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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mounting data support a causal connection between high-normal fibrinogen levels and atherosclerotic cardiovascular disease. There is clearly a thrombogenic component to atherosclerosis and the onset of clinical manifestations. This offers the possibility to better identify high-risk candidates and also to protect them by reducing blood fibrinogen concentration or blocking its action. The relationship of antecedent fibrinogen to the subsequent development of cardiovascular disease is examined, based on 18 years of surveillance of a cohort of 1274 men and women aged 47 to 79 years who participated in the Framingham Study. The association with the development of peripheral arterial disease and cardiac failure is now examined in addition to previously studied relationships to coronary heart disease and stroke. In men and women, there is a significant age-adjusted relationship of fibrinogen level to coronary heart disease and to cardiovascular disease in general. In women, a significant relationship to cardiac failure and peripheral arterial disease, but not to stroke, was also found. These data on women are unique as they are not available elsewhere. Age-adjusted cardiovascular, all-cause, and coronary heart disease mortality were all related to fibrinogen in both sexes. In men, fibrinogen impact was the greatest for stroke and the least for peripheral arterial disease. For women, the impact on coronary heart disease was greatest. The absolute risk for an elevated fibrinogen level was greatest for coronary heart disease in both sexes. Average fibrinogen values are higher in women and in persons with other risk factors, including hypertension, cigarette smoking, diabetes, obesity, and elevated hematocrit. However, there is an independent contribution of fibrinogen to cardiovascular disease in general and coronary disease in particular, on adjustment for coexistent risk factors. Fibrinogen enhances the risk of cardiovascular disease in hypertensives, diabetics, and cigarette smokers. About half the cardiovascular risk of cigarette smoking appears due to the higher fibrinogen values. Now, five prospective studies document the excess incidence of cardiovascular events in persons with elevated fibrinogen levels within the "normal range." Each standard deviation increase in fibrinogen is associated with a 30% increment of coronary heart disease in men and a 40% increase in women. Fibrinogen should be added to the list of major cardiovascular risk factors. Trials of intervention to lower fibrinogen in high-risk coronary candidates are needed.
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PMID:Update on fibrinogen as a cardiovascular risk factor. 134 96

A male fat distribution pattern with abdominal obesity increases the risk for hypertension and cardiovascular disease, and is closely linked to a number of metabolic aberrations including insulin resistance. Recent observations suggest that changes in the peripheral vasculature may be of pathophysiological importance for the development of hypertension and its associated metabolic disturbances. We therefore investigated the hemodynamic correlates of abdominal obesity. A central fat distribution was found to be associated with a specific hemodynamic profile, characterized by elevated total peripheral resistance and lower cardiac output. In response to sympathoadrenal activation during mental stress, the normal cardiac output-dependent pressor response was reversed into a systemic vasoconstrictor response. There was a direct relationship between degree of abdominal obesity (expressed as waist-hip ratio) and fasting serum insulin. Furthermore, the stress-induced increase in total peripheral resistance correlated positively with fasting serum insulin concentration, whereas there was an inverse relation between serum insulin and cardiac output and heart rate. In a second study, the circulatory responses to stress during physiological hyperinsulinemia were investigated. During hyperglycemic hyperinsulinemia the central hemodynamic response to stress was changed into a systemic vasoconstrictor response. In the forearm the physiological vasodilation during stress was markedly attenuated, suggesting that insulin may have peripheral vascular effects. In conclusion, central obesity is associated with a specific hemodynamic pattern characterized by higher total peripheral resistance and lower cardiac output, and a vasoconstrictor response to psychosocial stress. This hemodynamic response pattern may be related to insulin metabolism.
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PMID:Hemodynamics of the male fat distribution pattern. 134 31

A number of risk factors/indicators for cardiovascular disease, mainly stroke and coronary artery disease, have been established. Most powerful among the traditional risk factors are hypertension, cigarette smoking and elevated serum cholesterol. All three can successfully be modified by therapeutic intervention, which in turn will result in reduced risks. In recent years several novel risk indicators have been identified. The most powerful of these appears to be increased left ventricular mass, particularly when diagnosed with echocardiographic technique. Again, it is possible to reduce this risk factor, for instance by antihypertensive therapy, but the independent risk reduction attributable to this manoeuvre remains to be determined. Other novel risk indicators are male type adipose distribution, reduced insulin sensitivity and a number of newly detected lipoprotein fractions. At present little is known about the value of intervention against these factors in terms of risk reduction. It can be concluded that a structured concerted effort at reducing established risk factors such as arterial hypertension, elevated serum cholesterol and cigarette smoking is desirable for forming the basis of preventive strategies in cardiology. As regards some of the novel risk indicators, some of which appear more powerful than the old established ones, further research is needed before a clear opinion can be formulated regarding the value of intervention.
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PMID:The key issues in preventive cardiology. 134 36

