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Primary and secondary prevention of cardiovascular disease in the elderly.

Cardiovascular disease is the commonest cause of death and hospitalization in patients 65 years of age or older. The main offenders among the cardiovascular disorders in this age are CHD and hypertension. Many non-pharmacologic and pharmacologic measures in the middle-aged persons have confirmed for many years the effectiveness of primary and secondary prevention. Multiple intervention trials in the recent years have also demonstrated the effectiveness of these measures in patients 65 years of age and older. A summary of the main primary and secondary non-pharmacologic and pharmacologic measures that have been proven to be effective and useful in elderly patients has been presented with particular attention to hypertension and CHD. It also has been demonstrated that elderly patients have the capacity to follow the instructions of their physicians and that, as younger patients, they respond to these measures.

Aged↗

Description and validation of a Markov model of survival for individuals free of cardiovascular disease that uses Framingham risk factors.

BACKGROUND: Estimation of cardiovascular disease risk is increasingly used to inform decisions on interventions, such as the use of antihypertensives and statins, or to communicate the risks of smoking. Crude 10-year cardiovascular disease risk risks may not give a realistic view of the likely impact of an intervention over a lifetime and will underestimate of the risks of smoking. A validated model of survival to act as a decision aid in the consultation may help to address these problems. This study aims to describe the development of such a model for use with people free of cardiovascular disease and evaluates its accuracy against data from a United Kingdom cohort. METHODS: A Markov cycle tree evaluated using cohort simulation was developed utilizing Framingham estimates of cardiovascular risk, 1998 United Kingdom mortality data, the relative risk for smoking related non-cardiovascular disease risk and changes in systolic blood pressure and serum total cholesterol total cholesterol with age. The model's estimates of survival at 20 years for 1391 members of the Whickham survey cohort between the ages of 35 and 65 were compared with the observed survival at 20-year follow-up. RESULTS: The model estimate for survival was 75% and the observed survival was 75.4%. The correlation between estimated and observed survival was 0.933 over 39 subgroups of the cohort stratified by estimated survival, 0.992 for the seven 5-year age bands from 35 to 64, 0.936 for the ten 10 mmHg systolic blood pressure bands between 100 mmHg and 200 mmHg, and 0.693 for the fifteen 0.5 mmol/l total cholesterol bands between 3.0 and 10.0 mmol/l. The model significantly underestimated mortality in those people with a systolic blood pressure greater than or equal to 180 mmHg (p = 0.006). The average gain in life expectancy from the elimination of cardiovascular disease risk as a cause of death was 4.0 years for all the 35 year-old men in the sample (n = 24), and 1.8 years for all the 35 year-old women in the sample (n = 32). CONCLUSIONS: This model accurately estimates 20-year survival in subjects from the Whickham cohort with a systolic blood pressure below 180 mmHg.

Adult↗

Endothelial function in health and disease: new insights into the genesis of cardiovascular disease.

The vascular endothelium secretes factors that not only modulate blood vessel tone, but also participate in the development and progression of atherosclerosis through their effects on platelet adhesion and aggregation, thrombogenicity, and cell proliferation. Altered activities of these substances in patients with risk factors for cardiovascular disease (e.g., hypercholesterolemia, hypertension, diabetes, aging, postmenopausal status, smoking, and infections) appear to underlie the atherosclerotic process. There is increasing evidence from both preclinical studies and clinical trials that nitric oxide (NO) plays a pivotal role in the pathophysiology of arteriosclerosis. This review describes the role of NO in human health and disease and summarizes strategies currently being used to measure and improve endothelial dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗

Molecular genetic analysis in mild hyperhomocysteinemia: a common mutation in the methylenetetrahydrofolate reductase gene is a genetic risk factor for cardiovascular disease.

