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PubMed2006

Analysis of cardiovascular disease and kidney outcomes in multidisciplinary chronic kidney disease clinics: complex disease requires complex care models.

PURPOSE OF REVIEW: Chronic kidney disease is recognized as being highly prevalent in the population, and associated with morbidity and mortality relative to the general population. The complexity of patients and the multiplicity of interventions required to maintain health has forced clinicians to develop different models of healthcare delivery. This publication reviews the current literature on specific interventions to reduce progression of chronic kidney disease and cardiovascular disease, and studies the examination of outcomes of patients exposed to different healthcare delivery models. Specifically we examine the rationale and outcomes of those seen in multidisciplinary clinics. RECENT FINDINGS: Current evidence supports the use of rennin-angiotensin system blockers, reduction of blood pressure and proteinuria and phosphate control. Additional less robust studies support the need for attention to anemia, hyperparathryoidism, and other more "kidney specific" risk factors. The attendance of identified chronic kidney disease patients at multidisciplinary clinics appears to improve survival once dialysis is started. Despite aggressive management, not all patients are able to meet clinical targets associated with improved outcomes. SUMMARY: The recognition of the complexity of chronic kidney disease care and the need to develop and test models of care in addition to the single interventions is a challenge for both researchers and clinicians. Current data support the use of multidisciplinary clinics in improving outcomes of referred patients. Future research will help to refine and define appropriate care models for this growing chronic kidney disease population.

Calcium↗
PubMed2005

Vascular nitric oxide and oxidative stress: determinants of endothelial adaptations to cardiovascular disease and to physical activity.

Cardiovascular disease is the single leading cause of death and morbidity for Canadians. A universal feature of cardiovascular disease is dysfunction of the vascular endothelium, thus disrupting control of vasodilation, tissue perfusion, hemostasis, and thrombosis. Nitric oxide bioavailability, crucial for maintaining vascular endothelial health and function, depends on the processes controlling synthesis and destruction of nitric oxide as well as on the sensitivity of target tissue to nitric oxide. Evidence supports a major contribution by oxidative stress-induced destruction of nitric oxide to the endothelial dysfunction that accompanies a number of cardiovascular disease states including hypertension, diabetes, chronic heart failure, and atherosclerosis. Regular physical activity (exercise training) reduces cardiovascular disease risk. Numerous studies support the hypothesis that exercise training improves vascular endothelial function, especially when it has been impaired by preexisting risk factors. Evidence is emerging to support a role for improved nitric oxide bioavailability with training as a result of enhanced synthesis and reduced oxidative stress-mediated destruction. Molecular targets sensitive to the exercise training effect include the endothelial nitric oxide synthase and the antioxidant enzyme superoxide dismutase. However, many fundamental details of the cellular and molecular mechanisms linking exercise to altered molecular and functional endothelial phenotypes have yet to be discovered. The working hypothesis is that some of the cellular mechanisms contributing to endothelial dysfunction in cardiovascular disease can be targeted and reversed by signals associated with regular increases in physical activity. The capacity for exercise training to regulate vascular endothelial function, nitric oxide bioavailability, and oxidative stress is an example of how lifestyle can complement medicine and pharmacology in the prevention and management of cardiovascular disease.

Adaptation, Physiological↗
PubMed1993

Serum cholesterol in young men and subsequent cardiovascular disease.