Left ventricular hypertrophy (LVH) is an independent risk indicator of cardiovascular disease. Obtaining reversal of hypertension-induced cardiac hypertrophy seems to be a desirable objective of antihypertensive treatment. A total of 2,357 patients were included in a meta-analysis on the effect of antihypertensive pharmacological therapy on LVH. Overall left ventricular mass (LVM) was reduced by 11.9% (95% confidence interval (CI) 10.1-13.7) in parallel with a reduction of mean arterial pressure of 14.9% (CI 14.0 to 15.8). When evaluating the effect of first-line therapies on calculated LVM using the same formula for all studies, the absolute reductions in g were 44.7 (ACE-inhibitors), 22.8 (beta-blockers), 26.9 (calcium antagonists) and 21.4 (diuretics) when adjusted for differences between studies (ANCOVA). It can be concluded that effective antihypertensive therapy reduces LVM. ACE-inhibitors, beta-blockers and calcium antagonists reduce LVM by reducing wall hypertrophy, the effect of ACE-inhibitors being the most pronounced. Diuretics reduce LVM mainly through an effect on left ventricular inner diameter. How these effects affect prognosis is still an open question.
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PMID:Regression of left ventricular hypertrophy--a meta-analysis. 134 56

Doxazosin, an alpha 1-adrenergic inhibitor, has been shown to decrease hypertension and plasma lipids, especially total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), thus reducing certain risk factors associated with increased incidence of cardiovascular disease. One preliminary report indicated that the decrease in LDL-C in hypercholesterolemic hamsters treated with doxazosin was associated with a reduction in fatty streak formation. However, since the effects of doxazosin on plasma lipids, aortic fatty streak development, or the relationship between the two have not been studied in a dose-dependent manner, these effects were further investigated over varying doses of doxazosin (0, 1, 5, 10, and 20 mg/kg body wt/day) during a 10-week period. Doxazosin administration was associated with a dose-dependent decrease in LDL-C of 2%, 29%, 52%, and 60%, whereas the degree of fatty streak formation was reduced 11%, 45%, 76%, and 92% compared with controls, with the first statistically significant decrease for both parameters at the 10 mg/kg dose. Significant correlations between LDL-C concentrations and fatty streak area suggest that doxazosin altered aortic lipid infiltration primarily by its effect on plasma lipids. However, the 20 mg/kg dose of doxazosin significantly decreased lesion area compared with the 10 mg/kg dose without a further effect on plasma lipid concentrations. Three animals at these higher doses demonstrated no stainable lipid inclusions while maintaining plasma lipid values similar to their cohorts. These exceptions to the lipid-lesion relationship raise the possibility of additional effects of doxazosin, which may occur independent of or in concert with lipoprotein cholesterol lowering, on lesion formation.
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PMID:Dose-related effects of doxazosin on plasma lipids and aortic fatty streak formation in the hypercholesterolemic hamster model. 135 67

The strongest predictors of cardiovascular disease in women have been shown to be diabetes, high blood pressure, cigarette smoking, and, to a lesser degree, hypertriglyceridemia. The difference in risk between men and premenopausal women has been explained by the following widely held hypothesis: androgens lower plasma concentrations of high-density lipoprotein (HDL), particularly the HDL-2 subfraction, and increase plasma concentrations of low-density lipoprotein (LDL). In contrast, estrogens have the opposite effect, raising plasma concentrations of HDL, particularly HDL-2, and lowering plasma concentrations of LDL. After the menopause, it is believed that the protective effect of estrogens in women is lost and the incidence of heart disease rises to equal that in men. This paper provides a brief review of the effect of endogenous and exogenous androgens on lipoprotein metabolism in men and women, and considers the relevance of these findings to the choice of progestogens used in oral contraceptive preparations.
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PMID:Mechanism of action/effects of androgens on lipid metabolism. 135 63