Mild hyperhomocysteinemia is an established risk factor for cardiovascular disease. Genetic aberrations in the cystathionine beta-synthase (CBS) and methylenetetrahydrofolate reductase (MTHFR) genes may account for reduced enzyme activities and elevated plasma homocysteine levels. In 15 unrelated Dutch patients with homozygous CBS deficiency, we observed the 833T-->C (I278T) mutation in 50% of the alleles. Very recently, we identified a common mutation (677C-->T; A-->V) in the MTHFR gene, which, in homozygous state, is responsible for the thermolabile phenotype and which is associated with decreased specific MTHRF activity and elevated homocysteine levels. We screened 60 cardiovascular patients and 111 controls for these two mutations, to determine whether these mutations are risk factors for premature cardiovascular disease. Heterozygosity for the 833T-->C mutation in the CBS gene was observed in one individual of the control group but was absent in patients with premature cardiovascular disease. Homozygosity for the 677C-->T mutation in the MTHFR gene was found in (15%) of 60 cardiovascular patients and in only 6 (approximately 5%) of 111 control individuals (odds ratio 3.1 [95% confidence interval 1.0-9.2]). Because of both the high prevalence of the 833T-->C mutation among homozygotes for CBS deficiency and its absence in 60 cardiovascular patients, we may conclude that heterozygosity for CBS deficiency does not appear to be involved in premature cardiovascular disease. However, a frequent homozygous mutation in the MTHFR gene is associated with a threefold increase in risk for premature cardiovascular disease.

Alleles↗

Vitamin D and its analogues: do they protect against cardiovascular disease in patients with kidney disease?

BACKGROUND: Patients with chronic kidney disease (CKD) are at high risk for cardiovascular disease, and despite recent advances in hypertension control, anemia management, and dialysis adequacy, mortality remains high. Improved understanding of nontraditional risk factors, including those present at early phases in CKD, may lead to novel therapeutic strategies. CKD has been demonstrated to be an independent risk factor for cardiovascular disease in the general population, but data are lacking as to the associated potential abnormalities that occur in association with reduced glomerular filtration rate (GFR), which may contribute to this increased risk. Data are accumulating regarding the role of abnormalities of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) in cardiovascular disease. Vitamin D deficiency is present even in the early stages of CKD. Vitamin D plays a central role in calcium-phosphorus homeostasis, regulation of PTH, and formation and maintenance of bone. However, until recently, vitamin D has not been considered to have a biologic role in CKD beyond mineral regulation, or has been considered as a negative factor contributing to soft tissue and cardiovascular calcification. In light of recent observational studies showing an association of vitamin D therapy and survival benefit in hemodialysis patients, the effects of vitamin D on cardiovascular system have become a heavily debated issue. METHODS: A Medline search was performed to identify relevant literature describing the role of vitamin D in the pathogenesis of cardiovascular disease. Both the experimental and clinical literatures in English were reviewed. RESULTS: The accumulating published data demonstrate both associative relationships and mechanisms for biologic plausibility. The following three potential mechanisms may be important for the protective effects of vitamin D against cardiovascular disease mortality: vitamin D can inhibit various aspects of inflammation, which have been established as a key pathogenic mechanism in atherosclerosis; vitamin D exerts an antiproliferative effect on myocardial cell hypertrophy and proliferation, which underlies the pathogenesis of congestive heart failure; and vitamin D acts as a negative endocrine regulator for the renin-angiotensin system, which itself plays an important independent role in hypertension and cardiovascular health. CONCLUSION: Vitamin D deficiency might be an underestimated nonclassical risk factor for cardiovascular disease in CKD. Based on a review of the evidence, from both basic science and clinical studies, this article supports the possible protective role of vitamin D beyond its effect on mineral metabolism, and suggests the need for ongoing evaluation of the role of vitamin D in cardiovascular health in the CKD population.

Cardiovascular Diseases↗

Effects of a school-based intervention to reduce cardiovascular disease risk factors in elementary-school children: the Cardiovascular Health in Children (CHIC) study.

