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PubMed1999

Influence of pattern of drinking on cardiovascular disease and cardiovascular risk factors--a review.

There is an established inverse relationship between the regular light consumption of alcohol (5-10 g/day) and the incidence of coronary artery disease (CAD). This association has several biologically plausible mechanisms with dose-dependent effects of alcohol to increase HDL cholesterol, lower plasma fibrinogen and inhibit platelet aggregation. However, such a protective effect against atheroma cannot be considered in isolation from known adverse effects on blood pressure and triglycerides or possible detrimental effects of episodic or binge drinking on several other cardiovascular end-points and risk factors. In subjects with pre-existing CAD, an alcoholic binge can increase both silent myocardial ischaemia and angina. During withdrawal following binge drinking, marked fluctuations in blood pressure together with heightened platelet activation and adverse changes in the balance of fibrinolytic factors, may offer an explanation for the reported association between episodic heavy drinking and ischaemic stroke. This has been seen particularly in young males and extends further to an increase in both subarachnoid haemorrhage and intracerebral haemorrhage after binge drinking. Intervention studies in man have shown acute increases in blood pressure in men who drink predominantly at weekends, compared to longer-term pressor effects in regular daily drinkers. We have been unable, however, to reproduce the finding of unfavourable effects of binge drinking on the lipid profile that have been reported in animal studies and man. Binge drinking may also induce cerebrovascular spasm or cause both ventricular and supraventricular arrhythmias, especially atrial fibrillation. Alcohol-induced arrhythmia has been postulated as the basis for alcohol-related sudden coronary death in those subjects with pre-existing CAD. Hence, further exploration of any protective association of alcohol against CAD needs to carefully consider the implications of pattern of drinking for the relationship. The modulating influences of co-timing of drinking with meals, cigarette smoking or illicit drug use also need to be evaluated. Without such vital information, public health advice on alcohol and CAD will be limited in its scope and potentially flawed in its impact.

Alcohol Drinking↗
PubMed1976

Community surveillance for coronary heart disease: the Framingham Cardiovascular Disease survey. Comparisons with the Framingham Heart Study and previous short-term studies.

It appears likely that intervention trials on a community scale against one or more coronary heart disease risk factors will begin in the near future. Prerequisite to the evaluation of the effectiveness of these trials is the accurate determination of coronary heart disease incidence rates. The Framingham Cardiovascular Disease Survey was undertaken to test the hypothesis that a short-term surveillance study of a defined population can generate accurate incidence rates for at least some categories of cardiovascular disease and that these rates are comparable with those obtained by longitudinal survey of the same population. In conjunction with the 1970 U.S. census, a 1 year survey was made of all new coronary heart disease events occurring in the town of Framingham, Mass. Surveillance was performed by several methods that were intentionally overlapping. During the study period, 244 coronary heart disease events occurred. Despite the relatively small size of the population, many of the well established epidemiologic characteristics of this disease were evident. The rates obtained by the cardiovascular disease survey were comparable with those obtained by the Framingham Heart Study, for the harder end points of myocardial infarction and death from coronary heart disease, but much smaller for the softer end point of angina pectoris, especially in women. These data and those from similar studies indicate that periodic short-term surveillance studies of target populations of major intervention programs can provide an economic method of generating incidence data for the evaluation of the impact of such programs on myocardial infarction and death from coronary heart disease.

Age Factors↗
PubMed2000

Proteinuria as a risk factor for cardiovascular disease and mortality in older people: a prospective study.

BACKGROUND: The prognostic significance of proteinuria in older people is not well defined. We examined the associations between proteinuria and incident coronary heart disease, cardiovascular mortality, and all-cause mortality in older people. SUBJECTS AND METHODS: Casual dipstick proteinuria was determined in 1,045 men (mean [+/- SD] age 68 +/- 7 years) and 1,541 women (mean age 69 +/- 7 years) attending the 15th biennial examination of the Framingham Heart Study. Participants were divided by grade of proteinuria: none (85.3%), trace (10.2%), and greater-than-trace (4.5%). Cox proportional hazards analyses were used to determine the relations of baseline proteinuria to the specified outcomes, adjusting for other risk factors, including serum creatinine level. RESULTS: During 17 years of follow-up, there were 455 coronary heart disease events, 412 cardiovascular disease deaths, and 1,214 deaths. In men, baseline proteinuria was associated with all-cause mortality (hazards ratio [HR] = 1.3, 95% confidence interval [CI] 1.0 to 1.7 for trace proteinuria; HR = 1.3, 95% CI 1.0 to 1.8 for greater-than-trace proteinuria; P for trend = 0.02). In women, trace proteinuria was associated with cardiovascular disease death (HR = 1. 6, 95% CI 1.1 to 2.4), and all-cause mortality (HR = 1.4, 95% CI 1.1 to 1.7). CONCLUSION: Proteinuria is a significant, although relatively weak, risk factor for all-cause mortality in men and women, and for cardiovascular disease mortality in women.

