UMLS:C0020538 - FACTA Search

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

This article reviews important advances in the understanding and treatment of hypercholesterolemia and persistently high blood pressure in children. Two plant sterols, sitosterol and sitostanol, have been tested in prepubertal and adolescent children with hypercholesterolemia and appear promising. The advantages and disadvantages of family history in screening algorithms for atherosclerotic disease are discussed. Additionally, the apolipoproteins are being used more frequently to screen for cardiovascular risk. A rare genetic disease, familial defective apolipoprotein B-100, causes hypercholesterolemia. The distinction between this disease and familial hypercholesterolemia has therapeutic implications. Two studies show that in utero exposures influence the future development of hypertension. Intrauterine cocaine exposure was associated with persistently elevated blood pressure during later childhood. The mechanism may involve the sympathetic nervous system. Retarded fetal growth appears to be a risk factor for the presence of hypertension during adult years in men.
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PMID:Hypertension and atherosclerosis in children. 819 65

Coronary artery disease is the leading cause of death in the United States. Serum cholesterol is a widely used screening test to detect persons at high risk for coronary artery disease, including those with familial hypercholesterolemia. However, universal screening of currently healthy persons is not without risk. Previous experience in screening for sickle cell anemia and hypertension has shown that these risks include misunderstanding of test results, misdiagnosis, labeling, stigmatization, and decreased psychological well-being. Results of screening programs may be misused by industry or insurance companies to exclude individuals from positions or benefits. Consideration of these harms suggests that screening should not be implemented until certain safeguards are in place. Physicians and the public should be educated about the potential risks and benefits of screening. Screening tests should be accurate, reliable, valid, and of demonstrated sensitivity. Informed consent for screening should be obtained. Follow-up surveillance and recommended treatments, including dietary counseling and drug therapy, should be available to all individuals identified as being at high risk regardless of their socioeconomic status. Finally, procedures to protect the right to privacy of individuals and their families should be implemented well in advance of the actual screening.
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PMID:Psychological and ethical considerations in screening for disease. 821

In familial hypercholesterolemia (FH) elevated Lp(a) concentrations are more frequent than in the general Caucasian population, but the clinical relevance of Lp(a) as a risk-factor in this group of patients is controversial. In 91 adult patients with heterozygous FH due to LDL-receptor defect we analyzed the correlation between Lp(a) concentrations, presence of coronary heart disease (CHD) and degree of atherosclerosis of the carotid arteries assessed by duplex scan. Coronary heart disease was present in 32 patients (24 males, 8 females). In the group without CHD the median of the Lp(a) distribution was 23 mg/dl, in the group with CHD 43 mg/dl (P < 0.05). The median of Lp(a) was 8 mg/dl in patients without pathological changes in the duplex scan of the carotids, 13 mg/dl in the group with intimal thickening, 25 mg/dl in patients with non-obstructing plaques, and 45 mg/dl in presence of > 30% luminal obstruction (P < 0.01). The role of Lp(a) as an independent risk factor was analyzed by stepwise logistic regression together with age, sex, LDL-, HDL-cholesterol, serum triglycerides, smoking status and presence of hypertension. For the prediction of CHD only age, HDL cholesterol and gender reached statistical significance. Lp(a) was, however, the lipoprotein parameter with the highest discriminative strength for the presence of a pathological duplex scan (P = 0.016), followed by LDL- (P = 0.03), and HDL-cholesterol (P = 0.03). These results provide direct evidence for a close correlation between Lp(a) and the rate of progression of atherosclerosis in FH, already at early, asymtomatic stages.
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PMID:Relation of lipoprotein(a) to coronary heart disease and duplexsonographic findings of the carotid arteries in heterozygous familial hypercholesterolemia. 821 4

