cross-sectional studies have shown associations of various cardiovascular risk factors with aortic pulse wave velocity, a measure of aortic stiffness, but the long-term impact of these factors on aortic stiffness is unknown.
In 3,769 men and women from the Whitehall II cohort, a wide range of traditional and novel cardiovascular risk factors were determined at baseline (1991–1993) and aortic pulse wave velocity was measured at follow-up (2007–2009). The prospective associations between each baseline risk factor and aortic pulse wave velocity at follow-up were assessed through sex stratified linear regression analysis adjusted for relevant confounders. Missing data on baseline determinants were imputed using the Multivariate Imputation by Chained Equations.
Among men, the strongest predictors were waist circumference, waist-hip ratio, heart rate and interleukin 1 receptor antagonist, and among women, adiponectin, triglycerides, pulse pressure and waist-hip ratio. The impact of 10 centimeter increase in waist circumference on aortic pulse wave velocity was twice as large for men compared with women (men: 0.40 m/s (95%-CI: 0.24;0.56); women: 0.17 m/s (95%-CI: −0.01;0.35)), whereas the opposite was true for the impact of a two-fold increase in adiponectin (men: −0.30 m/s (95%-CI: −0.51;−0.10); women: 0.61 m/s (95%-CI: −0.86;−0.35)).
In this large prospective study, central obesity was a strong predictor of aortic stiffness. Additionally, heart rate in men and adiponectin in women predicted aortic pulse wave velocity suggesting that strategies to prevent aortic stiffening should be focused differently by sex.
Traditional atherosclerotic risk factors predict long-term cardiovascular disease events but are poor predictors of near-term events.
To determine whether elevated levels of d-dimer and biomarkers of inflammation were more closely associated with near-term than long-term mortality in patients with lower-extremity peripheral arterial disease (PAD) and whether greater increases in biomarker levels were associated with higher mortality rates during the first year after the increase than during later years.
Prospective cohort study with a mean follow-up of 3.4 years.
Academic medical center.
377 men and women with PAD.
Mortality within 1 year after biomarker measurement, 1 to 2 years after biomarker measurement, and 2 to 3 years after biomarker measurement. Cox regression analyses were used to evaluate associations of biomarkers levels and changes in biomarkers with cardiovascular and all-cause mortality. Hazard ratios were calculated for each 1-unit increase in log1.5(biomarker level). Analyses were adjusted for age, sex, race, comorbid conditions, ankle–brachial index, and other confounders.
Seventy-six patients (20%) died during follow-up. Higher levels of d-dimer, C-reactive protein, and serum amyloid A were associated with higher all-cause mortality among patients who died within 1 year after biomarker measurement (hazard ratio, 1.20 [95% CI, 1.08 to 1.33], 1.13 [CI, 1.05 to 1.21], and 1.12 [CI, 1.04 to 1.20], respectively; P < 0.001, P < 0.001, and P = 0.003) and among patients who died 1 to 2 years after biomarker measurement (hazard ratio, 1.14 [CI, 1.02 to 1.27], 1.15 [CI, 1.06 to 1.24], and 1.13 [CI, 1.04 to 1.24]; P = 0.022, P = 0.001, and P = 0.005]). However, higher levels of each biomarker were not associated with all-cause mortality for deaths occurring 2 to 3 years after biomarker measurement. Similar results were observed for cardiovascular mortality. Greater increases in each biomarker were associated with higher all-cause and cardiovascular mortality during the following year.
The small number of deaths limited the statistical power of the analyses.
Among persons with PAD, circulating levels of d-dimer and inflammatory markers are higher in the 1 to 2 years before death than in periods more remote from death. Increasing levels of d-dimer and inflammatory biomarkers are independently associated with higher mortality in persons with PAD.
