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PubMed1998

A review of vitamins A, C, and E and their relationship to cardiovascular disease.

Cardiovascular disease (CVD), particularly in the form of coronary artery disease, is the leading cause of death in the United States. Research in the past 10 years links pathogenic low-density lipoprotein (LDL) modification to oxidation damage by free radicals. This review summarizes the major findings of CVD-related epidemiologic research and clinical trials conducted in the past 5 years on vitamins A, C, and E. Vitamin supplementation behaviors are discussed. In prospective studies, the intake of vitamins A, C, and E has been correlated with lower mortality rates. When recent clinical trials and oxidation studies are analyzed, the weight of evidence suggests that 100-400 IU of daily vitamin E over 2 years or more may be most efficacious in reducing low-density lipoprotein oxidation and positively influencing mortality rates from CVD in primary care. Research also supports vitamin E supplementation in patients with known CAD or a history of transient ischemic attacks. Persons with diabetes or hypertension as well as smokers may benefit from supplemental vitamin C intake. Targeted antioxidant vitamin intake should be included in CVD risk assessment and primary preventive counseling efforts.

Adult↗
PubMed2003

Correlation between inflammatory periodontal diseases and cardiovascular diseases.

AIMS: Since cardiovascular diseases can exhibit a possible connection with chronic periodontal diseases, the aim of the present study was to examine the presence of periodontal impairment in patients with coronary heart diseases (CHD). METHODS: For this purpose periodontal charts were raised for 101 patients (78 male, 23 female, mean age 61.8 +/- 10.5 years) with cardiovascular diseases; comparison was drawn between theses charts and those for a control group of 101 healthy patients (59 male, 42 female, mean age 56.6 +/- 9.9 years). Over and above the dental diagnosis (probing depth [mm], vitality, tooth mobility, plaque index (PI), inclination towards sulcus bleeding) each related to 6 characteristic teeth, various habitual aspects (diet, smoke and drink patterns, stress, body weight) were recorded. RESULTS: Within the CHD-group the periodontal chart revealed for all teeth examined a mean probing depth of 3.4 +/- 1.1mm, with the corresponding reading for the control group being 2.8 +/- 0.9 mm. The mean bleeding index (Van-der-Weiden) read 1.1 +/- 0.7 for the CHD-group and 0.7 +/- 0.6 for the control group. The mean plaque index reading was 1.4 +/- 0.9 for the group suffering from heart diseases and 0.7 +/- 0.8 for the control group. Comparison of these periodontal charts showed statistically significant differences (p<= 0.01), whereas mean degrees of tooth mobility did not differ in a statistically significant way. In summary, the results described hint at a correlation between an existent coronary heart disease and the presence of a periodontitis. CONCLUSION: However, also for consideration below are further influential factors, such as diet, individual life conduct, smoking habits, Body-Mass-Index or microbiological aspects.

Adult↗
PubMed2002

Pulses and lipaemia, short- and long-term effect: potential in the prevention of cardiovascular disease.

Cardiovascular disease (CVD) is the leading cause of death in most developed countries. Most CVD deaths are preventable through life-style measures such as diet, exercise and avoidance of cigarette smoking. Decreased intake of saturated fat and cholesterol and increased intake of cholesterol-reducing foods, such as pulses, deserve a high priority for activities designed to prevent CVD. Epidemiological and observational studies indicate that habitual intakes of large amounts of dietary fibre or of vegetables are associated with significantly lower rates of CVD. Studies over four decades document the hypocholesterolaemic effect of pulses and soyabeans. We performed a meta-analysis of eleven clinical trials that examined the effects of pulses (not including soyabeans) on serum lipoproteins. Intake of non-soya pulses was associated with these changes: fasting serum cholesterol, -7.2 %, 95 % CI -5.8, -8.6 %; LDL-cholesterol, -6.2 %, 95 % CI -2.8, -9.5 %; HDL-cholesterol, +2.6 %, 95 % CI +6.3, -1.0 %; triacylglycerols, -16.6 %, 95 % CI -11.8 %, -21.5 %; and body weight, -0.9 %, 95 % CI +2.2 %, -4.1 %. The hypocholesterolaemic effects of pulses appear related, in estimated order of importance, to these factors: soluble dietary fibre, vegetable protein, oligosaccharides, isoflavones, phospholipids and fatty acids, saponins and other factors. Intake of pulses may also reduce risk for CVD by favourable effects on blood pressure, glycaemia and risk for diabetes, and risk for obesity. Overall, the available evidence indicates that regular consumption of pulses may have important protective effects on risk for CVD.

