Factors influencing the relation between alcohol and cardiovascular disease

PURPOSE OF REVIEW: Light-to-moderate alcohol intake is known to have cardioprotective properties in some subsets of the population. This review focuses on factors that modify the relation between alcohol and cardiovascular disease. RECENT FINDINGS: Several large American studies have shown that the J-shaped relation is influenced by age and coronary heart disease risk-factor status since only middle-aged and elderly and those already at risk of developing coronary heart disease seem protected by drinking alcohol. It has also been suggested that only those who have a steady - in contrast to a binge - intake of alcohol have benefits with regard to cardiovascular disease. Prospective studies from the UK, Sweden and Denmark have further suggested that wine drinkers have a lower mortality than beer and spirits drinkers. SUMMARY: The J-shaped relation between alcohol intake and cardiovascular disease seems to be influenced by age, gender, drinking pattern and type of alcohol.     

Alcohol abstinence and mortality in a general population sample of adults in Germany: A cohort study

BackgroundEvidence suggests that people who abstain from alcohol have a higher mortality rate than those who drink low to moderate amounts. However, little is known about factors that might be causal for this finding. The objective was to analyze former alcohol or drug use disorders, risky drinking, tobacco smoking, and fair to poor health among persons who reported abstinence from alcohol drinking in the last 12 months before baseline in relation to total, cardiovascular, and cancer mortality 20 years later.Methods and findingsA sample of residents aged 18 to 64 years had been drawn at random among the general population in northern Germany and a standardized interview conducted in the years 1996 to 1997. The baseline assessment included 4,093 persons (70.2% of those who had been eligible). Vital status and death certificate data were retrieved in the years 2017 and 2018.We found that among the alcohol-abstinent study participants at baseline (447), there were 405 (90.60%) former alcohol consumers. Of the abstainers, 322 (72.04%) had met one or more criteria for former alcohol or drug dependence or abuse, alcohol risky drinking, or had tried to cut down or to stop drinking, were daily smokers, or self-rated their health as fair to poor. Among the abstainers with one or more of these risk factors, 114 (35.40%) had an alcohol use disorder or risky alcohol consumption in their history. Another 161 (50.00%) did not have such an alcohol-related risk but were daily smokers. The 322 alcohol-abstinent study participants with one or more of the risk factors had a shorter time to death than those with low to moderate alcohol consumption. The Cox proportional hazard ratio (HR) was 2.44 (95% confidence interval (CI), 1.68 to 3.56) for persons who had one or more criteria for an alcohol or drug use disorder fulfilled in their history and after adjustment for age and sex. The 125 alcohol-abstinent persons without these risk factors (27.96% of the abstainers) did not show a statistically significant difference from low to moderate alcohol consumers in total, cardiovascular, and cancer mortality. Those who had stayed alcohol abstinent throughout their life before (42; 9.40% of the alcohol-abstinent study participants at baseline) had an HR 1.64 (CI 0.72 to 3.77) compared to low to moderate alcohol consumers after adjustment for age, sex, and tobacco smoking. Main limitations of this study include its reliance on self-reported data at baseline and the fact that only tobacco smoking was analyzed as a risky behavior alongside alcohol consumption.ConclusionsThe majority of the alcohol abstainers at baseline were former alcohol consumers and had risk factors that increased the likelihood of early death. Former alcohol use disorders, risky alcohol drinking, ever having smoked tobacco daily, and fair to poor health were associated with early death among alcohol abstainers. Those without an obvious history of these risk factors had a life expectancy similar to that of low to moderate alcohol consumers. The findings speak against recommendations to drink alcohol for health reasons.

In this cohort study conducted over 20 years, Ulrich John and colleagues examine the relationship between alcohol abstinence and mortality in a German adult population.     

New insights into the emerging effects of inflammatory response on HDL particles structure and function

According to the increasing results, it has been well-demonstrated that the chronic inflammatory response, including systemic lupus erythematosus, rheumatoid arthritis, and inflammatory bowel disease are associated with an increased risk of atherosclerotic cardiovascular disease. The mechanism whereby inflammatory response up-regulates the risk of cardio-metabolic disorder disease is multifactorial; furthermore, the alterations in high density lipoprotein (HDL) structure and function which occur under the inflammatory response could play an important modulatory function. On the other hand, the serum concentrations of HDL cholesterol (HDL-C) have been shown to be reduced significantly under inflammatory status with remarked alterations in HDL particles. Nevertheless, the potential mechanism whereby the inflammatory response reduces serum HDL-C levels is not simply defined but reduces apolipoprotein A1 production. The alterations in HDL structure mediated by the inflammatory response has been also confirmed to decrease the ability of HDL particle to play an important role in reverse cholesterol transport and protect the LDL particles from oxidation. Recently, it has been shown that under the inflammatory condition, diverse alterations in HDL structure could be observed which lead to changes in HDL function. In the current review, the emerging effects of inflammatory response on HDL particles structure and function are well-summarized to elucidate the potential mechanism whereby different inflammatory status modulates the pathogenic development of dyslipidemia.