BACKGROUND: The increased risk of cardiovascular disease associated with higher serum cholesterol levels in middle-aged persons has been clearly established, but there have been few opportunities to examine a potential link between serum cholesterol levels measured in young men and clinically evident premature cardiovascular disease later in life. METHODS: We performed a prospective study of 1017 young men (mean age, 22 years) followed for 27 to 42 years to quantify the risk of cardiovascular disease and total mortality associated with serum cholesterol levels during early adult life. The mean serum cholesterol level at entry was 192 mg per deciliter (5.0 mmol per liter). RESULTS: During a median follow-up of 30.5 years, there were 125 cardiovascular-disease events, 97 of which were due to coronary heart disease. The serum cholesterol level at base line was strongly associated with the incidence of events related to coronary heart disease and cardiovascular disease, as well as to total mortality and mortality due to cardiovascular disease. The risks were similar whether the events occurred before or after the age of 50. In a proportional-hazards analysis adjusted for age, body-mass index (the weight in kilograms divided by the square of the height in meters), the level of physical activity, coffee intake, change in smoking status, and the incidence of diabetes and hypertension during follow-up, a difference in the serum cholesterol level at base line of 36 mg per deciliter (0.9 mmol per liter)--the difference between the 25th and 75th percentiles of cholesterol level in the study population at base line--was associated with an increased risk of cardiovascular disease (relative risk, 1.72; 95 percent confidence interval, 1.39 to 2.14), coronary heart disease (relative risk, 2.01; 95 percent confidence interval, 1.59 to 2.53), and mortality due to cardiovascular disease (relative risk, 2.02; 95 percent confidence interval, 1.23 to 3.32). A difference in the base-line serum cholesterol level of 36 mg per deciliter was significantly associated with an increased risk of death before the age of 50 (relative risk, 1.64; 95 percent confidence interval, 1.03 to 2.61), but not with the overall risk of death (relative risk, 1.21; 95 percent confidence interval, 0.93 to 1.58). CONCLUSIONS: These findings indicate a strong association between the serum cholesterol level measured early in adult life in men and cardiovascular disease in midlife.

Adult↗
PubMed1995

Subclinical disease as an independent risk factor for cardiovascular disease.

BACKGROUND: The primary aim of the present study was to determine the relation between measures of subclinical cardiovascular disease and the incidence of clinical cardiovascular disease among 5201 adults 65 years of age or older who were participating in the Cardiovascular Health Study. METHODS AND RESULTS: A new method of classifying subclinical disease at baseline examination in the Cardiovascular Health Study included measures of ankle-brachial blood pressure, carotid artery stenosis and wall thickness, ECG and echocardiographic abnormalities, and positive response to the Rose Angina and Claudication Questionnaire. Participants were followed for an average of 2.39 years (maximum, 3 years). For participants without evidence of clinical cardiovascular disease at baseline, the presence of subclinical disease compared with no subclinical disease was associated with a significant increased risk of incident total coronary heart disease including CHD deaths and nonfatal MI and angina pectoris for both men and women. For individuals with subclinical disease, the increased risk of total coronary heart disease was 2.0 for men and 2.5 for women, and the increased risk of total mortality was 2.9 for men and 1.7 for women. The increased risk changed little after adjustment for other risk factors, including lipoprotein levels, blood pressure, smoking, and diabetes. CONCLUSIONS: The measurement of subclinical disease provides an approach for identifying high-risk older individuals who may be candidates for more active intervention to prevent clinical disease.

Aged↗
PubMed1996

Socio-economic factors in cardiovascular disease.

INCREASING RATES OF CARDIOVASCULAR DISEASE AMONG LOWER SOCIO-ECONOMIC GROUPS: Evidence from English studies indicates that not only is cardiovascular disease mortality more common among lower social classes, but there is an inverse social gradient. For example, one study showed that the higher the employment grade the lower the mortality, a finding that also held for most of the major causes of death. Between the early 1970s and early 1980s, coronary heart disease mortality rates declined by 15% in men in non-manual occupations and increased by 1% in manual occupations. Differences could not be attributed to medical care alone. This widening social gap in mortality rates has continued, and a similar pattern has been observed in other countries. EAST-WEST DIFFERENCES: Through the 1950s and 1960s, cardiovascular mortality and life expectancy were similar in central European countries on both sides of the iron curtain. From the late 1960s, however, there was marked divergence in mortality rates with improvement in the West and stagnation or deterioration in the countries of central and eastern Europe. After 1989 with the lifting of the iron curtain, Russia and some other eastern countries began to show a marked deterioration in life expectancy. In Russia life expectancy appears to have declined from 63 to 59 years in about 4 years. CURRENT RESEARCH ON MULTIPLE PATHWAYS: As we understand more of the biological mechanisms underlying the pathogenesis of cardiovascular disease, the more it becomes clear that these processes have multiple influences driving them. In our current research, we are using a model of potential pathways linking socio-economic status to diabetes mellitus and coronary heart disease in an attempt to confirm or refute the links in this model.