Body Weight↗
PubMed2004

Optimal management of hyperlipidemia in primary prevention of cardiovascular disease.

Cardiovascular disease (CVD) in the developed countries continues to grow at an epidemic proportion. There are a significant number of young adults with no clinical evidence of CVD, but who have two or more risk factors that predispose them to CV events and death. Many of these risk factors are modifiable, and by controlling these factors, the CVD burden can be decreased significantly. Recent statistics have shown that, if all major forms of CVD were eliminated, the life expectancy would rise by almost 7 years. Hence it is imperative that primary prevention efforts should be initiated at a young age to avert decades of unattended risk factors. Hyperlipidemia has been linked to CVD almost a century ago. Since then various clinical trials have not only supported this link, but have also shown the CV benefits in aggressively treating patients with hyperlipidemia. In this generation, we have various therapeutic agents that are capable of reducing the elevated lipid levels. With drugs like statins, we are able to reduce the risk of CVD by about 30% and avoid major adverse events. Newer drugs are being researched and introduced in the treatment of hyperlipidemia in humans. These can be used in combination therapy resulting in optimal levels of lipids. The new National Cholesterol Education Program (NCEP)/Adult Treatment Panel III (ATP III) guidelines have come as a wake-up call to clinicians about primary prevention of CVD through strict lipid management and multifaceted risk management approach in the prevention of CVD.

Cardiovascular Diseases↗
PubMed2001

Homocysteine, folate, and cardiovascular disease.

Cardiovascular disease (CVD) continues to be one of the main causes of mortality in the western world, however approximately only two-thirds of all episodes can be attributed to traditional environmental and genetic risk factors. Over the past decade it has emerged that a moderate elevation in plasma concentrations of the amino acid homocysteine (tHcy) constitutes a risk factor for atherosclerotic vascular disease in the coronary, cerebral and peripheral vessels. Furthermore, this association is a graded one with no apparent threshold and is independent of, but may enhance the effect of conventional risk factors. Plasma homocysteine is determined by both genetic and nutritional factors. The B-vitamins folate, B-12 and B-6 all play a key role in homocysteine metabolism and in fact it has been proposed that about two-thirds of all cases of hyperhomocysteinemia are due to an inadequate status of one or all of these vitamins. Of the three, folate appears to be the most important determinant and has been shown to significantly lower homocysteine concentration when administered at doses ranging from 0.2 to 10 mg/d in both healthy and hyperhomocysteinemia subjects. There is considerable variation in the rate of CVD mortality between northern and southern European countries. A common dietary element in regions with lower CVD incidence i.e. southern European countries appears to be the higher consumption of fruit and vegetables. In the past this protective effect of fruit and vegetables has been primarily attributed to antioxidants. Fruit and vegetables are however also one of the main sources of folate in the diet, contributing to more than 30% of total dietary folate intake (even in countries where consumption of fruit and vegetables is low). Thus, in light of the evidence that folate may play a role in primary prevention of CVD via homocysteine-lowering the protective effect of fruit and vegetables may be partly explained by folate.

Antioxidants↗
PubMed1998

Dental plaque, platelets, and cardiovascular diseases.

Cardiovascular diseases, including atherosclerosis and myocardial ischemia, occur as a result of a complex set of genetic and environmental factors. During periodontitis, dental plaque microorganisms may disseminate through the blood to infect the vascular endothelium and contribute to the occurrence of atherosclerosis and risk of myocardial ischemia and infarction. Myocardial ischemia and infarction are often preceded by acute thromboembolic events. In an in vitro model of thrombosis, certain dental plaque bacteria induce platelets to aggregate. Aggregation of platelets is induced by the platelet aggregation-associated protein [PAAPJ expressed on plaque bacteria, including Streptococcus sanguis and Porphyromonas gingivalis. Intravenous infusion of S. sanguis into rabbits has been shown previously to cause changes in the electrocardiogram (ECG), heart rate, blood pressure, and cardiac contractility. These changes are consistent with the occurrence of myocardial infarction. The ECG changes are now shown to begin within 30 seconds after infusion of PAAP+ S. sanguis, followed by alterations in blood pressure and respiratory rate. These changes occurred intermittently over a 30-minute period and changed within one heartbeat to a normal pattern and suddenly back to abnormal. Intermittent ECG abnormalities were seen in 13 of 15 rabbits, including left axis deviation, ST-segment depression, preventricular contractions, alternans, and bigemnia. Dose-dependent thrombocytopenia, accumulation of 111Indium-labeled platelets in the lungs, and tachypnea also occurred. No changes occurred with the PAAp- strain. The data indicated that PAPP+ S. sanguis interacts with circulating platelets, inducing thromboemboli to cause the pulmonary and cardiac abnormalities. During periodontitis, therefore, PAAP+ S. sanguis and P. gingivalis bacteremia may contribute to the chance of acute thromboembolic events.

