Vegetarianism, coronary disease risk factors and coronary heart disease

Recent studies of vegetarians confirm a lower risk of fatal heart disease amongst such subjects. Lipid levels are lower in vegetarians, even when the diet of comparable meat-eaters is low in fat. This may partly explain the lower mortality, but it is not clear whether the absence of meat or some other aspect of the vegetarian diet is causal in this relationship.     

Homocysteine, vitamins B6, B12, folate, and risk of coronary artery disease in patients undergoing diagnostic coronary angiography

Summary. Homocysteine and vitamins B were correlated with coronary artery disease in patients undergoing diagnostic coronary angiography. 160 patients having ≧1 stenosis (G1), 55 patients having normal coronary arteries (G2) and 171 healthy volunteers (G3) were prospectively recruited. Homocysteine levels were significantly higher in patients, particulary in those with normal coronary angiograms, than in healthy subjects (13.8 ± 6.3 μmol/L in G1 (p < 0.0001) and 15.2 ± 8.8 μmol/L in G2 (p < 0.0001) versus 10.1 ± 3.1 μmol/L in G3). Homocysteine levels were not related to the extent of coronary artery disease. In patients with normal angiogram, vitamin B12 and folate levels were significantly higher compared with the other groups (p < 0.05 and p < 0.001, respectively) showing that vitamin B deficiency was not involved in the hyperhomocysteinemia. In conclusion, homocysteine and vitamins B levels do not contribute to discriminate for the presence of coronary artery disease in patients undergoing diagnostic coronary angiography. Homocysteine levels, however, were higher in patients referred for coronary angiography than in healthy controls. Received November 7, 1998, Accepted February 20, 1999     

Leptin receptors are expressed in coronary arteries, and hyperleptinemia causes significant coronary endothelial dysfunction

Obesity is associated with marked increases in plasma leptin concentration, and hyperleptinemia is an independent risk factor for coronary artery disease. As a result, the purpose of this investigation was to test the following hypotheses: 1) leptin receptors are expressed in coronary endothelial cells; and 2) hyperleptinemia induces coronary endothelial dysfunction. RT-PCR analysis revealed that the leptin receptor gene is expressed in canine coronary arteries and human coronary endothelium. Furthermore, immunocytochemistry demonstrated that the long-form leptin receptor protein (ObRb) is present in human coronary endothelium. The functional effects of leptin were determined using pressurized coronary arterioles (<130 microm) isolated from Wistar rats, Zucker rats, and mongrel dogs. Leptin induced pharmacological vasodilation that was abolished by denudation and the nitric oxide synthase inhibitor N(omega)-nitro-l-arginine methyl ester and was absent in obese Zucker rats. Intracoronary leptin dose-response experiments were conducted in anesthetized dogs. Normal and obese concentrations of leptin (0.1-3.0 microg/min ic) did not significantly change coronary blood flow or myocardial oxygen consumption; however, obese concentrations of leptin significantly attenuated the dilation to graded intracoronary doses of acetylcholine (0.3-30.0 microg/min). Additional experiments were performed in canine coronary rings, and relaxation to acetylcholine (6.25 nmol/l-6.25 micromol/l) was significantly attenuated by obese concentrations of leptin (625 pmol/l) but not by physiological concentrations of leptin (250 pmol/l). The major findings of this investigation were as follows: 1) the ObRb is present in coronary arteries and coupled to pharmacological, nitric oxide-dependent vasodilation; and 2) hyperleptinemia produces significant coronary endothelial dysfunction.     

Educational status,coronary heart disease,and coronary risk factor prevalence in a rural population of India.

OBJECTIVE--To define the association between educational level and prevalence of coronary heart disease and coronary risk factors in India. DESIGN--Total community cross sectional survey with a doctor administered questionnaire, physical examination, and electrocardiography. SETTING--A cluster of three villages in rural Rajasthan, western India. SUBJECTS--3148 residents aged over 20 (1982 men, 1166 women) divided into various groups according to years of formal schooling. RESULTS--Illiteracy and low educational levels were associated with less prestigious occupations (agricultural and farm labouring) and inferior housing. There was an inverse correlation of educational level with age (rank correlation: mean -0.45, women -0.49). The prevalence of coronary heart disease (diagnosed by electrocardiography) was significantly higher among uneducated and less educated people and showed an inverse relation with education in both sexes. Among uneducated and less educated people there was a higher prevalence of the coronary risk factors smoking and hypertension. Educational level showed a significant inverse correlation with systolic and diastolic blood pressure. Logistic regression analysis with adjustment for age showed that educational level had an inverse relation with prevalence of electrocardiographically diagnosed coronary heart disease (odds ratio: men 0.82, women 0.53), hypertension (men 0.88, women 0.56), and smoking (men 0.73, women 0.65) but not with hypercholesterolaemia and obesity. The inverse relation of coronary heart disease with educational level abated after adjustment for smoking, physical activity, body mass index, and blood pressure (odds ratio: men 0.98, women 0.78). CONCLUSION--Uneducated and less educated people in rural India have a higher prevalence of coronary heart disease and of the coronary risk factors smoking and hypertension.     