OBJECTIVE: To test a classroom-based intervention to reduce cardiovascular disease risk factors in elementary school children. STUDY DESIGN: This was a randomized, controlled field trial in 12 schools across North Carolina, stratified by geographic region and urban/rural setting. Subjects were 1274 third and fourth graders (48% boys). The intervention, taught by regular classroom and physical education teachers, provided all children an 8-week exercise program and 8 weeks of classes on nutrition and smoking. Data were analyzed at the school level with survey regression models and at the individual level with multivariate analysis of variance and analysis of covariance models; 95% confidence intervals were computed. RESULTS: Children in the intervention group had significantly greater knowledge (7.9% more correct) and a significant increase in self-reported physical activity than children in the control group. Trends for the intervention group were a reduction in total cholesterol level (-5.27 mg/dl), an increase in aerobic power, a reduction in body fat, and smaller rise in diastolic blood pressure than control children. CONCLUSIONS: This classroom-based, public health approach improved children's cardiovascular disease risk profiles; it is practical and fairly easy to incorporate into the school day. All children directly receive the potential benefits of the intervention without a risk of labeling. This program can improve health knowledge, habits, and health outcomes of young children at a time when health habits are being formed.

Cardiovascular Diseases↗

Prevalence of cardiovascular diseases among older adults. The Cardiovascular Health Study.

The Cardiovascular Health Study is a population-based longitudinal study of 5,201 adults aged 65 years and older. Prevalences of myocardial infarction, angina pectoris, congestive heart failure, peripheral artery disease, stroke, and transient ischemic attack were ascertained between June 1989 and May 1990 in participants recruited from Forsyth County, North Carolina; Washington County, Maryland; Sacramento County, California; and Pittsburgh, Pennsylvania. A medical history was taken to obtain self-reports of prevalent disease. For all participants, use of nitrates was ascertained to document angina, electrocardiograms were used to document prevalent myocardial infarction, and ankle-arm blood pressure studies were used to document peripheral artery disease. Self-reports of disease that were not confirmed by examination findings were further investigated by examination of medical records. Reported disease that was confirmed by examination findings or by medical records was classified as "definite." Disease that was documented by examination, but not reported by the participant, was classified as "unreported." The prevalence rates of definite myocardial infarction and angina were 11% and 15%, respectively, among men aged 65-69 years, 18% and 17% among men aged 80-84 years, 4% and 8% among women aged 65-69 years, and 3% and 13% among women aged 80-84 years. Twenty-three percent of men and 38% of women with electrocardiographic evidence of myocardial infarction did not report it. These results suggest that prevalent disease estimates based only on self-report may underestimate the prevalence of cardiovascular diseases in older Americans.

Age Factors↗

Dietary recommendations for coronary heart disease prevention: implications for non-cardiovascular diseases.

In order to reduce the lipoprotein-related risk of coronary heart disease, nutritional recommendations have been formulated for use by communities prone to atherosclerosis and its complications. As such recommendations are potentially of widespread application they require careful scrutiny to assess possible risks as well as benefits. Epidemiological, clinical and experimental data concerning relationships between these nutrients and non-cardiovascular diseases are reviewed with emphasis on cancer mortality. Changes in intake of fats, including polyunsaturated fat, of cholesterol, carbohydrate, fibre, sodium and beta-carotene are discussed, and evidence of a relationship between serum cholesterol concentration and cancer is examined. These considerations offer reasonable reassurance as to the safety of recent dietary recommendations for the reduction of coronary heart disease.

Carotenoids↗

Crucial role of interferon-gamma and stimulated macrophages in cardiovascular disease.