Animals↗
PubMed2000

Diabetes and cardiovascular disease.

Cardiovascular disease (CVD) is the most frequent and costly complication of type 2 diabetes. In this review, we examine the impact of diabetes on CVD. Shedding some light on the diabetes/CVD relationship are epidemiologic studies, which focused on Native Americans, who collectively experienced little or no diabetes or CVD in the past, but experience both conditions in epidemic proportions today. Almost half of the Native Americans studied had diabetes at baseline. When CVD events were stratified by diabetic status, the relative CVD risk among diabetic men was twice that of nondiabetic men, and the risk among diabetic women was threefold that of nondiabetic women. Among all CVD events, diabetes accounted for 56% in men and 78% in women; most CVD deaths occurred in those with diabetes. Recent attention has focused on defining the relative strength of CVD risk factors in diabetic populations. In many populations, low-density lipoprotein (LDL) cholesterol is lower in diabetic individuals. However, in American Indians, every 10-mg/dL increase in LDL cholesterol has been associated with a 12% increase in CVD risk and every 10-mg/dL decrease in high-density lipoprotein (HDL) cholesterol was associated with an 8% increase in CVD risk. Albuminuria is an important predictor of CVD in diabetic populations. Those with macroalbuminuria had a CVD risk that was four to five times that of diabetic individuals without albuminuria. Other CVD risk factors in diabetes that have come under recent scrutiny in other populations are increased levels of fibrinogin, and C-reactive protein, and leukocytosis. Angiogenic response may be lower in diabetic individuals, and the possible role of infection is being examined in diabetic patients. LDL cholesterol and albuminuria should be the targets of preventive strategies, and promising new areas such as cytokines, growth factor, and the role of infection should be further explored.

Albuminuria↗
PubMed2003

PASSCLAIM - Diet-related cardiovascular disease.

Cardiovascular disease (CVD) has a multifactorial aetiology and many potential risk markers are known. As it was not feasible to discuss all markers and their possible interactions in relation to all aspects of CVD, selections had to be made in this paper. In the context of claims and functional foods, emphasis was placed on those aetiological processes and risk markers that have been shown previously to be modified by diet: lipid and lipoprotein metabolism, haemostatic function, oxidative damage, homocysteine metabolism, and blood pressure. Except for methodological and biological characteristics of these biomarkers, their relationships with the risk of CVD are discussed. For LDL and HDL cholesterol, fasting triacylglycerol, homocysteine, and blood pressure well-validated, easy applicable, and generally accepted biomarkers exist. For haemostatic function and oxidative damage validation of markers with respect to CVD or intermediate clinical markers is recommended. For diet-related CVD, however, the ultimate question is whether changes in the biomarker are truly related to changes in risk. Only for LDL cholesterol and blood pressure does consensus exist among scientists for a possible application as enhanced function claims. For HDL, triacylglycerol, and homocysteine, and in particular for haemostatic function and oxidative damage, however, formal proof is lacking that diet-induced changes in these biomarkers alter the risk of CVD. At the same time, it should be emphasised that CVD is multifactorial. Therefore it does not seem justified that a change in one particular biomarker is enough evidence to substantiate a claim. There are examples of food components or drugs that one biomarker is changed in a favourable way, but at the same time another biomarker is changed in an unfavourable way. Therefore, studies to further validate generic predictors for the CVD risk should be initiated.

Animals↗
PubMed1997

Therapeutic implications of the epidemiology and timing of myocardial infarction and other cardiovascular diseases.

