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The association between alcohol intake and atherosclerotic cardiovascular disease (CVD) in epidemiological studies is consistent and shows some protection from CVD at consumption levels of one to two drinks per day, but a sharp increase in CVD associated with three or more drinks per day. Analyses of potential mediators of effects of alcohol on CVD show that it increases high density lipoprotein (HDL) cholesterol levels and favourably influences thrombotic factors, especially fibrinogen, and also fibrinolytic factors. Some evidence also suggests moderate alcohol consumption may reduce insulin resistance. However, studies also show an adverse effect of alcohol, particularly at higher doses, on blood pressure (leading to hypertension) and directly on the myocardium (leading to arrhythmias and myocardiopathy). Statistical modelling of the alcohol-CVD relationship is consistent in several studies, with a protective pathway via elevated HDL cholesterol and an adverse pathway through elevated blood pressure. Other possible mediators influenced by alcohol have not yet been examined in this type of analysis. The French Paradox has led to speculation that wine is the only protective alcoholic beverage for CVD, or at least that it has a stronger effect. Multiple non-ethanol components of wine have been studied in the laboratory and have been shown to have antioxidant or anticoagulant effects. Although wine does appear more protective in ecological studies, studies within cohorts show similar effects across alcoholic beverages, suggesting confounding in ecological studies by diet, lifestyle, or other variables. The key component of alcoholic beverages thus appears to be ethanol, consistent with the known potent effects of ethanol on HDL cholesterol and thrombotic factors. The upswing in CVD risk with three or more drinks per day is sharp and emphasizes that benefit from alcohol is limited to moderate consumption only. This upswing also cautions against any public health recommendation to drink alcohol, since many persons will not or cannot limit their intake to moderate levels.
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PMID:Do known cardiovascular risk factors mediate the effect of alcohol on cardiovascular disease? 994 92

Compelling evidence from clinical trials confirms the benefits of secondary prevention for patients with known coronary disease. Preventive therapies initiated after myocardial infarction can extend overall survival, reduce subsequent myocardial infarction, decrease the need for revascularization, and improve quality of life. All patients with atherosclerotic cardiovascular disease should be considered for lipid lowering therapy, antiplatelet agents, beta-blockers, and control of hypertension. Long-term therapy with angiotensin-converting enzyme inhibitors should be continued in patients with systolic dysfunction. Hormone replacement therapy has not been shown to benefit postmenopausal women when initiated after myocardial infarction. Smoking cessation, weight control, exercise, and appropriate diet represent important behavioral modifications.
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PMID:Current therapies for secondary prevention after myocardial infarction. 1019 75

Although branch retinal artery occlusion (BRAO) is a relatively benign disease in terms of permanent visual impairment, the associated systemic diseases confer significant morbidity and mortality. The following systemic disorders can be found among patients presenting with a retinal artery occlusion: hypertension (59%), significant atherosclerotic cardiovascular disease (21%), diabetes mellitus (15% to 21%), left-sided valvular heart disease (5%), and cerebrovascular accidents (5%). These underlying systemic diseases are often responsible for a significant reduction in life expectancy and are in many cases potentially treatable conditions. A thorough cardiovascular examination (including a carotid duplex ultrasonography) may identify these occult diseases, and a prompt and effective treatment may improve the quantity and quality of patients' lives by reducing the risk of further arterial occlusive events.
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PMID:Branch retinal artery occlusion in systemic diseases: a case report. 1035 55

Elevated blood pressure has consistently been associated with increased prevalence of preclinical atherosclerosis and with increased risk of clinical atherosclerotic cardiovascular disease (CVD). However, there is no prospective evidence of the association between blood pressure and the progression of preclinical atherosclerosis. We therefore investigated the relationships of systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure to the 4-year increase in the measures of early carotid atherosclerosis, the mean and maximal common carotid intima-media thickness (IMT), assessed by B-mode ultrasonography, in 1026 men aged 42 to 60 years. Men with the SBP of <120, 120 to 126, 127 to 134, 135 to 143, and >143 mm Hg (fifths) had an increase in the mean IMT of 0.074, 0.090, 0.110, 0.136, and 0.158 mm per 4 years (P<0.001 for difference between groups, P<0.001 for linear trend) and in the maximal IMT of 0.212, 0.221, 0.279, 0.286, and 0.315 mm per 4 years, (P<0.001, P<0.001), respectively, adjusting for other atherosclerotic risk factors, including DBP. Also, pulse pressure, when adjusted for other risk factors including mean arterial pressure, was directly associated with the IMT increase. DBP was not independently related to the IMT increase. This is the first documentation to show that mildly elevated SBP and pulse pressure accelerate the progression of preclinical atherosclerosis. This study provides further evidence for the finding that systolic hypertension is a more important risk factor for atherosclerosis and consequent CVD than diastolic hypertension. Therefore, more attention should be paid to the level of SBP in the evaluation of CVD risk and in the treatment of hypertension.
Hypertension 1999 Jul
PMID:Blood pressure and the progression of carotid atherosclerosis in middle-aged men. 1040 23