Age Factors↗
PubMed1992

The health consequences of smoking. Cardiovascular diseases.

Cigarette smoking is a major cause of atherosclerotic diseases. Cardiovascular diseases (CVD) remain the leading disease cause of death and disability in the United States. Smoking contributes to much of the premature and overall disease burden from CVD. Smoking affects the physiologic, pathologic, hematologic, and metabolic factors that lead to the initiation, progression, and sequelae of atherosclerosis. Smoking cessation reduces the progression of atherosclerosis and the subsequent morbidity, mortality, and years of productive life lost from CVD.

Arteriosclerosis↗
PubMed2006

Cardiovascular disease in diabetes.

Diabetes is associated with a marked increase in the risk of atherosclerotic vascular disorders, including coronary, cerebrovascular, and peripheral artery disease. Cardiovascular disease (CVD) could account for disabilities and high mortality rates in patients with diabetes. In this paper, we review the molecular mechanisms for accelerated atherosclerosis in diabetes, especially focusing on postprandial hyperglycemia, advanced glycation end products (AGEs) and the renin-angiotensin system. We also discuss here the potential therapeutic strategy that specifically targets CVD in patients with diabetes.

Animals↗
PubMedDate not supplied

The association between educational level and risk of cardiovascular disease fatality among women with cardiovascular disease.

BACKGROUND: The inverse relation of socioeconomic status with incident cardiovascular diseases (CVDs) has been well established. However, few data are available describing this relation among ethnically diverse women with prevalent CVD. Using education as a proxy for socioeconomic status, we examined its relation to CVD mortality among women with established CVD. SUBJECTS: Data from 2,157 women with CVD at baseline, who participated in nine long-term U.S. cohort studies, were pooled. METHODS: Cox regression models adjusted for history of diabetes mellitus, total cholesterol, systolic and diastolic blood pressure, body mass index, smoking, race/ethnicity, and age at baseline were used to estimate hazard ratios for CVD mortality between non-high school graduates and high school graduates. RESULTS: During a mean follow-up time of 11.5 years, 615 CVD deaths were observed. There was an age-dependent (p = .003) inverse association between education and CVD mortality among women with CVD. At age 60, the risk of dying due to CVD among non-high school graduates was more than twice greater than that of high school graduates (hazard ratio = 2.34; 95% CI 1.27-4.29). At age 65, the hazard ratio decreased to 1.31 (95% CI 1.00-1.71). By age 70, there was no difference in the hazard of dying between high school graduates and nongraduates (hazard ratio = 1.01; 95% CI .85-1.21). CONCLUSIONS: Our results show that among women with CVD, educational level was a significant, and age-dependent, predictor of fatal CVD independent of other traditional risk factors. These women are an important high-risk population to target secondary prevention and educational efforts.

Adult↗
PubMed2000

Renal disease as a risk factor for cardiovascular disease.

Cardiovascular disease is the major cause of death in patients with end-stage renal disease (ESRD). ESRD patients are almost invariably hypertensive. They all have acquired combined hyperlipidemia and increased Lp(a), hyperhomocysteinemia, decreased physical activity, psychosocial stress, insulin resistance, procoagulant factors, left ventricular hypertrophy, and increased oxidative stress. Diabetes mellitus, a major risk factor for both cardiovascular disease and ESRD, has become the commonest cause of ESRD. If ESRD patients choose to smoke, the additive risk is profound. Moreover, ESRD patients are becoming older and are often menopausal if female. Finally, ESRD patients have a dramatic tendency for vascular and cardiac calcification, probably related to hyperphosphatemia and hyperparathyroidism. Cardiovascular disease is also a major risk in patients with decreased renal function of nearly any degree. Data from the HDFP study showed that patients with a serum creatinine concentration > 1.5 mg/dl had a profoundly higher risk of cardiovascular disease than patients with creatinine values below this value. These data were recently corroborated in the HOPE study. Microalbuminuria (MAU), with or without diabetes mellitus, indicates increased cardiovascular disease risk even without decreases in glomerular filtration rate. We found earlier that nondiabetic hypertensive patients with MAU had much higher rates of myocardial infarction, stroke, and peripheral vascular disease, than similar hypertensive patients without MAU. In conclusion, the presence of decreased renal function or MAU is a major cardiovascular risk factor. ESRD can be regarded as a catastrophic risk factor. Prophylactic measures known to be effective in reducing the risk from cardiovascular disease are grossly underused. Unfortunately, they are less effective in patients with renal disease, and new strategies are needed.