Cardiovascular diseases (CVD) account for almost 50% of the 2 million deaths annually in the United States. Coronary heart disease (CHD) (ie, myocardial infarction, sudden death) account for the largest proportion (32%) of this mortality. Over the last 3 decades both CVD and age-adjusted coronary death rates have fallen dramatically. However, crude CVD (and CHD) incidence is actually increasing, almost exclusively as a function of rising CVD incidence amongst older Americans. Population groups at highest for premature CVD complications include African-Americans, diabetics, men, smokers, and those with high levels of single risk factors (ie, stage III hypertension). Individuals with multiple CVD risk factors as well as those with manifestations of blood pressure (BP)-related target-organ damage (TOD) (ie, left ventricular hypertrophy, hypercreatinemia) are at an inordinately high risk for clinical events. CVD events do not randomly occur throughout the 24-h time period. The peak incidence of myocardial infarction (MI), thrombotic stroke, sudden cardiac death, and transient myocardial ischemia is between 6 am and 12 noon. During the morning hours coinciding with the peak incidence of CVD events, coronary vasomotor tone, plasma catecholamines, and platelet aggregability are at their highest levels while coronary blood flow and plasma fibrinolytic activity are at their lowest levels of the day. Moreover, BP rapidly rises from its nocturnal nadir during the early morning hours. Prevention of pressure-related CVD events in hypertensive patients over the long term can be best accomplished by controlling BP throughout the 24 h time period with drugs that do not adversely impact (or favorably affect) other metabolic, neurohormonal, and hemostatic parameters. BP control (minimally to <140/90 mm Hg) may be particularly important in the early morning hours since elevated BP and/or rapidly rising BP is a plausible biological trigger for the aforementioned CVD events. One effective strategy for achieving this goal is to utilize antihypertensive drugs with long therapeutic half-lives. Such agents will provide smooth whole-day BP control and also will minimize the loss of BP control during time period(s) between missed medication doses in the setting of therapeutic non-compliance. Practitioners should give due consideration to nocturnal administration of antihypertensive drugs prescribed once-daily as a means of achieving more effective morning BP control.

Cardiovascular Diseases↗
PubMed1988

The care of elderly patients with cardiovascular disease.

Cardiovascular disease is a major clinical problem in the elderly, with coronary heart disease the most frequent cause of death and with hypertension present in as many as 50% of these patients. The cardiovascular manifestations of aging must be differentiated from those due to disease. There are clinical manifestations and responses to therapy in the elderly that differ from those in younger patients. The extent of diagnostic and therapeutic procedures undertaken should be based on the patient's physiologic age, the presence and severity of concomitant diseases, mental status and cognitive ability, and the patient's expectations from medical care. Preventive approaches are also warranted.

Age Factors↗
PubMed2006

Prevention of cardiovascular disease in patients with rheumatic diseases.

Cardiovascular disease (CVD), the leading cause of death in the USA, has emerged as an important comorbidity in the rheumatic diseases. As disease-modifying therapies have resulted in better disease control and decreases in disease-associated mortality, it is now apparent that the prevalence of CVD and cardiovascular (CV) events is significantly increased in a number of rheumatic disorders when compared with age and gender-matched subjects from the general population. Investigations into the mechanisms of CVD in the general population have provided insights into potential mechanisms in rheumatic disease patients and possible aetiologies for their increased risk. Although there are no evidence-based guidelines for CV risk factor screening and interventions specific to patients with rheumatic disease, the best current approach utilizes evidence-based recommendations for the general population (and higher-risk subgroups) modified by what is known of CV risk factor and event prevalence in these patients.

Cardiovascular Diseases↗
PubMed2006

Detection of chronic kidney disease in patients with or at increased risk of cardiovascular disease: a science advisory from the American Heart Association Kidney And Cardiovascular Disease Council; the Councils on High Blood Pressure Research, Cardiovascular Disease in the Young, and Epidemiology and Prevention; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: developed in collaboration with the National Kidney Foundation.

Chronic kidney disease (CKD) occurs commonly in patients with cardiovascular disease. In addition, CKD is a risk factor for the development and progression of cardiovascular disease. In this advisory, we present recommendations for the detection of CKD in patients with cardiovascular disease. CKD can be reliably detected with the combined use of the Modification of Diet in Renal Disease equation to estimate glomerular filtration rate and a sensitive test to detect microalbuminuria. All patients with cardiovascular disease should be screened for evidence of kidney disease with these two determinations.

American Hospital Association↗
PubMed2002

[Computer program for diagnosis, monitoring, and prophylaxis of cardiovascular diseases].

Cardiovascular diseases remain the main cause of death among adult population; their incidence can be reduced only using an effective system of primary and secondary prevention. The aim of our study was to develop software for automated recognition of cardiovascular risk factors, prognosis, and evaluation of dyslipoproteinemia phenotypes in lipid centers. Prognostic indexes, lipidogram values are estimated, and the program detects the risk factors (overweight, poor physical training, irrational nutrition, tobacco smoking, etc.) and predicts the summary risk of coronary disease. Neuronal network was used for evaluating the types of dyslipoproteinemias and for cardiovascular prognosis. The input vectors were lipid and lipoprotein concentrations. Output neurons were diagnostic signs of dislipoproteinemia phenotypes or cardiovascular prognosis.