Traditional approaches to control the epidemic of blood pressure-related atherosclerotic cardiovascular disease (ASCVD) have largely focused on drug therapy in persons with hypertension. Still, nonpharmacologic therapy, also termed lifestyle modification, has an important and expanding role that complements drug therapy. Specifically, nonpharmacologic therapies can serve as initial therapy in Stage 1 hypertensive patients, facilitate medication step down or withdrawal in patients with well-controlled hypertension, prevent hypertension in high-risk populations, and reduce blood pressure in normotensive individuals and thereby lower their risk of ASCVD. Traditional lifestyle modifications that reduce blood pressure include sodium reduction, weight loss, moderation of alcohol intake, and increased physical activity. Such strategies have been prominently advocated in the Fifth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Recommendations to increase potassium, magnesium, and calcium intake were based primarily on general health considerations, not for control of high blood pressure. In its sixth and most recent report (JNC VI) published in 1997, the Joint National Committee has extended its recommendations. In addition to the traditional lifestyle recommendations, the JNC VI advocates increased potassium intake for control of high blood pressure. Furthermore, this policy-making body now recommends a healthy dietary pattern, that is, one that is rich in fruits, vegetables, and low-fat dairy products, and reduced in saturated fat, total fat, and cholesterol. This diet, which was rigorously evaluated in the Dietary Approaches to Stop Hypertension (DASH) clinical trial, substantially lowered blood pressure in normotensive and hypertensive individuals. These recent developments reinforce the hypothesis that multiple dietary factors influence blood pressure. Nonpharmacologic approaches have enormous potential as a means to reduce blood pressure and control hypertension, thereby preventing the occurrence of ASCVD. The current challenge to health care providers, government officials, and the general public is to develop and implement effective clinical and public health strategies that lead to desirable lifestyle modifications.
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PMID:Nonpharmacologic therapies that reduce blood pressure: a fresh perspective. 1041 Feb 98

In a cross-sectional study of 293 nondiabetic patients (169 men and 124 women) referred for the diagnosis and treatment of hyperlipidemia, our specific aim was to determine whether fasting serum insulin independently contributes to the prediction of atherosclerotic cardiovascular disease (ASCVD) status. Of the 169 men and 124 women, 65 (38%) and 44 (35%), respectively, had ASCVD with at least one of the following: unstable angina, myocardial infarction (MI), angioplasty, coronary artery bypass graft (CABG), claudication, transient ischemic attack, or ischemic stroke. In addition, 42% and 38% had fasting hyperinsulinemia (> or =20 microU/mL). Fasting serum insulin of 20 microU/mL or higher was very common in women (59% to 100%) and men (67% to 88%) when hypertension, obesity, top-decile triglyceride (TG), and bottom-decile high-density lipoprotein cholesterol (HDLC) were concurrent in various combinations. ASCVD events (present or absent) were dependent variables in a stepwise logistic regression model with explanatory variables including age, gender, race, hypertension, cigarette smoking, ASCVD in first-degree relatives at age 55 years or less, Quetelet Index, fasting serum insulin, a gender x insulin interaction term, anticardiolipin antibodies (ACLAs) IgG and IgM, total cholesterol to HDLC ratio, TG, lipoprotein(a) [Lp(a)], and homocysteine. The risk odds ratio for ASCVD (109 events and 184 nonevents) for subjects with top-decile insulin (vthe bottom nine deciles) was 3.71, with a 95% confidence interval (CI) of 1.62 to 8.9 (P = .002). For patients with MI and/or CABG and/or angioplasty ([MCA] 63 events and 184 nonevents), the risk odds ratio for top-decile insulin versus the rest was 5.07 (95% CI, 1.83 to 14.8, P = .002). For patients with MCA at age 55 or less, the gender x insulin interaction term was significant (P = .0004); the risk odds ratio for men with top-decile insulin was 13.28 (95% CI, 3.82 to 51.65, P = .0001). Hyperinsulinemia is very common in nondiabetic hyperlipidemic women and men. Fasting serum insulin, a crude, simple, practical, and inexpensive measure, independently and uniformly improved the prediction of ASCVD status beyond traditional risk factors and lipid variables in patients referred for treatment of hyperlipidemia.
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PMID:Contribution of fasting hyperinsulinemia to prediction of atherosclerotic cardiovascular disease status in 293 hyperlipidemic patients. 1058 54

Atherosclerotic cardiovascular disease is a major health problem in the United States. In particular, coronary heart disease (CHD) is the leading cause of death in men and women in the United States, as well as in other industrialized countries. Extensive observational epidemiologic data within and between populations have strongly linked such various factors as untreated hypertension, diabetes, cigarette smoking, and lipid abnormalities to the development of CHD. With respect to lipoprotein parameters, elevated total and low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C) have been strongly associated with CHD risk. Emerging evidence suggests that other lipoprotein abnormalities also are associated with premature CHD, including elevated levels of lipoprotein(a), triglyceride-rich lipoproteins such as small very-low-density lipoproteins and intermediate-density lipoproteins, small and dense LDL particles, and the magnitude of postprandial lipemia. Extensive primary and secondary clinical trial evidence has established that favorably altering dyslipidemias through diet and a variety of pharmacologic agents produces clear improvements in CHD end points. The extent of this benefit depends on the presence or absence of clinical atherosclerotic disease, as well as other CHD risk factors, and the severity of one or more lipoprotein abnormalities. CHD patients and individuals with multiple risk factors, but free of clinical CHD, derive the greatest absolute benefit from lipid treatment directed at reducing LDL-C. The dyslipidemias that impart high risk are severely elevated LDL-C (> 200 mg/dL), combined high LDL-C and low HDL-C (< 35 mg/dL), and combined hyperlipidemias (non-HDL-C > 200 mg/dL with low HDL). The purpose of this review is to aid the primary care physician in identifying these important dyslipidemias and to critically analyze the relative importance of various lipoproteins on atherosclerotic risk.
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PMID:Clinical diagnosis of lipid disorders. 1068 61