Cardiovascular inflammation is a key contributor to the development of atherosclerosis and the prediction of cardiovascular events among healthy women. An emerging literature suggests biomarkers of inflammation vary by geography of residence at the state-level, and are associated with individual-level socioeconomic status. Associations between cardiovascular inflammation and state-level socioeconomic conditions have not been evaluated. The study objective is to estimate whether there are independent associations between state-level socioeconomic conditions and individual-level biomarkers of inflammation, in excess of individual-level income and clinical covariates among healthy women.
The authors examined cross-sectional multilevel associations among state-level socioeconomic conditions, individual-level income, and biomarkers of inflammation among women (n = 26,029) in the Women's Health Study, a nation-wide cohort of healthy women free of cardiovascular diseases at enrollment. High sensitivity C-reactive protein (hsCRP), soluble intercellular adhesion molecule-1 (sICAM-1) and fibrinogen were measured between 1993 and 1996. Biomarker levels were examined among women within quartiles of state-level socioeconomic conditions and within categories of individual-level income.
The authors found that favorable state-level socioeconomic conditions were correlated with lower hsCRP, in excess of individual-level income (e.g. state-level real per capital gross domestic product fixed effect standardized Βeta coefficient [Std B] -0.03, 95% CI -0.05, -0.004). Individual-level income was more closely associated with sICAM-1 (Std B -0.04, 95% CI -0.06, -0.03) and fibrinogen (Std B -0.05, 95% CI -0.06, -0.03) than state-level conditions.
We found associations between state-level socioeconomic conditions and hsCRP among healthy women. Personal household income was more closely associated with sICAM-1 and fibrinogen than state-level socioeconomic conditions. Additional research should examine these associations in other cohorts, and investigate what more-advantaged states do differently than less-advantaged states that may influence levels of cardiovascular inflammation among healthy women.
C-reactive protein; Geography; Income; Inflammation; Multilevel analysis; Poverty; Socioeconomic factors; Women's health
People with type 2 diabetes mellitus are at high risk for cardiovascular disease. In some studies, the mortality rate among people with this condition has been equivalent to that among people with cardiovascular disease. We compared cardiovascular mortality between incident cases of diabetes and cardiovascular disease.
The study population was part of a random sample of 4376 men from Quebec, Canada, aged 35 to 64 years, who did not have cardiovascular disease in 1974 and who were followed until 1998. Three groups of incident cases were identified: diabetes without cardiovascular disease, first cardiovascular event (myocardial infarction, unstable angina or stroke) without diabetes, and both cardiovascular disease and diabetes. These cases were age-matched to a control group without diabetes or cardiovascular disease.
During the 24-year follow-up period, new diabetes without cardiovascular disease was documented in 137 men. A first cardiovascular event without diabetes was documented in 527 men. Relative to the 627 controls, men with 1 of the 2 diseases of interest had higher cardiovascular mortality (age-adjusted relative risk [RR] 3.11, 95% confidence interval [CI] 1.96–4.92) for those with diabetes and 4.46 (95% CI 3.15–6.30) for those with cardiovascular disease). However, within the first 5 years after diagnosis, men with cardiovascular disease had higher cardiovascular mortality than men with diabetes (age-adjusted RR 2.03, 95% CI 1.01–4.08).
Men with isolated type 2 diabetes and men with isolated cardiovascular disease had similar cardiovascular mortality rates several years after initial diagnosis of either condition. These findings reinforce the need to prevent and optimally manage diabetes and cardiovascular disease.
Self-reported health perceptions such as physical distress and quality of life are suggested independent predictors of mortality and morbidity in patients with established cardiovascular disease. This study examined the associations between these factors and three years incidence of cardiovascular events in a population of elderly men with long term hyperlipidemia.
We studied observational data in a cohort of 433 men aged 64–76 years from a prospective, 2 × 2 factorial designed, three-year interventional trial. Information of classical risk factors was obtained and the following questionnaires were administered at baseline: Hospital Anxiety and Depression Scale, Physical Symptom Distress Index and Life Satisfaction Index. The occurrence of cardiovascular death, myocardial infarction, cerebrovascular incidences and peripheral arterial disease were registered throughout the study period. Continuous data with skewed distribution was split into tertiles. Hazard ratios (HR) were calculated from Cox regression analyses to assess the associations between physical distress, quality of life and cardiovascular events.