Inflammation and immune activation are crucially involved in the pathogenesis of atherosclerosis and cardiovascular disease. Accordingly, markers of inflammation such as fibrinogen, ferritin, C-reactive protein or neopterin are found in patients with vascular diseases, correlating strongly with the extent of disease and predicting disease progression. Neopterin formation by human monocyte-derived macrophages and dendritic cells is induced by the pro-inflammatory cytokine interferon-gamma, which is released by activated T-lymphocytes. Human macrophages are centrally involved in plaque formation, and interferon-gamma and macrophages are also of importance in the development of oxidative stress for antimicrobial and antitumoural defence within the cell-mediated immune response. Interferon-gamma also stimulates the enzyme indoleamine-2,3-dioxygenase, which degrades tryptophan to kynurenine. Again, macrophages are the most important cell type executing this enzyme reaction, but also other cells like dendritic cells, endothelial cells or fibroblasts can contribute to the depletion of tryptophan. Likewise, enhanced tryptophan degradation was reported in patients with coronary heart disease and was found to correlate with enhanced neopterin formation. In chronic diseases such as in cardiovascular disease, biochemical reactions induced by interferon-gamma may have detrimental consequences for host cells. In concert with other pro-inflammatory cytokines, interferon-gamma is the most important trigger for the formation and release of reactive oxygen species (ROS). Chronic ROS-production leads to the depletion of antioxidants like vitamin C and E and glutathione, with a consequence that oxidative stress develop. Oxidative stress plays a major role in the atherogenesis and progression of cardiovascular disease, and it may also account for the irreversible oxidation of other oxidation-sensitive substances like B-vitamins (e.g. folic acid and B12). They are essential cofactors in homocysteine-methionine metabolism. Associations between moderate hyperhomocysteinaemia and cellular immune activation are found in several diseases including coronary heart disease, and data indicate that hyperhomocysteinaemia may develop as a consequence of immune activation. Homocysteine accumulation in the blood is established as an independent risk factor for cardiovascular disease. Homocysteine itself has the capacity to further enhance oxidative stress. Interferon-gamma appears to be a central player in atherogenesis and in the development and progression of cardiovascular disease. Anti-inflammatory and immunosuppressive treatment (e.g. with non-steroidal anti-inflammatory drugs or statins) may among other consequences, also contribute to a slow-down of the adverse effects of interferon-gamma.

Animals↗

Erectile dysfunction is a marker for cardiovascular disease: results of the minority health institute expert advisory panel.

INTRODUCTION: Cardiovascular disease and its related comorbidities are associated with significant morbidity and mortality and affect a disproportionately large number of African Americans and Hispanics. The prevalence of cardiovascular disease is increasing worldwide, which underscores the urgency to improve methods of prevention and early detection. AIM: To develop a risk assessment and management algorithm for primary care patients with erectile dysfunction (ED) that facilitates diagnosis, early intervention, and prevention of cardiovascular disease. METHODS: The Minority Health Institute (MHI) convened an Expert Advisory Panel of cardiologists and urologists to design a new practice model algorithm that uses ED as a clinical tool for early identification of men with systemic vascular disease. A draft of the algorithm was presented at a national symposium and comments from symposium participants were considered in the development of the final algorithm. MAIN OUTCOME MEASURES AND RESULTS: Erectile dysfunction is common and has long been considered a secondary complication of cardiovascular disease, diabetes, hypertension, and dyslipidemia. However, a growing body of evidence challenges this view, suggesting instead that ED is an early manifestation of atherosclerosis and a precursor to systemic vascular disease. Endothelial dysfunction is the etiologic factor linking ED and cardiovascular disease. CONCLUSIONS: The recognition of ED as an early sign of systemic cardiovascular disease offers an opportunity for prevention, particularly in high-risk and underserved minority populations. The MHI algorithm stipulates that all men 25 years old and older regardless of sexual dysfunction complaints should be asked about ED. The presence of ED should prompt an aggressive assessment for cardiovascular risk and occult systemic vascular disease.

Algorithms↗

Coping process theory: a tool to reduce stress and cardiovascular disease.

1. Associations exist between stress and cardiovascular disease. This article presents the coping process theory as a possible strategy to reduce the incidence of cardiovascular disease. 2. The occurrence of coronary heart disease may be reduced by using the coping process to manage stress in the workplace. If the disease is present, coping with the stress of having the disorder diminishes its recurrence. 3. Social support is a valuable coping resource; its association with cardiovascular disease is demonstrated.

Adaptation, Psychological↗

Gender, ethnicity, and cardiovascular disease.

Although the influence of gender and ethnicity on cardiovascular disease has been understudied, cardiovascular nurse researchers have contributed significantly to the existing body of knowledge. This article distinguishes between the constructs of "gender versus sex'' and "ethnicity versus race,'' acknowledging that the terms are often used interchangeably in research. A sampling of the substantial contributions of cardiovascular nurse researchers related to gender and ethnicity in the areas of symptoms of cardiovascular disease; risk factors and prevention; delay in seeking care, diagnosis, and treatment; recovery and outcomes; and cardiac rehabilitation is highlighted. Recommendations for future research include publishing research data by gender and ethnicity subgroups even though statistical comparisons may not be feasible, and increasing cardiovascular disease research in minority populations such as Asian Americans, Pacific Islanders, Native Americans, and Hispanics. Finally, we challenge cardiovascular nurse researchers to shift from the documentation of disparities toward designing and testing of interventions to eliminate health disparities.