     

Alcohol consumption and the risk of incident atrial fibrillation among people with cardiovascular disease

Background:

Moderate alcohol consumption may reduce cardiovascular events, but little is known about its effect on atrial fibrillation in people at high risk of such events. We examined the association between moderate alcohol consumption and the risk of incident atrial fibrillation among older adults with existing cardiovascular disease or diabetes.

Methods:

We analyzed data for 30 433 adults who participated in 2 large antihypertensive drug treatment trials and who had no atrial fibrillation at baseline. The patients were 55 years or older and had a history of cardiovascular disease or diabetes with end-organ damage. We classified levels of alcohol consumption according to median cut-off values for low, moderate and high intake based on guidelines used in various countries, and we defined binge drinking as more than 5 drinks a day. The primary outcome measure was incident atrial fibrillation.

Results:

A total of 2093 patients had incident atrial fibrillation. The age- and sex-standardized incidence rate per 1000 person-years was 14.5 among those with a low level of alcohol consumption, 17.3 among those with a moderate level and 20.8 among those with a high level. Compared with participants who had a low level of consumption, those with higher levels had an increased risk of incident atrial fibrillation (adjusted hazard ratio [HR] 1.14, 95% confidence interval [CI] 1.04–1.26, for moderate consumption; 1.32, 95% CI 0.97–1.80, for high consumption). Results were similar after we excluded binge drinkers. Among those with moderate alcohol consumption, binge drinkers had an increased risk of atrial fibrillation compared with non–binge drinkers (adjusted HR 1.29, 95% CI 1.02–1.62).

Interpretation:

Moderate to high alcohol intake was associated with an increased incidence of atrial fibrillation among people aged 55 or older with cardiovascular disease or diabetes. Among moderate drinkers, the effect of binge drinking on the risk of atrial fibrillation was similar to that of habitual heavy drinking.A trial fibrillation is associated with an increased risk of stroke and a related high burden of mortality and morbidity, both in the general public and among patients with existing cardiovascular disease.^1,2 The prevalence of atrial fibrillation increases steadily with age, as do the associated risks, and atrial fibrillation accounts for up to 23.5% of all strokes among elderly people.³Moderate alcohol consumption has been reported to be associated with a reduced risk of cardiovascular disease and all-cause death,^1,2 whereas heavy alcohol intake and binge drinking have been associated with an increased risk of stroke,⁴ cardiovascular disease and all-cause death.^5,6 Similarly, heavy drinking and binge drinking are associated with an increased risk of incident atrial fibrillation in the general population.⁷ However, the association between moderate drinking and incident atrial fibrillation is less consistent and not well understood among older people with existing cardiovascular disease.In this analysis, we examined whether drinking moderate quantities of alcohol, and binge drinking, would be associated with an increased risk of incident atrial fibrillation in a large cohort of people with existing cardiovascular disease or diabetes with end-organ damage who had been followed prospectively in 2 long-term antihypertensive drug treatment trials.     

The HDL hypothesis: does high-density lipoprotein protect from atherosclerosis?

There is unequivocal evidence of an inverse association between plasma high-density lipoprotein (HDL) cholesterol concentrations and the risk of cardiovascular disease, a finding that has led to the hypothesis that HDL protects from atherosclerosis. This review details the experimental evidence for this “HDL hypothesis”. In vitro studies suggest that HDL has a wide range of anti-atherogenic properties but validation of these functions in humans is absent to date. A significant number of animal studies and clinical trials support an atheroprotective role for HDL; however, most of these findings were obtained in the context of marked changes in other plasma lipids. Finally, genetic studies in humans have not provided convincing evidence that HDL genes modulate cardiovascular risk. Thus, despite a wealth of information on this intriguing lipoprotein, future research remains essential to prove the HDL hypothesis correct.     