After three years, 49 cardiovascular events were registered, with similar incidence among subjects with and without established cardiovascular disease. In multivariate analyses adjusted for age, smoking, systolic blood pressure, serum glucose, HADS-anxiety and treatment-intervention, physical distress was positively associated (HR 3.1, 95% CI 1.2 – 7.9 for 3rd versus 1st tertile) and quality of life negatively associated (HR 2.6, 95% CI 1.1–5.8 for 3rd versus 1st tertile) with cardiovascular events. The association remained statistically significant only for physical distress (hazard ratio 2.8 95% CI 1.2 – 6.8, p < 0.05) when both variables were evaluated in the same model.
Physical distress, but not quality of life, was independently associated with increased risk of cardiovascular events in an observational study of elderly men predominantly without established cardiovascular disease.
Trial registration: NCT00764010
To evaluate the risk of cardiovascular disease in patients with rheumatoid arthritis exposed to glucocorticoids.
Retrospective analysis of exposure to glucocorticoids in a prospective cohort of 353 patients with rheumatoid arthritis followed from June 2001 up to November 2011 for incident cardiovascular disease in a hospital-based outpatient cohort in the Netherlands. Hazard ratios with 95%-confidence intervals were calculated for the association between different types of exposure to glucocorticoids and incident cardiovascular disease. Associations were adjusted for demographics, cardiovascular risk factors and disease related parameters.
Recent and current exposure to glucocorticoids were associated with incident cardiovascular disease, as was a longer duration of exposure and cumulative exposure to glucocorticoids. Adjustment for disease activity and severity negated the association.
In observational studies the finding of incident cardiovascular disease in patients with rheumatoid arthritis exposed to glucocorticoids is strongly confounded by indication due to high disease activity. The adverse cardiovascular effects of glucocorticoids might be balanced by positive effects working through inflammation control.
Positive association between cardiovascular diseases and osteoporosis is important because it concerns two major public health problems. Men and women with cardiovascular diseases (including severe abdominal aortic calcification (AAC) and peripheral arterial disease) tend to have lower areal and volumetric bone mineral density (BMD) as well as faster bone loss, although findings vary according to skeletal site. On one hand, severe forms of cardiovascular diseases (heart failure, myocardial infarction, hypertension, severe AAC) are associated with higher risk of osteoporotic fracture, especially hip fracture. This link was found in the studies based on healthcare databases and the cohort studies. On the other hand, low BMD, history of fragility fracture, vitamin D deficit and increased bone resorption are associated with higher risk of major cardiovascular events (myocardial infraction, stroke, cardiovascular mortality). Moreover, osteocalcin secreted by osteoblasts may be involved in the regulation of energetic and cardiovascular metabolism. The association between both pathologies depends partially on the shared risk factors, and also on the mechanisms that are involved in the regulation of bone and cardiovascular metabolism. Interpretation of the data should take into account methodological limitations: representativeness of the cohorts, quality of the registers and the information obtained from questionnaires, severity of diseases, number of events (statistical power) and their temporal closeness, availability of the information on potential confounders. It seems that patients with severe form of osteoporosis would benefit from assessment of the cardiovascular status and vice versa. However, official guidelines for the clinical practice are still lacking.