Black or African American↗

[The role of aspirin in the primary prevention of cardiovascular disease].

For persons without cardiovascular disease, the benefit of aspirin in primary prevention has been controversial until the recent publication of several major randomized controlled trials. Since then, several medical societies recommend that clinicians discuss aspirin prevention with adults at high cardiovascular risk. Patients with low cardiovascular risk are unlikely to benefit from aspirin, as potential harms (hemorrhagic strokes, gastrointestinal bleedings) may outweigh benefits. Aspirin should be recommended in primary prevention only in patients with a 10-year cardiovascular risk > or = 10% or in diabetic patients aged > or = 40 years with a concomitant cardiovascular risk factor, after assessing contraindications for aspirin and individual's preferences for the risks and benefits associated with aspirin.

Aspirin↗

Homocysteine lowering with folic acid and vitamin B supplements: effects on cardiovascular disease in older adults.

Cardiovascular disease (CVD) is the leading cause of death in older men and women and contributes significantly to morbidity in later life. Folic acid and other vitamin B deficiencies and elevated total plasma homocysteine levels are associated with increased cardiovascular risk in geriatric patients, but recent studies have questioned the importance of these risk factors in older people. Data on the effects of homocysteine-lowering therapy (e.g. folic acid and vitamin B supplements) on surrogate CVD endpoints, such as atherosclerotic progression, endothelial function, inflammation and hypercoagulation, are conflicting. Findings from randomised clinical trials using clinical CVD outcomes show that folic acid and vitamin B supplements may not provide cardiovascular protection. Furthermore, these findings raise questions about whether the combination of folic acid and B vitamins may actually be harmful. Other large randomised clinical trials are underway to help clarify the role of folic acid and vitamin B supplements in CVD prevention in older people. Data to date do not support use of homocysteine-lowering therapies in either middle-aged or older adults.

Adult↗

Childhood maltreatment as a risk factor for adult cardiovascular disease and depression.

BACKGROUND: Traumatic experiences in childhood are linked to adult depression and cardiovascular disease. Depression is twice as common in women than men, and depression after cardiovascular events is more common in women than men. However, sex differences in these relationships have not been comprehensively investigated using a nationally representative sample in which demographic factors related to these illnesses can be controlled. METHOD: Data come from the Part 2 sample of the U.S. National Comorbidity Survey, a nationally representative sample containing over 5000 adults. Relationships between childhood maltreatment (sexual abuse, physical abuse, neglect), adult depression (DSM-III-R), and cardiovascular disease were examined using multiple logistic regression models with a specific emphasis on the evaluation of sex differences. RESULTS: Childhood maltreatment was associated with a significant increase in cardiovascular disease for women only and with a significant increase in lifetime depression for both genders. A history of childhood maltreatment removed the natural protection against cardiovascular disease for women and depression for men. Although depression and cardiovascular disease were correlated, depression did not contribute to the prediction of cardiovascular disease in women when controlling for history of childhood maltreatment. CONCLUSIONS: Gender is important in evaluating potential psychiatric and physical correlates of childhood maltreatment. Maltreatment is a potent risk factor for cardiovascular disease in women and for depression in both women and men. Effective clinical assessment should recognize the role of childhood abuse or neglect in adult health and disease. Research on the consequences of childhood maltreatment should focus on both psychiatric and physical outcomes.

Adolescent↗

Pet ownership and risk factors for cardiovascular disease.