Moderate acute intake of de-alcoholized red wine, but not alcohol, is protective against radiation-induced DNA damage ex vivo -- results of a comparative in vivo intervention study in younger men

Moderate intake of wine is associated with reduced risk of cardiovascular disease and possibly cancer however it remains unclear whether the potential health benefits of wine intake are due to alcohol or the non-alcoholic fraction of wine. We therefore tested the hypothesis that the non-alcoholic fraction of wine protects against genome damage induced by oxidative stress in a crossover intervention study involving six young adult males aged 21-26 years. The participants adhered to a low plant phenolic compound diet for 48 h prior to consuming 300 mL of complete red wine, de-alcoholized red wine or ethanol on separate occasions 1 week apart. Blood samples were collected 0.5, 1.0 and 2.0 h after beverage consumption. Baseline and radiation-induced genome damage was measured using the cytokinesis-block micronucleus assay and total plasma catechin concentration was measured. Consumption of de-alcoholized red wine significantly decreased the gamma radiation-induced DNA damage at 1 and 2 h post-consumption by 20%. In contrast alcohol tended to increase radiation-induced genome damage and complete wine protected against radiation-induced genome damage relative to alcohol. The observed effects were only weakly correlated with the concentration of total plasma catechin (R=-0.23). These preliminary data suggest that only the non-alcoholic fraction of red wine protects DNA from oxidative damage but this effect cannot be explained solely by plasma catechin.     

The Association between Triglyceride/High-Density Lipoprotein Cholesterol Ratio and All-Cause Mortality in Acute Coronary Syndrome after Coronary Revascularization

Aims

High triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C) are cardiovascular risk factors. A positive correlation between elevated TG/HDL-C ratio and all-cause mortality and cardiovascular events exists in women. However, utility of TG to HDL-C ratio for prediction is unknown among acute coronary syndrome (ACS).

Methods

Fasting lipid profiles, detailed demographic data, and clinical data were obtained at baseline from 416 patients with ACS after coronary revascularization. Subjects were stratified into three levels of TG/HDL-C. We constructed multivariate Cox-proportional hazard models for all-cause mortality over a median follow-up of 3 years using log TG to HDL-C ratio as a predictor variable and analyzing traditional cardiovascular risk factors. We constructed a logistic regression model for major adverse cardiovascular events (MACEs) to prove that the TG/HDL-C ratio is a risk factor.

Results

The subject’s mean age was 64 ± 11 years; 54.5% were hypertensive, 21.8% diabetic, and 61.0% current or prior smokers. TG/HDL-C ratio ranged from 0.27 to 14.33. During the follow-up period, there were 43 deaths. In multivariate Cox models after adjusting for age, smoking, hypertension, diabetes, and severity of angiographic coronary disease, patients in the highest tertile of ACS had a 5.32-fold increased risk of mortality compared with the lowest tertile. After adjusting for conventional coronary heart disease risk factors by the logistic regression model, the TG/HDL-C ratio was associated with MACEs.

Conclusion

The TG to HDL-C ratio is a powerful independent predictor of all-cause mortality and is a risk factor of cardiovascular events.     

Genetic causes of high and low serum HDL-cholesterol

Plasma levels of HDL cholesterol (HDL-C) have a strong inherited basis with heritability estimates of 40-60%. The well-established inverse relationship between plasma HDL-C levels and the risk of coronary artery disease (CAD) has led to an extensive search for genetic factors influencing HDL-C concentrations. Over the past 30 years, candidate gene, genome-wide linkage, and most recently genome-wide association (GWA) studies have identified several genetic variations for plasma HDL-C levels. However, the functional role of several of these variants remains unknown, and they do not always correlate with CAD. In this review, we will first summarize what is known about HDL metabolism, monogenic disorders associated with both low and high HDL-C levels, and candidate gene studies. Then we will focus this review on recent genetic findings from the GWA studies and future strategies to elucidate the remaining substantial proportion of HDL-C heritability. Comprehensive investigation of the genetic factors conferring to low and high HDL-C levels using integrative approaches is important to unravel novel pathways and their relations to CAD, so that more effective means of diagnosis, treatment, and prevention will be identified.     