STUDY OBJECTIVE: To examine associations between measures of work stress (that is, the combination of high effort and low reward) and cardiovascular risk factors. DESIGN: Cross sectional first screening of a prospective cohort study. SETTING AND PARTICIPANTS: The study was conducted among 5720 healthy employed men and women living in the greater Stockholm area aged 19-70 years. All analyses were restricted to subjects with complete data (n = 4958). The investigation of associations between indicators of effort-reward imbalance and cardiovascular risk factors was restricted to the age group 30-55 years (n = 3427). MAIN RESULTS: Subjects reporting high effort and low reward at work had a higher prevalence of well known risk factors for coronary heart disease. After adjustment for relevant confounders, associations between a measure of extrinsic effort and reward (the effort-reward ratio) and hypertension (multivariate prevalence odds ratio (POR) 1.62- 1.68), increased total cholesterol (upper tertile 220 mg/dl)(POR = 1.24) and the total cholesterol/high density lipoprotein(HDL)- cholesterol ratio (upper tertile 4.61)(POR 1.26-1.30) were found among men. Among women a measure of high intrinsic effort (immersion) was related to increased low density lipoprotein (LDL)-cholesterol (upper tertile 130 mg/dl)(POR 1.37-1.39). Analyses of variance showed increasing mean values of LDL cholesterol with an increasing degree of the effort-reward ratio among men and increased LDL-cholesterol among women with high levels of intrinsic effort (upper tertile of immersion). CONCLUSIONS: Findings lend support to the hypothesis that effort-reward imbalance represents a specific constellation of stressful experience at work related to cardiovascular risk. The relation was not explained by relevant confounders (for example, lack of physical exercise, body weight, cigarette smoking).
Kidney disease and hypertension commonly coexist, yet the direction of their association is still debated.
To evaluate whether early kidney dysfunction, measured by serum cystatin C levels and urinary albumin excretion, predates hypertension in adults without clinically recognized kidney or cardiovascular disease.
Observational cohort study using data from 2000 to 2005.
The MESA (Multi-Ethnic Study of Atherosclerosis), a community-based study of subclinical cardiovascular disease in adults age 45 to 84 years.
2767 MESA participants without prevalent hypertension, cardiovascular disease, or clinically recognized kidney disease (an estimated glomerular filtration rate <60 mL/min per 1.73 m2 or microalbuminuria).
Cystatin C was measured by using a nephelometer, and urinary albumin and creatinine were measured from a spot morning collection. The primary outcome was incident hypertension, defined as systolic blood pressure of at least 140 mm Hg, diastolic blood pressure of at least 90 mm Hg, or use of an antihypertensive medication.
During a median follow-up of 3.1 years, 19.7% of the cohort (545 participants) developed hypertension. After adjustment for established hypertension risk factors, each 15-nmol/L increase in cystatin C was associated with a statistically significant 15% greater incidence of hypertension (P = 0.017). The highest sex-specific quartile of urinary albumin–creatinine ratio was associated with a statistically insignificant 16% greater incidence of hypertension (P = 0.192) compared with the lowest quartile. No statistical evidence suggested a multiplicative interaction.
Unmeasured characteristics may have confounded observed associations of kidney markers with hypertension. Follow-up was relatively short. Hypertension that may have occurred between study visits or hypertension that was not captured by standard cuff measurements may have been missed.
Differences in kidney function, indicated by cystatin C levels, are associated with incident hypertension among individuals without clinical kidney or cardiovascular disease. These population-based findings complement experimental work implicating early kidney damage in the pathogenesis of essential hypertension.
Perturbed sleep might contribute to cardiovascular disease by accelerating atherosclerosis. Sleep is poor in Alzheimer caregivers who are also a group at increased cardiovascular risk. Objective: To test the hypothesis that impaired sleep relates to elevated levels of biomarkers of atherosclerosis in community-dwelling elderly and that this association would possibly be stronger in caregivers than in non-caregiving controls.
We studied 97 Alzheimer caregivers and 48 non-caregiving controls (mean age 71 ± 8 years, 72% women) who underwent wrist actigraphy at their homes. Measures of objective sleep were averaged across 3 consecutive nights. The Pittsburgh Sleep Quality Index was administered by an interviewer to rate subjective sleep quality. Morning fasting blood samples were collected to determine measures of inflammation, coagulation and endothelial dysfunction.