Adult↗
PubMed2025

Post-genome-wide association study dissects genetic vulnerability and risk gene expression of Sj&#xf6;gren's disease for cardiovascular disease.

OBJECTIVES: This study aims to clarify the genetic associations between Sj&#xf6;gren's Disease (SD) and cardiovascular disease (CVD) outcomes, and to conduct an in-depth exploration of specific pleiotropic susceptibility genes. METHODS: We performed two-sample and multivariable Mendelian randomization (MR) analysis to investigate the association between SD and the risk of ischemic heart disease (IHD) and stroke. Linkage disequilibrium score regression (LDSC) and Bayesian co-localization analyses were employed to assess the genetic associations between traits. Cross-phenotype analyses were employed to identify shared variants and genes, followed by a Transcriptome-Wide Association Study (TWAS) and Multi-marker Analysis of Genomic Annotation (MAGMA) based on Multi-Trait Analysis of GWAS (MTAG) results. To validate the pleiotropic genes, we further analyzed tissue-specific differentially expressed genes (DEGs) related to SD using RNA sequencing data. RESULTS: The two-sample and multivariable MR analyses revealed that SD confers a genetic vulnerability to IHD and stroke. LDSC and co-localization analyses indicated a strong genetic linkage between SD and CVDs. Cross-phenotype analyses identified 38 and 37 pleiotropic single nucleotide polymorphisms (SNPs) for SD-Stroke and SD-IHD, respectively, primarily located within the MHC class region on 6p21.32:33 loci. Additionally, TWAS and MAGMA analyses identified pleiotropic genes located outside the MHC regions-seven associated with stroke (UHRF1BP1, SNRPC, BLK, FAM167A, ARHGAP27, C8orf12, and PLEKHM1) and two associated with IHD (UHRF1BP1 and SNRPC). Proxy variants within these genes in SD suggested an increased causal risk for stroke or IHD. Co-localization analysis further reinforced that SD and stroke share significant SNPs within the loci of FAM167A, BLK, C8orf12, SNRPC, and UHRF1BP1. DEG analysis revealed a significant up-regulation of the identified genes in SD-specific tissues. CONCLUSIONS: SD appears genetically predisposed to an increased risk of CVDs. Moreover, this research not only identified pleiotropic genes shared between SD and CVDs, but also, for the first time, detected key gene expressions that elevate CVD risk in SD patients-findings that may offer promising therapeutic targets for patient management.

Humans↗
PubMed1997

Mortality from coronary heart disease and cardiovascular disease among adult U.S. Hispanics: findings from the National Health Interview Survey (1986 to 1994).

OBJECTIVES: We sought to estimate the coronary heart disease (CHD) and cardiovascular disease (CVD) mortality experience of U.S. Hispanics. BACKGROUND: Limited information is available concerning the mortality from CHD among U.S. Hispanics, the nation's second largest minority group. METHODS: The study used data from the National Health Interview Survey (1986 to 1994), including representative national samples of 246,239 non-Hispanic whites, 38,042 blacks and 14,965 Hispanics who were > or = 45 years old at baseline. Mean follow-up of mortality was 5 years (range 1 to 10). RESULTS: During the follow-up period, 27,702 whites (11%), 4,976 blacks (13%) and 1,061 Hispanics (7%) died. Among men, the age-adjusted total mortality per 100,000 person-years was 3,089 in whites and 2,466 in Hispanics, and among women, it was 1,897 and 1,581 in whites and Hispanics, respectively. The Hispanic/white mortality rate ratio for CHD was 0.77 (95% confidence interval [CI] 0.64 to 0.93) and 0.82 (95% CI 0.66 to 1.01) for men and women, respectively. The rate ratio was 0.79 (95% CI 0.68 to 0.91) and 0.80 (95% CI 0.69 to 0.94), respectively, for mortality from cardiovascular diseases. Given the lower all-cause mortality in Hispanics, the proportion of total deaths due to CHD and CVD was similar between the two populations for the same gender and were, respectively, 29.7% and 44.7% in white men, 28.1% and 44.3% in Hispanic men, 24.9% and 43.2% in white women and 24.1% and 41% in Hispanic women. CONCLUSIONS: These data from a cohort of a large national sample are consistent with vital statistics that show that all-cause, CHD and CVD mortality is approximately 20% lower among adult Hispanics than among whites in the United States.