Behavior↗
PubMed2004

Periodontal disease and biomarkers related to cardiovascular disease.

Periodontal disease is a chronic infection of the gums characterized by a loss of attachment between the tooth and bone, and by bone loss. We evaluated cross-sectionally the association between periodontal disease and C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor necrosis factor receptors 1 and 2. The final sample consisted of 468 men (ages 47-80 yrs), participating in the Health Professional Follow-up Study, who provided blood and were free of CVD, diabetes, and cancer. In multivariate regression models controlling for age, cigarette smoking, alcohol intake, physical activity, and aspirin intake, self-reported periodontal disease was associated with significantly higher levels of CRP (30% higher among periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher). Based on our data, periodontal disease showed significant associations with biomarkers of endothelial dysfunction and dyslipidemia, which may potentially mediate the association between periodontal and cardiovascular disease.

Age Factors↗
PubMed1979

Cardiovascular disease and trace metals.

Cardiovascular disease is a major cause of morbidity and mortality in the U.K. and other developed countries. In the U.K., mortality from coronary heart disease has increased progressively over the past 25 years, particularly in males. This paper examines the possible role of trace metals in the development of cardiovascular disease, with particular reference to the effects of cobalt, cadmium and lead in myocardial disease, atherosclerosis and hypertension. It is concluded that cobalt is an unimportant factor in community levels of cardiovascular disease, that cadmium has striking effects on blood pressure in animals and that there is some evidence for an association between environmental lead and high blood pressure.

Blood Pressure↗
PubMedDate not supplied

[Immunology of cardiovascular diseases in children].

Cardiovascular diseases in children are most usually caused by the disturbances in the immune system. The disease very often occurs after infections with a secondary immune response to the cardiovascular system; lately there are more frequently secondary responses after surgical treatment on the heart. Passive transfer of maternal antibodies through the placenta results particularly in congenital complete heart block in newborns and infants. Rheumatic heart disease is the most usual manifestation of humoral and cell-mediated reactivity in patients. Due to cardiotoxicity of eosinophils, endomyocardial diseases with eosinophilia are developed. There is a problem of arteritis of the coronary arteries as part of some allergic diseases, especially of Kawasaki disease. Immunologically mediated diseases of the cardiovascular system in children need further studies.

Cardiovascular Diseases↗
PubMed1987

Geochemistry, soils and cardiovascular diseases.

The hypothesis is presented that deficiencies or excesses in the content or availability of trace elements in rocks and soils, or in water flowing through them, may be a possible cause of certain chronic diseases, including cardiovascular ones. The geographic distribution of cardiovascular diseases is often associated with geochemical differences. This trend is particularly evident in the United States and in Europe, with higher rates for cardiovascular mortality in areas underlain by soils that are poor in most essential trace elements. Confirmation of this trend is found in connection with the degree of mineralization of local water supplies. Areas that are served by soft waters usually show higher rates of cardiovascular mortality and other forms of cardiovascular pathology, compared with the areas that are served by hard waters. Such a negative association between water hardness and cardiovascular pathology is evident in many countries, both industrialized and developing ones.

Cardiovascular Diseases↗
PubMed1998

Novel risk factors for vascular disease: the homocysteine hypothesis of cardiovascular disease.