There were independent associations between decreased subjective sleep quality and increased levels of fibrin D-dimer (p = 0.022, ΔR2 = 0.029) and von Willebrand factor antigen (p = 0.029, ΔR2 = 0.034) in all participants. Percent sleep (p = 0.025) and subjective sleep quality (p = 0.017) were lower in caregivers than in controls. In caregivers, the correlation between decreased percent sleep and elevated levels of interleukin-6 (p = 0.042, ΔR2 = 0.039) and C-reactive protein (p < 0.10, ΔR2 = 0.027) was significantly stronger than in controls.
Perceived impairment in sleep related to increased coagulation activity and endothelial dysfunction in all participants, whereas objectively impaired sleep related to inflammation activity in caregivers. The findings provide one explanation for the increased cardiovascular risk in elderly poor sleepers and dementia caregivers in particular.
Cardiovascular disease; Coagulation; Inflammation; Psychological stress; Sleep
C-reactive protein (CRP), a marker of inflammation, has been associated with cardiovascular disease. Risk of cardiovascular disease is increased in migraineurs with aura. Results from a clinical report, case control- and a cohort study suggest that CRP is elevated in migraineurs compared to nonmigraineurs. We examined the proposed association in a case-control study nested within two large population-based studies.
The relationship between migraine and CRP (hs-CRP) was studied in 5906 men and women age 55.0 (±8.5) years in the Reykjavik Study and 1345 men and women age 27.7 (±5.5) years from the Reykjavik Study for the Young. A modified version of the International Headache Society criteria was used to categorize people into migraineurs (2 or more symptoms) or nonmigraineurs. Migraineurs with visual or sensory symptoms were further defined as having migraine with aura (MA) or without aura (MO).
Multivariable-adjusted CRP levels were similar in migraineurs and nonmigraineurs (0.83 vs. 0.79mg/l, p=0.44) for men and (0.87 vs. 0.87mg/l, p=0.90) for women. When further stratified by migraine aura and age, no differences were found between nonmigraineurs, MO and MA among men. In women MO, CRP was borderline higher than among nonmigraineurs and MA (1.01mg/l vs. 0.81 and 0.75mg/l, p=0.08 and p=0.08) in age group 19–34 years but significantly lower in age group 60–81 years (0.52mg/l vs. 1.07 and 1.01mg/l, p=0.007 and p=0.03).
CRP levels were not increased among migraine sufferers compared to nonmigraineurs. Older women migraineurs without aura had lower CRP values compared to nonmigraineurs and migraineurs with aura.
C-reactive protein (hs-CRP); cardiovascular disease; epidemiology; inflammation; migraine
Atherosclerotic cardiovascular disease is a major health problem around the world. Obesity is a primary risk factor for atherosclerosis and is associated with increased morbidity and mortality of cardiovascular diseases. However, the precise molecular pathways underlying this close association remain poorly understood. Adipokines are cytokines, chemokines and hormones secreted by adipose tissue that couple the regulation of lipid accumulation, inflammation, and atherogenesis, and therefore serve to link obesity with cardiovascular disorders. Obesity-related disorders including metabolic syndrome, diabetes, atherosclerosis, hypertension, and coronary artery disease are associated with dysregulated adipokine(s) expression. Recent studies demonstrate the proinflammatory effects as well as atherogenic properties of adipokines. Adipokines also participate in the regulation of endothelial function, which is an early event in atherosclerosis. By contrast, adiponectin, an adipocyte-derived hormone, exerts anti-inflammatory, anti-atherogenic and vascular protective effects. Furthermore, there is an interactive association among adipokines, by which adipokines reciprocally regulate each other’s expression. Understanding this interplay may reveal plausible mechanisms for treating atherosclerosis and coronary heart disease by modulating adipokine(s) expression. In this review, we discuss insights into the role and the therapeutic potential of adipokines as mediators of atherosclerosis.
Obesity; Inflammation; Adipokines; Endothelial function; Atherosclerosis
Although television viewing time is detrimentally associated with intermediate cardiovascular risk factors, the relationship with incident total (i.e. combined fatal and non-fatal) cardiovascular disease (CVD), non-fatal CVD and coronary heart disease is largely unknown. This study examined whether television viewing time is associated with these three outcomes, independently of physical activity energy expenditure and other confounding variables.