Hypertension (HT) has been known since times immemorial to be one of the major causes of morbidity and mortality. It contributes to atherosclerotic cardiovascular disease, increasing its risk 2-3 times and is also associated with dyslipidemia, insulin resistance, glucose intolerance and obesity (1). The age of onset of hypertension is now earlier than before, making it essential that early detection of people who could be future hypertensives is done. Therefore, cardiovascular reactivity to stress in predicting future hypertension becomes important. In this fast paced age most people are exposed to mental stress which is the most common and prevalent form of stress. Increase in blood pressure (BP) in response to emotional arousal is well known, but support for this hypothesis of reactivity in predicting future hypertension is limited. We are attempting here to put forth a review of the various endeavours done so far to support this hypothesis.
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PMID:Role of cardiovascular reactivity to mental stress in predicting future hypertension. 1068 21

Hypertension is estimated to affect 43 to 56 million adults or 24% to 31% of the US population and is emerging as a major health problem in some countries in the Third World. Hypertension contributes to all the major atherosclerotic cardiovascular disease outcomes.
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PMID:Home blood pressure monitoring. 1117 48

Microalbuminuria, i.e., slightly elevated albumin excretion in the urine, is considered a novel atheroslerotic risk factor. This supposition is based partly on two preliminary minor studies, partly on the current knowledge within the fields of diabetes mellitus and arterial hypertension. The aims of the present series of studies were 1) to examine whether a relationship exists between microalbuminuria and atherosclerotic cardiovascular disease in the general population, and 2) to illuminate possible pathophysiological mechanisms underlying this association. The studies were performed as sub-studies of the Copenhagen City Heart Study and the Monica Population Study. In the 3rd Copenhagen City Heart Study a cross-sectional analysis comprising 2,613 individuals without diabetes mellitus or renal- or urinary tract disease revealed a positive association between overnight urinary albumin excretion rate and a history of acute myocardial infarction. This association was independent of age, sex, conventional atherosclerotic risk factors, and glomerular filtration rate. Participants with a urinary albumin excretion rate exceeding the upper decile (7 micrograms/min) in the entire study population had a higher frequency of previous acute myocardial infarction than the others. In order to assess the time sequence of the observed association, this population will be followed prospectively. In the 1st Monica Population Study in Copenhagen County, 2,085 individuals without diabetes, mellitus, cardiovascular disease, or renal or urinary tract disease were followed for 10 years. Participants with a urinary albumin/creatinine concentration ratio exceeding the upper decile (0.65, mg/mmol) in the entire study population had a relative risk of 2.3 for developing ischaemic heart disease as compared to participants with a lower urinary albumin/creatinine concentration ratio. This predictive effect was independent of age, sex, and conventional atherosclerotic risk, factors, but it was not known whether participants with a urinary albumin/creatinine concentration ratio above the upper decile had severe subclinical atherosclerosis already at entrance to the study. A group of individuals with persistent microalbuminuria, and an age- and sex-matched control group with persistent normoalbuminuria underwent a clinical physiological and biochemical investigation program. None had developed clinically present atherosclerotic cardiovascular disease. Microalbuminuria was defined as a urinary albumin excretion rate exceeding the upper decile in the entire study population, normoalbuminuria as a lower urinary albumin excretion rate. Measurements of glomerular filtration rate and tubular function made it unlikely that the difference in urinary albumin excretion between the two study groups was due to local renal conditions exclusively, although reductions in both glomerular charge selectivity and size selectivity were observed in the microalbuminuric individuals. Individuals with persistent microalbuminuria had increased systemic transvascular albumin leakage to a level similar to that seen among individuals with severe clinical atherosclerosis. This could be explained neither by differences in blood pressure or concentration of plasma lipoproteins, both of which were more atherogenic in the microalbuminuric individuals, nor by differences in plasma volume or albumin concentration, antropometric factors, insulin sensitivity, or smoking habits. It is hypothesized that the systemic transvascular leakiness may also include lipoproteins, thus allowing for an increased lipid insudation into the vessel walls. The leakiness might be due to haemodynamic factors or structural or functional perturbations of the endothelium or the intracellular matrix beneath. Although endothelial dysfunction could not be demonstrated in the present studies, future research will focus on these possibilities.
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PMID:Microalbuminaria and the risk of atherosclerosis. Clinical epidemiological and physiological investigations. 1082 99


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