Echocardiographically determined left ventricular mass (LVM) is currently considered to be the most powerful risk indicator for cardiovascular disease, yielding prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors, high blood pressure included. It has been considered logical to try to obtain regression of cardiac hypertrophy, even though the risk-reducing implications of such a measure remain to be fully established. Experimental and clinical studies have shown that some classes of antihypertensive compounds are less effective than others in causing reversal of left ventricular hypertrophy (LVH) in spite of being similarly efficacious in lowering blood pressure. In order to extract the maximum amount of information from clinical studies, a meta-analysis was performed. This analysis included 109 treatment studies, each conformed to strict present rules. Only studies with pharmacological antihypertensive therapy and echocardiographically determined LVM were included. An analysis of the effect of the four first-hand antihypertensive treatment principles, adjusted for differences between studies with ANCOVA, showed that the ACE inhibitors, beta-blockers and calcium antagonists all reduce LVM by reversing wall hypertrophy and that the effect is most pronounced with ACE inhibitors. Diuretics reduce LVM mainly by a reduction in left ventricular diameter. If the difference in ability to reverse LVH, between ACE inhibitors and beta-blockers/diuretics would correspond to a difference in prognosis, then the outcome of antihypertensive therapy might be expected to improve. This hypothesis is currently under investigation.
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PMID:Regression of left ventricular hypertrophy--are there differences between antihypertensive agents? 136 88

Transgenic experimentation has become a crucial part of hypertension and atherosclerosis research, and is growing more important in several other areas of cardiovascular disease. It has recently made a particular contribution to understanding the role of the renin-angiotensin system in controlling hypertension. The study of blood pressure regulation, cardiac hypertrophy, atherogenesis and thrombosis are also benefiting from the transgenic approach.
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PMID:Transgenic animal models of cardiovascular disease. 136 20

The synthetic androgen methylandrostenediol (MAD) and the naturally occurring one, testosterone, both bring about hypertensive cardiovascular disease when chronically administered to rats. The pathogenesis of this form of experimental hypertension is thought to result from inhibition of steroid 11 beta-hydroxylase activity. In contrast to the above androgens, 19-nortestosterone, androstenedione and dehydroepiandrosterone (DHEA) have been reported to be without effect in elevating blood pressure. To examine the mechanism(s) involved, we have in this study compared the effects of a number of androgens on adrenal cytochrome P- 45011 beta enzyme and mRNA steady state levels. These parameters were also correlated with the ability of adrenal mitochondria isolated from these groups to hydroxylate 11-deoxycorticosterone (DOC) to corticosterone and 18-hydroxy-11-deoxycorticosterone (18-hydroxy-DOC). Rats treated for seven days with 10 mg per day of dihydrotestosterone, testosterone, 19-nortestosterone or MAD showed a profound decrease in cytochrome P-45011 beta mRNA levels (to less than 20% of controls). This was accompanied by similar changes in both the level and activity of the enzyme. Androstenedione and DHEA were less potent in effecting these changes. In addition, for MAD and testosterone we tested the dose dependence of these changes and found that increasing doses (0.1 mg to 10 mg per day) of either androgen caused progressive decreases in the parameters measured. To assess selectivity we also determined the steady state level of cytochrome P-450scc mRNA in rats treated with the various androgens. In contrast to what was found with cytochrome P-45011 beta, the mRNA transcript for cytochrome P-450scc was equal to or above control levels. We conclude that, in general, the extent of inhibition of cytochrome P-45011 beta enzyme and mRNA level by a given androgen correlates with its reported facility in producing hypertension in rats. Increased secretion of DOC continues to be a likely mechanism for the development of this hypertension but with some androgens extra-adrenal effects may be involved.
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PMID:The inhibition of rat adrenal cytochrome P-45011 beta gene expression by androgens. 138 7

Factors that can influence cardiovascular growth are becoming increasingly important for our understanding of such complex diseases as cardiac hypertrophy, coronary artery disease, atherosclerosis, and hypertension. Several proto-oncogenes were found to be involved in the regulation of abnormal cell growth in cardiovascular disease. It is also evident that some peptide hormones, which are well known to be involved in blood pressure control, may play a role as growth modulators. Angiotensin II is one such peptide. It elevates blood pressure through its direct vasoconstrictor, sympathomimetic, and (through release of aldosterone) sodium-retaining activity but also appears to have mitogenic actions. Interestingly, all components of the renin-angiotensin system were found locally in cardiovascular tissues. The question remains whether angiotensin can act directly as a growth factor or whether it does so indirectly by influencing or modulating cell growth factors. A better understanding of the renin-angiotensin system as a direct or indirect mediator for cardiovascular hypertrophy would offer new and interesting insights into the pathophysiology of hypertension and possibly novel options for the treatment of cardiovascular disease.
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PMID:The molecular basis of cardiovascular hypertrophy: the role of the renin-angiotensin system. 138 95


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