Estrogens, progestins, and coronary artery reactivity in atherosclerotic monkeys

It has been known for many years that sex hormones modulate vasodilator responses of arteries supplying the uterus with blood. Recently, it has been shown that sex hormones such as estrogen modulate vasomotor responses of other arteries, including coronary arteries. It is thought that modulation of vasodilator and constrictor responses of coronary arteries may be one mechanism by which estrogen affects the risk of coronary heart disease. Although several studies have examined the effects (and potential mechanisms) of estrogen on vasodilator responses of nonatherosclerotic arteries, few have focused on estrogen's effects on atherosclerotic coronary arteries. In studies of ovariectomized atherosclerotic female cynomolgus monkeys, both long-term (2 years) and short-term (20 min) estradiol treatment augments dilator responses to acetylcholine, but not nitroglycerin. Presumably, this indicates an effect of estradiol on endothelium-mediated dilator responses of coronary arteries. Addition of the progestin medroxyprogesterone acetate diminishes the beneficial effect of conjugated equine estrogens on these dilator responses. This is significant because a progestin is usually added to estrogen replacement to reduce the risk of endometrial and breast cancer associated with unopposed estrogen therapy. However, it would seem that not all progestins act similarly on vascular reactivity. Studies in monkeys indicate that addition of progesterone or the progestin medroxyprogesterone acetate does not diminish the beneficial effects of estrogen on coronary dilator responses. Thus it would appear that different estrogen/progestin combinations may affect vascular reactivity in different manners, There is also an effort being made to examine the potential of different kinds of estrogens on cardiovascular risk. Studies in monkeys indicate that one of the estrogens found in conjugated equine estrogens (17 alpha-dihydroequilenin) has estrogen effects on vascular reactivity without having detrimental effects on uterine pathology. The isoflavones “plant estrogens” found in soy protein also have estrogenic effects on vascular reactivity and inhibition.     

Lycopene,tomatoes, and coronary heart disease

Tomato and its major antioxidant component lycopene have recently been focused as important antioxidant nutrients because of their ability to reduce reactive oxygen species and to provide health benefits. Most of the studies were undertaken to determine the usefulness of lycopene against cancer and cardiovascular diseases. Epidemiological studies, however, yielded conflicting results. This study was undertaken to compare cardioprotective abilities of tomato juice and lycopene. Rats were gavaged either tomato juice or lycopene for 3 weeks. At the end of 3 weeks, isolated hearts were subjected to 30?min ischemia followed by 2?h of reperfusion. Both tomato juice and lycopene reduced the extent of lipid peroxidation; but only tomato juice, but not lycopene, improved post-ischemic ventricular function, and reduced myocardial infarct size and cardiomyocyte apoptosis. The results indicated for the first time that tomato juice, but not lycopene, possesses cardioprotective ability.     

Lycopene, tomatoes, and coronary heart disease

Tomato and its major antioxidant component lycopene have recently been focused as important antioxidant nutrients because of their ability to reduce reactive oxygen species and to provide health benefits. Most of the studies were undertaken to determine the usefulness of lycopene against cancer and cardiovascular diseases. Epidemiological studies, however, yielded conflicting results. This study was undertaken to compare cardioprotective abilities of tomato juice and lycopene. Rats were gavaged either tomato juice or lycopene for 3 weeks. At the end of 3 weeks, isolated hearts were subjected to 30 min ischemia followed by 2 h of reperfusion. Both tomato juice and lycopene reduced the extent of lipid peroxidation; but only tomato juice, but not lycopene, improved post-ischemic ventricular function, and reduced myocardial infarct size and cardiomyocyte apoptosis. The results indicated for the first time that tomato juice, but not lycopene, possesses cardioprotective ability.     

Lycopene,atherosclerosis, and coronary heart disease

Diets rich in fruits and vegetables containing carotenoids have been of interest because of their potential health benefit against chronic diseases such as cardiovascular diseases (CVD) and cancer. Interest particularly in lycopene is growing rapidly following the recent publication of epidemiological studies that have associated high lycopene levels with reductions in CVD incidence. Two studies were conducted. In the first one, we examined the role of lycopene as a risk-lowering factor with regard to acute coronary events and stroke in the prospective Kuopio Ischemic Heart Disease Risk Factor (KIHD) Study. The subjects were 725 middle-aged men free of coronary heart disease and stroke at the study baseline. In a Cox's proportional hazards' model adjusting for covariates, men in the lowest quartile of serum levels of lycopene had a 3.3-fold (P < 0.001) risk of the acute coronary event or stroke as compared with others. In the second study, we assessed the association between plasma concentration of lycopene and intima-media thickness of the common carotid artery wall (CCA-IMT) in a cross-sectional analysis of the Antioxidant Supplementation in the Atherosclerosis Prevention (ASAP) study data in 520 asymptomatic men and women. In a covariance analysis adjusting for common cardiovascular risk factors, low plasma levels of lycopene were associated with an 18% increase of IMT in men as compared with men in whom plasma levels were higher than median (P = 0.003 for difference). In women, the difference did not remain significant after the adjustments. On the basis of these works, it is evident that the circulating levels of lycopene play some role with regard to cardiovascular health in Finland, at least in men. We conclude that circulating levels of lycopene, a biomarker of tomato-rich food, may play a role in early stages of atherogenesis and may have clinical and public health relevance.     