A population-based cohort of 12,608 men and women (aged 61.4±9.0), free from stroke, myocardial infarction and cancer at baseline in 1998–2000 were followed up until 2007 (6.9±1.9 years). Participants self-reported education, smoking, alcohol use, antihypertensive, lipid lowering and antidepressant medication, disease history, total energy intake, sleep duration, physical activity and television viewing. BMI, waist circumference, blood pressure, triglycerides, HDL cholesterol and glycated haemoglobin (HbA1c) were measured by standardized procedures; a clustered metabolic risk score was constructed. Every one hour/day increase in television viewing was associated with an increased hazard for total (HR = 1.06, 95%CI = 1.03–1.08; 2,620 cases), non-fatal CVD (HR = 1.06, 95%CI = 1.03–1.09; 2,134 cases), and coronary heart disease (HR = 1.08, 95%CI = 1.03–1.13; 940 cases), independent of gender, age, education, smoking, alcohol, medication, diabetes status, CVD family history, sleep duration and physical activity energy expenditure. Energy intake, BMI, waist circumference, blood pressure, triglycerides, HDL cholesterol, HbA1c and the clustered metabolic risk score only partially mediated these associations.
These results indicate that the most prevalent leisure time (sedentary) behaviour, television viewing, independently contributes to increased CVD risk. Recommendations on reducing television viewing time should be considered.
Although erectile dysfunction (ED) has been associated with heart disease risk factors and large-vessel lower extremity arterial disease (LEAD), no community-based studies have reported the association between ED and small-vessel LEAD, despite the similar size of the arteries affected. We examined whether small-vessel LEAD is associated with ED, and whether this association is independent of cardiovascular risk factors and medications.
Methods and Results
Community-dwelling men, average age 71, completed the International Index of Erectile Function-5 questionnaire and had measurements recorded of toe-brachial index (TBI), a measure of small-vessel LEAD. TBI, 12 cardiovascular risk factors, and medications were used as categorical predictors in age-adjusted bivariate analyses, and as continuous covariates in multivariable linear regression analyses, to determine their independent association with severity of ED.
In the age-adjusted categorical model, the level of TBI (low, medium, high) was associated with the severity of ED (β = 0.364; 95% CI: 0.102, 0.625). In the final multivariable linear regression model, which controlled for age and systolic blood pressure, lower TBI (i.e., more severe small-vessel LEAD) was significantly and independently associated with more severe ED (β = 0.422; 95% CI: 0.019, 0.826).
The severity of small-vessel LEAD is significantly and independently associated with the severity of ED. The mechanism for this association remains to be determined, but these data are compatible with the hypothesis that concurrent ED and small-vessel LEAD signify a diffuse microvascular process involving multiple small-vessel arterial beds.
erectile dysfunction; lower extremity arterial disease; cardiovascular risk factors; epidemiology
Previous studies have suggested that subclinical abnormalities in TSH levels are associated with detrimental effects on the cardiovascular system.
To determine the relationship between baseline thyroid status and incident atrial fibrillation, incident cardiovascular disease, and mortality in older men and women not taking thyroid medication.
Design, Setting, and Patients
Participants were 3,233 US community-dwelling individuals aged 65 or over with baseline serum TSH levels who were enrolled in 1989–1990 in the Cardiovascular Health Study (CHS), a large, prospective cohort study.
Main Outcome Measures
Incident atrial fibrillation, coronary heart disease, cerebrovascular disease, cardiovascular death, and all-cause death assessed through June, 2002.