The possibility that modest elevations in the level of blood homocysteine (hyperhomocysteinaemia) could contribute to cardiovascular disease arose from investigation of patients with rare, severe homocysteine elevations caused by cystathionine beta-synthase deficiency. Such patients often had thromboembolic events before the age of 30 years. Since the established cardiovascular risk factors could only partly account for the occurrence and severity of vascular disease in the general population, other risk factors had to exist, and homocysteine elevation seemed to be a possible candidate. Australian case-control studies identified an association between mild homocysteine elevation and early-onset coronary disease, and also with chronic renal failure. Patients in the latter group have a high prevalence of unexplained vascular disease and particularly high homocysteine levels. Such elevations in levels of homocysteine in vascular patients could usually be normalised by daily supplementation with folic acid (1-5 mg) while in patients with chronic renal failure 5 mg of folic acid daily markedly reduced the increased concentrations of homocysteine. These initial observations have been confirmed by many investigators and biologically plausible mechanisms for homocysteine-induced vascular dysfunction, and particularly endothelial dysfunction, have been identified. However, associations between hyperhomocysteinaemia and other risk factors, such as smoking and hypertension, have also been documented and need to be controlled for when assessing any increase in risk that homocysteine may independently confer. Although it has been established that lowering the greatly elevated blood homocysteine levels in homocystinuria, due to cystathione beta-synthase deficiency, unquestionably reduces cardiovascular risk, it remains to be determined whether normalising mild homocysteine elevation could reduce cardiovascular risk. Trials to test this possibility have been initiated and others are planned.

Cardiovascular Diseases↗
PubMed2002

Studying genotype-phenotype relationships: cardiovascular disease as an example.

Cardiovascular disease is a multifactorial disorder resulting from the complex interaction of a plethora of both environmental and genetic factors. The "candidate gene" approach aims at identifying the genes contributing to cardiovascular disease assessing their entire polymorphic spectrum and the consequences of their combination in appropriate large association studies. In view of the sequence data available for the entire human genome, candidate sequences will more easily be traced and located in their chromosomal context. More powerful sequencing devices are available and will hopefully give reliable and reproducible data not only on the nucleotide sequence diversity in different populations throughout candidate regions of the human genome. The choice and the assessment of disease-related or intermediate phenotypes, especially in clinical settings, will be again more crucial in the future when the knowledge of gene sequence variation significantly increases. Identification of relevant genes and genetic variants involved in the different pathophysiological steps leading to cardiovascular disease may considerably improve our understanding of the mechanisms of the disease course. This may help to identify high-risk individuals and groups or subgroups in whom specific therapeutic interventions are indicated or necessary, leading to an individually adapted clinical management.

Cardiovascular Diseases↗
PubMed2006

Non-alcoholic fatty liver disease and increased risk of cardiovascular disease.

Non-alcoholic fatty liver disease (NAFLD) is present in up to one-third of the general population and in the majority of patients with cardio-metabolic risk factors such as abdominal obesity, type 2 diabetes and other components of the metabolic syndrome (MetS). Currently, the importance of NAFLD and its relationship to the MetS is increasingly recognized, and this has stimulated an interest in the possible role of NAFLD in the development of cardiovascular disease (CVD). Indeed, the impact of NAFLD on CVD risk deserves particular attention in view of the implications for screening/surveillance strategies in this growing number of patients. Recent evidence suggests that the severity of liver histology in NAFLD patients is closely associated with markers of early atherosclerosis such as greater carotid artery wall thickness and lower endothelial flow-mediated vasodilation independently of classical risk factors and components of the MetS. Moreover, NAFLD is associated with greater overall mortality and independently predicts the risk of future CVD events. Overall, the current body of evidence strongly suggests that NAFLD is likely to be associated with increased CVD risk, and raises the possibility that NAFLD may be not only a marker but also an early mediator of atherosclerosis.

Atherosclerosis↗
PubMed1995

Social class and cardiovascular disease--an update.

Cardiovascular disease is associated with a low social class position in numerous epidemiological studies. The mechanisms behind this finding are not fully known, although several factors may be of importance (e.g. lifestyle, neuroendocrine regulation, foetal deprivation). A better understanding of the biological basis for class-related disease may facilitate efforts in preventive medicine related to cardiovascular health.

Cardiovascular Diseases↗
PubMed2005

[A review of epidemiological studies about pulse wave velocity for prevention of cardiovascular disease].