Obesity, adiponectin and vascular inflammatory disease

PURPOSE OF REVIEW: Obesity is the most common risk factor for cardiovascular diseases in industrial countries. It is now clear that adipose tissue secretes various bioactive substances, conceptualized as adipocytokines, and that dysregulation of adipocytokines directly contributes to obesity-related diseases. Chronic inflammatory processes contribute to the development of atherosclerosis. In this review, the authors focus on the relationship between adiponectin, a recently discovered anti-atherogenic adipocytokine, and vascular inflammation. RECENT FINDINGS: Plasma concentrations of adiponectin, an adipocyte-specific protein, are reduced in obese subjects and in patients with type 2 diabetes and coronary artery disease. Adiponectin inhibits the expression of tumor necrosis factor-alpha-induced endothelial adhesion molecules, macrophage-to-foam cell transformation, tumor necrosis factor-alpha expression in macrophages and adipose tissues, and smooth muscle cell proliferation. In addition, adenovirus-expressed adiponectin reduces atherosclerotic lesions in a mouse model of atherosclerosis, and adiponectin-deficient mice exhibit an excessive vascular remodeling response to injury. Clinically, hypoadiponectinemia is closely associated with increased levels of inflammatory markers such as C-reactive protein and interleukin-6. SUMMARY: Adiponectin acts as an anti-inflammatory and anti-atherogenic plasma protein. Adiponectin is an endogenous biologically relevant modulator of vascular remodeling linking obesity and vascular disease.     

Antiatherogenic potential of red wine: clinician update

Complications of atherosclerosis remain the leading cause of morbidity and mortality in industrialized countries. Epidemiological studies have repeatedly demonstrated that moderate alcohol intake has a beneficial effect on cardiovascular disease. The purpose of this review is to examine the epidemiological and biological evidence supporting the intake of red wine as a means of reducing atherosclerosis. On the basis of epidemiological studies, moderate intake of alcoholic beverages, including red wine, reduces the risk of cardiovascular, cerebrovascular, and peripheral vascular disease in populations. In addition to the favorable biological effects of alcohol on the lipid profile, on hemostatic factors, and in reducing insulin resistance, the phenolic compounds in red wine appear to interfere with the molecular processes underlying the initiation, progression, and rupture of atherosclerotic plaques. Whether red wine is more beneficial than other types of alcohol remains unclear. Definitive data from a large-scale, randomized clinical end-point trial of red wine intake would be required before physicians can advise patients to use wine as part of preventative or medical therapies.     

Modulation of oxidative stress, inflammation, and atherosclerosis by lipoprotein-associated phospholipase A2

Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), also known as platelet-activating factor acetylhydrolase (PAF-AH), is a unique member of the phospholipase A(2) superfamily. This enzyme is characterized by its ability to specifically hydrolyze PAF as well as glycerophospholipids containing short, truncated, and/or oxidized fatty acyl groups at the sn-2 position of the glycerol backbone. In humans, Lp-PLA(2) circulates in active form as a complex with low- and high-density lipoproteins. Clinical studies have reported that plasma Lp-PLA(2) activity and mass are strongly associated with atherogenic lipids and vascular risk. These observations led to the hypothesis that Lp-PLA(2) activity and/or mass levels could be used as biomarkers of cardiovascular disease and that inhibition of the activity could offer an attractive therapeutic strategy. Darapladib, a compound that inhibits Lp-PLA(2) activity, is anti-atherogenic in mice and other animals, and it decreases atherosclerotic plaque expansion in humans. However, disagreement continues to exist regarding the validity of Lp-PLA(2) as an independent marker of atherosclerosis and a scientifically justified target for intervention. Circulating Lp-PLA(2) mass and activity are associated with vascular risk, but the strength of the association is reduced after adjustment for basal concentrations of the lipoprotein carriers with which the enzyme associates. Genetic studies in humans harboring an inactivating mutation at this locus indicate that loss of Lp-PLA(2) function is a risk factor for inflammatory and vascular conditions in Japanese cohorts. Consistently, overexpression of Lp-PLA(2) has anti-inflammatory and anti-atherogenic properties in animal models. This thematic review critically discusses results from laboratory and animal studies, analyzes genetic evidence, reviews clinical work demonstrating associations between Lp-PLA(2) and vascular disease, and summarizes results from animal and human clinical trials in which administration of darapladib was tested as a strategy for the management of atherosclerosis.     