Aged↗
PubMed2003

Diabetes mellitus: a cardiovascular disease.

Cardiovascular disease (CVD) is the major cause of morbidity and mortality in patients with diabetes mellitus (DM). The pathophysiology of CVD in diabetes involves traditional and novel cardiac risk factors, including hypertension, dyslipidemia, smoking, genetic factors, hyperglycemia, insulin resistance/hyperinsulinemia, metabolic abnormalities, oxidative/glycoxidative stress, inflammation, endothelial dysfunction, a procoagulant state and myocardial fibrosis. Specific vascular, myopathic and neuropathic alterations have been suggested to be responsible for the excessive cardiovascular morbidity and mortality in diabetes. These alterations manifest themselves clinically as coronary heart disease, congestive heart failure and/or sudden cardiac death. In order to contain the emerging epidemic of CVD in DM, diabetic patients should ideally have excellent glycemic control, a low normal blood pressure and low levels of low-density lipoprotein cholesterol, and be taking an angiotensin-converting enzyme inhibitor and aspirin, which may go some way to containing the emerging epidemic of CVD in DM.

Cardiovascular Diseases↗
PubMed2002

Periodontal disease and cardiovascular disease: epidemiology and possible mechanisms.

BACKGROUND: Many early epidemiologic studies reported an association between periodontal disease and cardiovascular disease. However, other studies found no association or nonsignificant trends. This report summarizes the evidence from epidemiologic studies and studies that focused on potential contributing mechanisms to provide a more complete picture of the association between periodontal and heart disease. TYPES OF STUDIES REVIEWED: The authors summarize the longitudinal studies reported to date, because they represent the highest level of evidence available regarding the connection between periodontal disease and heart disease. The authors also review many of the case-control and cross-sectional studies published, as well as findings from clinical, animal and basic laboratory studies. RESULTS: The evidence suggests a moderate association--but not a causal relationship--between periodontal disease and heart disease. Results of some case-control studies indicate that subgingival periodontal pathogenic infection may be associated with myocardial infarction. Basic laboratory studies point to the biological plausibility of this association, since oral bacteria have been found in carotid atheromas and some oral bacteria may be associated with platelet aggregation, an event important for thrombosis. Animal studies have shown that atheroma formation can be enhanced by exposure to periodontal pathogens. CONCLUSIONS: The accumulation of epidemiologic, in vitro, clinical and animal evidence suggests that periodontal infection may be a contributing risk factor for heart disease. However, legitimate concerns have arisen about the nature of this relationship. These are early investigations. Since even a moderate risk contributed by periodontal disease to heart disease could contribute to significant morbidity and mortality, it is imperative that further studies be conducted to evaluate this relationship. One particularly important study to be carried out is the investigation of a possible clinically meaningful reduction in heart disease resulting from the prevention or treatment of periodontal disease.

Acute-Phase Reaction↗
PubMed2006

Relation of brain natriuretic peptide levels to cognitive dysfunction in adults > 55 years of age with cardiovascular disease.

Cardiovascular disease (CVD) is associated with cognitive deficits long before the onset of stroke or dementia. Recent work has extended these findings and shown that patients with congestive heart failure also exhibit reduced cognitive performance. Brain natriuretic peptide (BNP) is used to help diagnose heart failure, but no study has examined whether BNP predicts cognitive dysfunction in older patients with CVD. BNP values and performance on the Dementia Rating Scale were assessed in 56 older adults with documented CVD. Forty-eight percent of the participants were women, and their average age was 70 +/- 8 years. All participants had Mini-Mental State Examination scores greater than the cutoff for dementia and no histories of neurologic or severe psychiatric disorders. The average BNP level was 122 +/- 202 pg/ml. Hierarchical regression analyses showed that log-transformed BNP levels predicted Dementia Rating Scale total score after adjusting for possible demographic and medical confounders (DeltaR2 = 0.09, F[1, 44] = 6.14, p = 0.017). Partial correlation analysis adjusting for these possible confounders showed a particularly strong relation to the conceptualization subtest (r = -0.44, p = 0.002), a measure of verbal and nonverbal abstraction abilities. In conclusion, the results of the present study provide the first evidence for an independent relation between BNP and cognitive dysfunction in older adults with CVD.

Age Factors↗