Early arteriosclerosis can be prevented by medication and life style changes. However, late cardiac disease, called cardiovascular disease, could be fatal or have severe sequelae. Therefore, it is important to develop a method for early diagnosis. Since no symptoms become evident until endothelial/vascular dysfunction, a simple and sensitive diagnostic method using a biological parameter needs to be developed for prevention and medical treatment. Pulse wave velocity (PWV) is a noninvasive and simple measure for evaluating arterial wall stiffness and several studies have indicated this is a good marker for vascular damage, although not all results were consistent. This review concerns the following three aspects: 1. PWV as a marker of vascular damage 2. PWV as a prognostic predictor 3. Brachial-ankle PWV (baPWV) Blood pressure is strongly related with PWV, along with BMI, fasting blood glucose, and cholesterol. However, no relation was rated cigarette smoking. While many reports have shown that rise of PWV can serve as a prognostic predictor of disease, the situation with baPWV remains unclear. It is to be expected that improvements in methods for PWV will greatly contribute to primary and secondary prevention in the future.

Aging↗
PubMed2005

Cardiovascular disease in children with chronic kidney disease.

In children with end-stage renal disease (ESRD), cardiovascular disease (CVD) mortality has not changed for the past 3 decades. Cardiac disease remains the second most common cause of death. Recent data demonstrate a high incidence and prevalence of traditional and chronic kidney disease (CKD)-related CVD risk factors in children. Early markers of cardiomyopathy, such as left ventricular hypertrophy (LVH) and left ventricular dysfunction (LV dysfunction), and early markers of atherosclerosis, such as increased carotid artery intima-media thickness (IMT) and carotid arterial wall stiffness, are frequently found in this patient population. Early identification of modifiable risk factors and treatment of asymptomatic CVD might lead to decrease of cardiovascular morbidity and mortality in young adults who developed CKD during childhood.

Adolescent↗
PubMed2001

Evidence-based nutrition and cardiovascular disease in the Asia-Pacific region.

The Asia-Pacific region is undergoing a major change in both food and health patterns, with a connection between the two more than likely. Evidence for certain traditional Asia-Pacific foods as protective agents against chronic non-communicable disease and cardiovascular disease (CVD), in particular, is growing at a time when their usage diminishes. The nature of the evidence to establish relevant Asia-Pacific food-health linkages will include randomised placebo-controlled clinical trials, but is much more extensive and meaningful. Okinawans have probably achieved one of the most successful food cultures from a health point of view and serve as a reference point for the Asia-Pacific region. The expert working party has produced, in November 2000, the 'Okinawan Recommendations on Nutrition and CVD in the Asia-Pacific region'.

Asia↗
PubMed2003

The action of ovarian hormones in cardiovascular disease.

The incidence of cardiovascular disease (CAD) differs between men and women, in part because of differences in risk factors and hormones. This sexual dimorphism means a lower incidence in atherosclerotic diseases in premenopausal women, which subsequently rises in postmenopausal women to eventually equal that of men. These observations point towards estrogen and progesterone playing a lifetime protective role against CAD in women. As exogenous estrogen and estrogen plus progesterone preparations produce significant reductions in low-density lipoprotein (LDL) cholesterol levels and significant increases in high-density lipoprotein (HDL) cholesterol, this should in theory lower the risk of CAD. However, results from oral contraceptive (OC) use and combined estrogen and progesterone hormone replacement therapy (HRT) have suggested that hormone replacement regimes do not provide cardiovascular protection. In fact, depending on the preparation and the presence or absence of genetic risk factors, an increased risk of cardiovascular diseases such as venous thrombosis, myocardial infarction (MI) and stroke have been observed. Interestingly, in the majority of studies the increase in risk was highest in the first year, after which an increase in risk was not observed, and in some studies a lower risk of CAD was evident after four or five years of exogenous hormone administration. While the debate continues about the merits of HRT, and several good reviews exist on the statistics of CAD in relation to exogenous hormones, we have decided to review the literature to piece together the physiological actions of estrogen and progesterone preparations on the individual mechanistic components leading to CAD; namely, the altered endothelium and the haemostatic balance between coagulation and fibrinolysis. We present possible mechanisms for how HRT and OCs protect against MI in the absence of cardiovascular risk factors but increase the incidence of MI in their presence. We also speculate on the roles played by hormones on the short- and long-term risks of cardiovascular disease.

Blood Coagulation↗