Calcinosis↗
PubMed2006

[Rheumatic diseases as risk factors for cardiovascular disease].

Cardiovascular disease is the leading cause of death in patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS) and systemic lupus erythematosus (SLE). In addition to mortality, cardiovascular morbidity is also markedly increased in these patients, compared with the general population. The increased cardiovascular risk can be explained only partially by an increased prevalence of classical risk factors for cardiovascular disease; it also appears to be related to inflammation. Prospective intervention trials aimed at the modification of cardiovascular risk factors are needed to determine the impact of cardiovascular risk reduction in patients with rheumatic disease. In addition to SLE, RA and AS should be acknowledged as new risk factors for cardiovascular disease.

Arthritis, Rheumatoid↗
PubMed2001

Efficacy of atorvastatin in achieving National Cholesterol Education Program low-density lipoprotein targets in women with severe dyslipidemia and cardiovascular disease or risk factors for cardiovascular disease: The Women's Atorvastatin Trial on Cholesterol (WATCH).

BACKGROUND: Recent studies have demonstrated that women at high risk for cardiovascular disease (CVD) benefit from cholesterol lowering to an extent similar to that of men. The ability to achieve established treatment goals for low-density lipoprotein cholesterol (LDL-C) in women with clearly defined risk factors has not been examined in detail. METHODS AND RESULTS: We have determined the efficacy and frequency of achieving target levels for LDL-C with atorvastatin on the basis of National Cholesterol Education Program Adult Treatment Panel II recommendations in 318 women according to the presence of CVD (198 women) or risk factors for CVD (120 women) and the presence of mixed dyslipidemia with obesity with or without CVD (72 women). Mean baseline LDL-C concentrations for women with established CVD were in the upper 10% of the distribution for age-matched North American women and, for those without CVD, were also extremely elevated and were in the top 5% of the LDL-C distribution for age-matched women in this population. The majority of participants without CVD (63%) reached LDL-C targets (LDL-C or=2 CVD risk factors) with 10 mg atorvastatin and 79% reached targets with up to 20 mg of atorvastatin. For women with established CVD, 34% achieved an LDL-C <or=100 mg/dL (2.6 mmol/L) with 10 mg and 60% reached this target with up to 20 mg of atorvastatin. With maximal titration to the LDL-C target, up to and including 80 mg atorvastatin, 87% of women without CVD and 80% of women with established CVD achieved LDL-C targets. The presence of mixed dyslipidemia with obesity did not affect the frequency of achieving LDL-C targets. CONCLUSION: Atorvastatin is very effective in achieving National Cholesterol Education Program Adult Treatment Panel II target concentrations for LDL-C in the majority of women with established CVD or CVD risk factors.

Adult↗
PubMed1990

Ten-year mortality from cardiovascular disease in relation to cholesterol level among men with and without preexisting cardiovascular disease.