OBJECTIVE: To compare risk factors for cardiovascular disease in pet owners and non-owners. DESIGN AND PATIENTS: Accepted risk factors for cardiovascular disease were measured in 5741 participants attending a free, screening clinic at the Baker Medical Research Institute in Melbourne. Blood pressure, plasma cholesterol and triglyceride values were compared in pet owners (n = 784) and non-owners (n = 4957). RESULTS: Pet owners had significantly lower systolic blood pressure and plasma triglycerides than non-owners. In men, pet owners had significantly lower systolic but not diastolic blood pressure than non-owners, and significantly lower plasma triglyceride levels, and plasma cholesterol levels. In women over 40 years old, systolic but not diastolic pressure was significantly lower in pet owners and plasma triglycerides also tended to be lower. There were no differences in body mass index and self-reported smoking habits were similar, but pet owners reported that they took significantly more exercise than non-owners, and ate more meat and "take-away" foods. The socioeconomic profile of the pet owners and non-owners appeared to be comparable. CONCLUSIONS: Pet owners in our clinic population had lower levels of accepted risk factors for cardiovascular disease, and this was not explicable on the basis of cigarette smoking, diet, body mass index or socioeconomic profile. The possibility that pet ownership reduces cardiovascular risk factors should therefore be investigated.

Animals↗

Is cardiovascular disease a risk factor in the development of axonal polyneuropathy?

OBJECTIVES: To determine if cardiovascular disease may be a risk factor in the development of chronic idiopathic axonal polyneuropathy (CIAP). METHODS: In this incidence case-control study, the prevalence of cardiovascular disease and risk factors in 97 patients with CIAP (mean age 67.5 (SD 7.9) years) and the prevalence of neuropathic features in 97 patients with peripheral arterial disease (PAD) (mean age 67.1 (SD 7.3) years) were investigated. The results were compared with those for 96 age and sex matched controls without diagnosed PAD or polyneuropathy (mean age 67.5 (SD 9.1) years). In a randomly chosen subgroup of 23 patients with CIAP, 42 patients with PAD, and 48 controls, an electrodiagnostic investigation was performed. RESULTS: Patients with CIAP more often had manifest cardiovascular disease and cardiovascular risk factors than controls (stroke 18% v 6% of patients, odds ratio (OR) 3.2 (95% confidence interval (CI) 1.8 to 5.9); heart disease 29% v 15%, OR 2.4 (95% CI 1.2 to 4.9); family history of cardiovascular disease 42% v 21%, OR 2.8 (95% CI (1.5 to 5.2); hypertension 56% v 39%, OR 2.0 (95% CI 1.1 to 3.6); hypercholesterolaemia 46% v 21%, OR 3.3 (95% CI 1.5 to 7.3); current smoking 38% v 23%, OR 2.1 (95% CI 1.1 to 3.9)). The prevalence of cardiovascular disease and cardiovascular risk factors was lower than in patients with PAD. Patients with PAD more often had polyneuropathy than controls (15% v 5%, OR 3.3 (95% CI 1.1 to 10.0)). There was a trend towards lower nerve conduction velocities and lower amplitudes on electrodiagnostic investigation compared with controls. CONCLUSION: This study shows that cardiovascular disease and CIAP often coexist, and therefore cardiovascular disease may be a cofactor in the development of CIAP.

Aged↗

Prevention of cardiovascular disease--opportunities for progress.

Steady progress has been made in the prevention of cardiovascular disease. There has been a favorable trend in major risk factor reduction and an average 3% annual decline in cardiovascular disease death rates over the past decade. Yet, CVD death rates still exceed that for many countries and not all segments of the U.S. population have benefited equally. Cardiovascular disease remains the leading cause of death and disability in this country. The role of epidemiologic research and prevention strategies in addressing this issue has been underestimated. Unresolved research questions require further epidemiologic research in order to improve application of known preventive measures and explore other approaches toward the prevention of cardiovascular disease. It is well established that attention to life-style changes and pharmacologic approaches can prevent cardiovascular disease in those at high risk and reduce the likelihood of subsequent cardiac events among patients with known cardiovascular disease. Furthermore, small changes in the distribution of risk factors through community intervention can have tremendous impact on cardiovascular disease morbidity and mortality. Preventive research requires an appropriate framework and plan to satisfy or exceed the needs in keeping with the national goals for Healthy People 2000. The National Heart, Lung, and Blood Institute has addressed this issue by creating a Task Force to develop research priorities for epidemiology and prevention.

Arteriosclerosis↗