Relationships between Diet,Alcohol Preference,and Heart Disease and Type 2 Diabetes among Americans

Although excessive alcohol consumption is a recognized cause of morbidity and mortality, many studies have linked moderate alcohol consumption to improved cardiovascular health and a lower risk of Type 2 Diabetes (T2D). Self-reported alcohol and diet data used to generate these results suffer from measurement error due to recall bias. We estimate the effects of diet, alcohol, and lifestyle choices on the prevalence and incidence of cardiovascular disease and T2D among U.S. adults using a nationally representative cohort of households with scanner data representing their food-at-home, alcohol, and tobacco purchases from 2007-2010, and self-reported health surveys for the same study participants from 2010-2012. Multivariate regression models were used to identify significant associations among purchase data and lifestyle/demographic factors with disease prevalence in 2010, and with incidence of new disease from 2011-2012. After controlling for important confounders, respondents who purchased moderate levels of wine were 25% less likely than non-drinkers to report heart disease in 2010. However, no alcohol-related expenditure variables significantly affected the likelihood of reporting incident heart disease from 2011-2012. In contrast, many types of alcohol-related purchases were associated with a lower prevalence of T2D, and respondents who purchased the greatest volumes of wine or beer—but not liquor—were less likely to report being diagnosed with T2D in 2011-2012 than non-drinkers.     

Anti-inflammatory drugs and atherosclerosis

PURPOSE OF REVIEW: Inflammation contributes to the formation and progression of atherosclerosis and the therapeutic potential of some anti-inflammatory drugs has been evaluated for possible antiatherosclerotic effects. This review will briefly describe the mechanisms underlying the inflammation-atherosclerosis connection, the effect of various anti-inflammatory therapies on atherosclerotic disease and a sampling of the potential targets and agents under evaluation. RECENT FINDINGS: Some agents with anti-inflammatory properties appear to have beneficial effects on atherosclerosis or subsequent risk for cardiovascular events, while others have been disappointing. The anti-inflammatory actions of statins have been linked retrospectively with their favorable effects on atherosclerosis progression and clinical outcomes. The cardiovascular safety of COX-2 inhibitors is being assessed prospectively in patients with atherosclerosis. Potential new therapeutic agents targeting other inflammatory mechanisms and oxidative stress are being evaluated in animal models and clinical trials. SUMMARY: Due to the contributory inflammatory pathways in atherosclerosis, the properties of existing and novel anti-inflammatory agents are being carefully and actively evaluated in cardiovascular disease. Advances in our understanding of both atherosclerosis and the inflammatory contributors may play an important role in future strategies to decrease the incidence of atherosclerotic cardiovascular disease.     

Glycemic index, postprandial glycemia and cardiovascular disease

PURPOSE OF REVIEW: Several lines of evidence indicate that exaggerated postprandial glycemia puts individuals without diabetes at greater risk of developing cardiovascular disease. In large, prospective observational studies, including meta-analyses, higher 120 min post-load blood glucose and glycated hemoglobin (a measure of average blood glucose level over time) independently predict cardiovascular mortality and morbidity in individuals without diabetes. These findings imply that the glycemic nature of dietary carbohydrates may also be relevant. We aim to provide a clearer perspective on how the glycemic impact of carbohydrates may modulate development of cardiovascular disease. RECENT FINDINGS: In ecological studies, average dietary glycemic index (a measure of the postprandial glycemic potential of carbohydrates) and glycemic load (average glycemic index x amount of carbohydrate) predicts coronary infarct and cardiovascular disease risk factors, including HDL cholesterol, triglycerides and C-reactive protein. In short-term intervention studies of overweight and hyperlipidemic patients, low glycemic index diets lead to improvements in cardiovascular disease risk factors, including reduced LDL cholesterol and improved insulin sensitivity, as well as greater body fat loss on energy-restricted diets. Molecular studies indicate that physiological hyperglycemia induces overproduction of superoxide by the mitochondrial electron-transport chain, resulting in inflammatory responses and endothelial dysfunction. SUMMARY: Taken together, the findings suggest that conventional high-carbohydrate diets with their high glycemic index may be suboptimal, particularly in insulin-resistant individuals. Because around one in four adults has impairments in postprandial glucose regulation, the glycemic potential of carbohydrates warrants further investigation in cardiovascular disease prevention.     