Analyses are reported for four groups defined according to thyroid function test results: subclinical hyperthyroidism, euthyroidism, subclinical hypothyroidism, and overt hypothyroidism. Individuals with overt thyrotoxicosis were excluded due to small numbers. Eighty-two percent of participants were euthyroid, 15% had subclinical hypothyroidism, 1.6% were overtly hypothyroid, and 1.5% had subclinical hyperthyroidism. After exclusion of those with prevalent atrial fibrillation, individuals with subclinical hyperthyroidism had a greater incidence of atrial fibrillation compared to the euthyroid group (67 events vs. 31 events per 1,000 person-years; p<.001, and an adjusted hazard ratio [AHR] of 1.98; 95% confidence interval [CI] 1.29–3.03). No differences were seen between the subclinical hyperthyroidism group and euthyroid group for incident coronary heart disease, cerebrovascular disease, cardiovascular death, or all-cause death. Likewise, there were no differences between the subclinical hypothyroidism or overt hypothyroidism groups and the euthyroid group for cardiovascular outcomes or mortality. Specifically, individuals with subclinical hypothyroidism had an AHR of 1.07 (95% CI, 0.90–1.28) for incident coronary heart disease.
Our data show an association between subclinical hyperthyroidism and the development of atrial fibrillation, but do not support the hypothesis that unrecognized subclinical hyperthyroidism or subclinical hypothyroidism is associated with other cardiovascular disorders or mortality.
Thyroid disease; cardiovascular disease; subclinical hyperthyroidism; subclinical hypothyroidism; cholesterol; atrial fibrillation; myocardial infarction; mortality; elderly; Cardiovascular Health Study
Objective To investigate whether varenicline is associated with an increased risk of serious cardiovascular events compared with another drug used for smoking cessation, bupropion.
Design Nationwide historical cohort study.
Setting Denmark, 2007-10.
Participants New users of varenicline (n=17 926) and bupropion (n=17 926).
Main outcome measures Individual level data on dispensed drug prescriptions, cardiovascular events, and potential confounders were linked between registries. Cox regression was used to estimate hazard ratios of cardiovascular events in analyses matched for propensity score. The primary outcomes at six months after start of treatment were acute coronary syndrome, ischaemic stroke, and cardiovascular death analysed individually and as a composite of any major event.
Results There were 57 major cardiovascular events among varenicline users (6.9 cases per 1000 person years) compared with 60 events among bupropion users (7.1 cases per 1000 person years); the hazard ratio for any major event was 0.96 (95% confidence interval 0.67 to 1.39). Varenicline use was not associated with an increased risk of acute coronary syndrome (1.20, 0.75 to 1.91), ischaemic stroke (0.77, 0.40 to 1.48), and cardiovascular death (0.51, 0.13 to 2.02). In subgroup analyses, the risk of any major cardiovascular event was not significantly different between patients with and without a history of cardiovascular disease (1.24 (0.72 to 2.12) and 0.83 (0.51 to 1.36), respectively; P=0.29).
Conclusions This cohort study found no increased risk of major cardiovascular events associated with use of varenicline compared with bupropion for smoking cessation. On the basis of the upper confidence limit, the data allowed the exclusion of a 40% increased risk of the composite outcome of any major cardiovascular event. While the estimates were less precise for specific outcomes, any differences would be small in absolute terms.
This study aimed at investigating whether cardiovascular risk factors and their impact on total risk estimation differ between men and women.
Cross-sectional cohort study.
Finnish cardiovascular risk subjects (n = 904) without established cardiovascular disease, renal disease, or known diabetes.
Main outcome measures
Ankle-brachial index (ABI), estimated glomerular filtration rate (eGFR), oral glucose tolerance test, and total cardiovascular risk using SCORE risk charts.
According to the SCORE risk charts, 27.0% (95% CI 23.1–31.2) of the women and 63.1% (95% CI 58.3–67.7) of the men (p < 0.001) were classified as high-risk subjects. Of the women classified as low-risk subjects according to SCORE, 25% had either subclinical peripheral arterial disease or renal insufficiency.
The SCORE system does not take into account cardiovascular risk factors typical in women, and thus underestimates their total cardiovascular risk. Measurement of ABI and eGFR in primary care might improve cardiovascular risk assessment. especially in women.
Ankle-brachial index; cardiovascular risk estimation; gender difference; glucose disorders; renal function