To determine the associations of total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol with mortality from coronary heart disease and cardiovascular disease, we studied 2541 white men who were 40 to 69 years old at base line and followed them for an average of 10.1 years. Seventeen percent had some manifestation of cardiovascular disease at base line, whereas the others did not. Among the men who had cardiovascular disease at base line, we found, after multivariate adjustment, that those with "high" blood cholesterol levels (above 6.19 mmol per liter) had a risk of death from cardiovascular disease, including coronary heart disease, that was 3.45 times higher (95 percent confidence interval, 1.63 to 7.33) than that for men with "desirable" blood cholesterol levels (below 5.16 mmol per liter). The corresponding hazard ratios were 5.92 (95 percent confidence interval, 2.59 to 13.51) for LDL cholesterol levels above 4.13 mmol per liter as compared with those below 3.35 mmol per liter, and 6.02 (95 percent confidence interval, 2.73 to 13.28) for HDL cholesterol levels below 0.90 mmol per liter as compared with those above 1.16 mmol per liter. All three lipid levels were also significant predictors of death from coronary heart disease alone (P less than 0.005). Total cholesterol and LDL cholesterol levels were also significant predictors of death from cardiovascular and coronary heart disease in men without preexisting cardiovascular disease, although at a lower level of absolute risk of death. Thus, the 10-year risk of death from cardiovascular disease for a man with preexisting cardiovascular disease increased from 3.8 percent to almost 19.6 percent with increasing levels of total cholesterol from "desirable" to "high," whereas the corresponding risk for a man who was free of cardiovascular disease at base line increased from 1.7 percent to 4.9 percent. Our findings suggest that total, LDL, and HDL cholesterol levels predict subsequent mortality in men 40 to 69 years of age, especially those with preexisting cardiovascular disease.

Adult↗
PubMed2004

Cardio: a web-based knowledge resource of genes and proteins related to cardiovascular disease.

BACKGROUND: Cardiovascular disease (CVD) is the leading killer for human. In order to understand the linkage between cardiovascular diseases and genes or proteins, it is essential to construct a database to organize the body of knowledge. While the existing molecular biological databases focus on the sequence and structural aspects of biological macromolecules, i.e. DNAs, RNAs and proteins, Cardio is the web-based system we built to provide a knowledge environment with visual interface to integrate information about major cardiovascular diseases in relation to genes and proteins. METHODS: We collected the information from the web by using a group of software we developed and used a relational database management system to manage the information of these data. RESULTS: Cardio consists of six sections: GENE, PROTEIN, DISEASE, DRUG, LINKS, and REFERENCE. Each section contains relevant information about the topic. Using a phenotype-driven approach, we can identify genetic mechanisms underlying the physiology and pathophysiology of specific cardiovascular disease, such as atherosclerosis, hypertension, heart failure, and stroke. CONCLUSION: The website titled "Database of Genes and Proteins Related to Cardiovascular Disease (Cardio)" is available at along with additional information on cardiovascular disease, supplementary materials and related figures.

Cardiovascular Diseases↗
PubMed2000

Diabetes mellitus: subclinical cardiovascular disease and risk of incident cardiovascular disease and all-cause mortality.

Previously diagnosed diabetes mellitus, newly diagnosed diabetes mellitus, and impaired glucose tolerance are important determinants of the risk of clinical cardiovascular disease (CVD). We have evaluated the relation of patients with subclinical CVD, diabetes, and impaired glucose tolerance and "normal" subjects and the risk of clinical CVD in the Cardiovascular Health Study. Diabetes (1343), impaired glucose tolerance (1433), and normal (2421) were defined by World Health Organization criteria at baseline in 1989 to 1990. The average follow-up was 6.4 years (mean age 73 years). Diabetics had a higher prevalence of clinical and subclinical CVD at baseline. Compared with diabetes in the absence of subclinical disease, the presence of subclinical CVD and diabetes was associated with significant increased adjusted relative risk of death (1.5, CI 0.93 to 2.41), relative risk of incident coronary heart disease (1.99, CI 1.25 to 3.19), and incident myocardial infarction (1.93, CI 0.96 to 3.91). The risk of clinical events was greater for participants with a history of diabetes compared with newly diagnosed diabetics at baseline. Compared with nondiabetic nonhypertensive subjects without subclinical disease, patients with a combination of diabetes, hypertension, and subclinical disease had a 12-fold increased risk of stroke. Fasting blood glucose levels were a weak predictor of incident coronary heart disease as were most other risk factors. Subclinical CVD was the primary determinant of clinical CVD among diabetics in the Cardiovascular Health Study.

Aged↗
PubMed2005

Abnormal ankle brachial indices may predict cardiovascular disease among diabetic patients without known heart disease.