Risk of dementia and alcohol and wine consumption: a review of recent results

The term dementia refers to a clinical syndrome of acquired intellectual disturbances produced by brain dysfunction. Dementia may result from a wide variety of disorders, including degenerative (e.g. Alzheimer's disease, AD), vascular (e.g. multi-infarct dementia), and traumatic (e.g. head injury). Long-term abuse of alcohol is related to the development of the Wernicke-Korsakoff's syndrome or alcohol dementia. However, light to moderate alcohol intake might also reduce the risk of dementia and AD. In Bordeaux (France), a population-based prospective study found that subjects drinking 3 to 4 standard glasses of wine per day (> 250 and up to 500 ml), categorized as moderate drinkers, the crude odds ratio (OR) was 0.18 for incident dementia (p < 0.01) and 0.25 for Alzheimer's disease (p < 0.03), as compared to the non-drinkers. After adjusting for age, sex, education, occupation, baseline cognitive performances and other possible confounders, the ORs were respectively 0.19 (p < 0.01) and 0.28 (p < 0.05). In the 922 mild drinkers (< 1 to 2 glasses per day) there was a negative association only with AD. after adjustment (OR = 0.55; p < 0.05). The inverse relationship between moderate wine drinking and incident dementia was explained neither by known predictors of dementia nor by medical, psychological or socio-familial factors. These results were confirmed from data of the Rotterdam study. Light-to-moderate drinking (one to three drinks per day) was significantly associated with a lower risk of any dementia (hazard ratio 0.58 [95% CI 0.38-0.90]) and vascular dementia (hazard ratio 0.29 [0.09-0.93]). No evidence that the relation between alcohol and dementia varied by type of alcoholic beverage was found. Stroke constitutes one of the most common causes of serious functional impairment in developed countries. Ischaemic strokes represent about 80% of all strokes. Several studies have been published and the overall conclusion is that heavy drinking is a risk factor for most stroke subtypes. Regular light to moderate drinking seemed to be associated with a decreased risk for ischaemic stroke.     

A prospective study of HDL-C and cholesteryl ester transfer protein gene mutations and the risk of coronary heart disease in the elderly

High density lipoprotein cholesterol (HDL-C) levels are inversely associated with the incidence of coronary heart disease (CHD) in middle-aged individuals; in the elderly, the association is less clear. Genetic factors, including variations in the cholesteryl ester transfer protein (CETP) gene, play a role in determining HDL-C levels. Controversy remains about whether CETP deficiency and the resultant rise in HDL-C are antiatherogenic, or whether CETP has the opposite effect due to its role in reverse cholesterol transport. In a seven-year follow-up of 2340 men aged 71-93 in the Honolulu Heart Program, the age-adjusted CHD incidence rates were significantly lower in men with high versus low HDL-C levels. After adjustment for age, hypertension, smoking, and total cholesterol, the relative risk of CHD for those with HDL-C levels >or=60 mg/dl, compared with those with HDL-C levels <40 mg/dl, was 0.6. Men with a CETP mutation had the lowest rates of CHD, although this was not statistically significant. These data indicate that HDL-C remains an important risk factor for CHD in the elderly. Whether a CETP mutation offers additional protection against CHD warrants further investigation.     

不同海拔地区藏族就诊人群血脂、血液黏度、HCY水平与心血管疾病的相关性研究

目的:探讨不同海拔地区藏族就诊人群血脂、血液黏度、HCY水平与心血管疾病的相关性。方法:采用回顾性分析的方法,将328例来自不同海拔地区的藏族就诊患者为三组,高海拔组(纳入99例),中海拔(纳入120例)和低海拔组(纳入109例),比较不同海拔高度组患者血压、血脂、血液黏度、HCY、疾病类型的差异,采用多元Logistic回归模型分析藏族就诊人群心血管疾病发病的影响因素。结果:不同海拔组收缩压、舒张压、血清HCY、TC、TG、HDL-C、LDL-C水平、全血黏度低切、中切、高切、血浆黏度和红细胞压积比较差异均有统计学意义(P0.05),随着海拔升高,收缩压、舒张压、血清HCY、TC、TG以及LDL-C、全血黏度低切、中切、高切、血浆黏度和红细胞压积水平显著升高(P0.05),而血清HDL-C水平显著下降。41.8%(137/328)的就诊者至少患有一种心血管疾病,和非心血管组比较,心血管疾病组年龄明显偏高,居住主要分布在中度及高度海拔地区,合并高血糖、高血脂、高HCY的比例均明显较高,差异均有统计学意义(P0.05)。年龄、海拔、高血糖、高血脂、高HCY均和心血管疾病相关(r=-0.230~0.334,P0.05)。多元Logistic回归分析显示年龄、居住地海拔、HCY水平、全血低切粘度、TG水平、LDL-C等因素是心血管疾病发生的危险因素,HDL-C是保护因素。结论:来自不同海拔地区的就诊人群在血压、血脂、血液黏度、HCY水平以及心血管疾病患者占比不同。年龄、居住地海拔、HCY水平、血液黏度、血脂水平等增加可能使高原藏族人群心血管疾病发生风险增加。