Coffee, caffeine, and coronary heart disease

PURPOSE OF REVIEW: This review summarizes and highlights recent advances in current knowledge of the relationship between coffee and caffeine consumption and risk of coronary heart disease. Potential mechanisms and genetic modifiers of this relationship are also discussed. RECENT FINDINGS: Studies examining the association between coffee consumption and coronary heart disease have been inconclusive. Coffee is a complex mixture of compounds that may have either beneficial or harmful effects on the cardiovascular system. Randomized controlled trials have confirmed the cholesterol-raising effect of diterpenes present in boiled coffee, which may contribute to the risk of coronary heart disease associated with unfiltered coffee consumption. A recent study examining the relationship between coffee and risk of myocardial infarction incorporated a genetic polymorphism associated with a slower rate of caffeine metabolism and provides strong evidence that caffeine also affects risk of coronary heart disease. Several studies have reported a protective effect of moderate coffee consumption, which suggests that coffee contains other compounds that may be beneficial. SUMMARY: Diterpenes present in unfiltered coffee and caffeine each appear to increase risk of coronary heart disease. A lower risk of coronary heart disease among moderate coffee drinkers might be due to antioxidants found in coffee.     

Thrombosis, physical activity, and acute coronary syndromes

Acute coronary syndromes (ACS) are common, life-threatening cardiac disorders that typically are triggered by rupture or erosion of an atherosclerotic plaque. Platelet deposition and activation of the blood coagulation cascade in response to plaque disruption lead to the formation of a platelet-fibrin thrombus, which can grow rapidly, obstruct coronary blood flow, and cause myocardial ischemia and/or infarction. Several clinical studies have examined the relationship between physical activity and ACS, and numerous preclinical and clinical studies have examined specific effects of sustained physical training and acute physical activity on atherosclerotic plaque rupture, platelet function, and formation and clearance of intravascular fibrin. This article reviews the available literature regarding the role of physical activity in determining the incidence of atherosclerotic plaque rupture and the pace and extent of thrombus formation after plaque rupture.     

Endothelium, arachidonic acid, and coronary vascular tone

Vasoactive mediators play an important role in the control of coronary vascular tone. Arachidonic acid (AA) metabolites and endothelium-derived vasoactive factors have been implicated in coronary vasoregulation. AA can be metabolized via three separate routes in blood vessels, mediated by cyclooxygenase, lipoxygenase, and cytochrome P-450-dependent monooxygenase enzymes. AA can evoke endothelium-dependent relaxations that are due in part to the formation of cytochrome P-450-dependent metabolites, inasmuch as drugs that modify cytochrome P-450 activity produce parallel changes in endothelium-dependent relaxations to AA. Moreover, some cytochrome P-450-derived metabolites formed biologically cause relaxations of isolated blood vessels. A cytochrome P-450-dependent pathway does not appear to contribute to endothelium-dependent relaxations induced by acetylcholine, which suggests that there may be a number of endothelium-derived relaxing factors (EDRFs). In addition, two endothelium-derived contractile factors have been described, including an unidentified cyclooxygenase metabolite of AA and a polypeptide isolated from cultured cells. As both prostaglandin I2 and acetylcholine-induced EDRF also inhibit platelet aggregation, endothelial injury and loss of these factors may predispose to vasospasm precipitated by release of platelet-derived mediators such as thromboxane A2 (TXA2) and 5-hydroxytryptamine. Unstable angina may be a clinical syndrome in which these events occur, which can be alleviated by inhibition of platelet activation and TXA2 formation with aspirin. Attenuation of endothelium-dependent relaxations can also occur without loss of endothelial cells. Neutrophil-endothelium interactions, precipitated by an ischemic episode, may initiate endothelial dysfunction and underlie the development of vasospasm in some conditions. Whether increased production of endothelium-derived contractile factors also occurs in vasospastic conditions remains to be determined.     

Phytoestrogens, cancer and coronary heart disease

Recent results obtained in collaboration with many other groups with regard to phytoestrogens (isoflavones and lignans) and breast cancer, prostate cancer and cardiovascular disease are presented and discussed in light of new developments in the field. Both isoflavones and lignans may be protective with regard to these diseases, but we do not yet understand some of the controversial results obtained. In this short communication the possible mechanisms of disease prevention were not discussed.