BACKGROUND: Cardiovascular disease remains the primary cause of diabetes-associated morbidity and mortality. Previous studies have failed to provide accurate, inexpensive, screening techniques to detect cardiovascular disease in diabetics. Ankle brachial indices (ABI) testing may be an effective screening technique for diabetics. METHODS AND RESULTS: The aim of this 100-subject clinical study was to determine cardiovascular disease prevalence, via perfusion stress testing, in diabetic patients having abnormal ABI (<0.90) and without known heart disease who were referred to the South Carolina Heart Center, Columbia, SC for nuclear perfusion stress testing. Study data were analyzed using frequency and descriptive statistics and 2-sample T-testing. Mean subject age was 62+/-11 years, ABI 0.76+/-13, and ejection fraction 60+/-12%. Perfusion stress testing detected 49 abnormal electrocardiograms, 36 subjects with coronary ischemia, 20 with diminished left ventricular function, and 26 subjects having significant thinning of the myocardium. There were 71 subjects who tested positive for at least one form of cardiovascular disease. The sole predictive variable reaching significance for the presence of cardiovascular disease was an ABI score <0.90 (p< or =0.0001). CONCLUSION: Cardiovascular disease may be predicted among diabetic patients via ABI scores and confirmed by nuclear perfusion testing.

Aged↗
PubMed2001

Prevention of cardiovascular disease and the future of cardiovascular disease epidemiology.

BACKGROUND: Coronary heart disease is preventable. The improved interpretation of risk factors, in vivo non-invasive measuring of arteries, brain and heart, and proven efficacy of both non-pharmacological and pharmaceutical therapies provides the model for both cardiovascular prevention programmes and new epidemiological studies. METHODS: Risk factors can be subdivided into those related to the development of atherosclerosis with relatively long incubation periods, and risk factors that moderate the changes in atherosclerotic plaque, thrombosis and fibrinolysis, i.e. those with short incubation periods, or proximate risk factors. RESULTS: The level of ApoB containing lipoproteins, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) are the primary determinants of atherosclerosis. Using non-invasive methods of measuring atherosclerosis, we can evaluate the efficacy of intervention to both prevent the development of atherosclerosis and the progression of disease. The importance of proximate risk factors, especially inflammatory markers, is less estimated than long incubation period factors. It is possible that a combination of measures of subclinical atherosclerosis and proximate risk factors may provide the best estimate of the risk of clinical disease, especially among higher risk older individuals. CONCLUSIONS: The measurement of subclinical disease and new proximate risk factors (i.e. inflammation, fibrinolysis) may be useful for comparing reported differences in rates of clinical disease among populations and monitoring the emerging epidemic of cardiovascular disease in countries that currently have low death rates due to cardiovascular disease.

Biomarkers↗
PubMed2023

Causal Associations of Sleep Apnea with Alzheimer's Disease and Cardiovascular Disease: a Bidirectional Mendelian Randomization Analysis.

BACKGROUND: Sleep apnea (SA) has been linked to an increased risk of dementia in numerous observational studies; whether this is driven by neurodegenerative, vascular or other mechanisms is not clear. We sought to examine the bidirectional causal relationships between SA, Alzheimer's disease (AD), coronary artery disease (CAD), and ischemic stroke using Mendelian randomization (MR). METHODS: Using summary statistics from four recent, large genome-wide association studies of SA (n=523,366), AD (n=64,437), CAD (n=1,165,690), and stroke (n=1,308,460), we conducted bidirectional two-sample MR analyses. Our primary analytic method was fixed-effects inverse variance weighted MR; diagnostics tests and sensitivity analyses were conducted to verify the robustness of the results. RESULTS: We identified a significant causal effect of SA on the risk of CAD (odds ratio (OR IVW ) =1.35 per log-odds increase in SA liability, 95% confidence interval (CI) =1.25-1.47) and stroke (OR IVW =1.13, 95% CI =1.01-1.25). These associations were somewhat attenuated after excluding single-nucleotide polymorphisms associated with body mass index (BMI) (OR IVW =1.26, 95% CI =1.15-1.39 for CAD risk; OR IVW =1.08, 95% CI =0.96-1.22 for stroke risk). SA was not causally associated with a higher risk of AD (OR IVW =1.14, 95% CI =0.91-1.43). We did not find causal effects of AD, CAD, or stroke on risk of SA. CONCLUSIONS: These results suggest that SA increased the risk of CAD, and the identified causal association with stroke risk may be confounded by BMI. Moreover, no causal effect of SA on AD risk was found. Future studies are warranted to investigate cardiovascular pathways between sleep disorders, including SA, and dementia.

Preprint↗