The genetic and environmental determinants of hypertension, lipid abnormalities, and coronary artery disease (CAD) have been studied for 15 years in Utah in population-based multigenerational pedigrees (2500 subjects among 98 pedigrees), twin pairs (74 monozygous and 78 dizygous), hypertensive siblings (131 sibships), siblings with CAD before age 55 (45 sibships), and anecdotally ascertained pedigrees with type II diabetes (271 subjects among 16 pedigrees), lipoprotein lipase deficiency (106 subjects in a single pedigree), and familial hypercholesterolemia (502 heterozygotes among 50 pedigrees). Estimates of heritability ranged from 20 to 75% for blood pressures and blood lipids. A strong positive family history predicts a future occurrence of hypertension (relative risk [RR] = 3.8) and CAD (RR = 12.7). Segregating single-gene effects were found for several 'intermediate phenotypes' associated with hypertension (erythrocyte sodium-lithium countertransport, intraerythrocytic sodium, a relative fat pattern, total urinary kallikrein excretion, and fasting insulin levels). Strong single-gene effects in segregation analysis were also found for low-density lipoprotein (LDL) cholesterol, lipoprotein (a) (Lp[a]), low high-density lipoprotein (HDL) cholesterol, and high apolipoprotein (apo) B. Deoxyribonucleic acid (DNA) markers of lipid abnormalities or hypertension have included LDL-receptor defects, lipoprotein lipase deficiency, high Lp(a), familial defective apo B, decreased quantitative levels of apo B, apo E phenotype, angiotensinogen, and 'glucocorticoid remediable aldosteronism (GRA) hypertension.' Also tested in Utah studies, but not found to be DNA markers for hypertension, were the genetic loci for the structural genes for renin and angiotensin-converting enzyme, and the sodium antiport system. In addition, important gene-gene interactions (LDL receptor with apo E2) and gene-environment interactions (kallikrein with potassium intake) were found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genetic basis of familial dyslipidemia and hypertension: 15-year results from Utah. 829 39

The familial lipoprotein disorder type III hyperlipoproteinemia (HPL) carries a marked increase in the risk of accelerated and premature atherosclerosis, but there is considerable variation among affected individuals in susceptibility to cardiovascular disease (CVD). We studied the influence of independent risk factors for atherosclerosis in 67 patients with clinically overt type III HPL and homozygosity for apolipoprotein (apo) E2. Among the different risk factors (lipid and lipoprotein levels, age, sex, body mass index, smoking status, hypertension, and diabetes mellitus) there was only a statistically significant difference in age between 25 patients with atherosclerosis and 42 patients without atherosclerosis. Serum lipoprotein (a), [Lp, (a)], levels were 30.6% higher in the atherosclerosis group, but this was not statistically significant. We conclude that (in contrast to familial hypercholesterolemia) elevated Lp (a) concentrations may not be regarded as a component of the clinical syndrome of type III HPL.
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PMID:Relation of cardiovascular risk factors to atherosclerosis in type III hyperlipoproteinemia. 837 May 76

Apolipoprotein B-100 (apo B-100) is the protein component of low density lipoprotein (LDL) responsible for its binding and clearance by LDL receptors (LDL-R). In familial defective apo B-100 (FDB), a mutation in apo B-100 at residue 3500 markedly reduces its affinity for LDL-R, often causing accumulation of defective LDL particles, and an increased proneness to coronary artery disease (CAD). In FDB heterozygotes, about 70% of the LDL particles are mutant, which may alter their atherogenicity relative to LDL containing normal apo B. Therefore, we compared CAD in heterozygous FDB with CAD in heterozygous familial hypercholesterolemia (FH), since raised LDL is usually present from birth in both conditions, and in FH the LDL particles that accumulate have normal apo B, as the inherited defect involves the LDL-R. The clinical presentation of coronary atherosclerosis and its angiographic appearance were examined in FDB and FH patients matched for conventional cardiac risk factors (hypertension, smoking, sex) and serum lipid levels. There was no significant difference between the FDB and FH patients (n=11 pairs) in the type of cardiac symptoms or their ages of onset (50 +/- 9 vs. 45 +/- 11 years). Coronary angiographic appearance was also similar in both groups (n=9 pairs). These observations suggest that LDL particles with the 3500 mutation in apo B have the same atherogenicity as LDL particles with normal apo B.
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PMID:Does the presence of the 3500 mutant apolipoprotein B-100 in low density lipoprotein particles affect their atherogenicity? 857 20

Calcium antagonists are well accepted in the prevention of ischaemia in patients with chronic stable angina, unstable angina, variant angina, and silent ischaemia, and in the treatment of hypertension. Although all of these compounds increase myocardial oxygen supply by reducing coronary tone and decrease myocardial oxygen demand by reducing systolic pressure and myocardial contractility, the magnitude of these effects may differ from one agent to another. Some calcium antagonists, such as verapamil and diltiazem, reduce heart rate and attenuate heart rate increases in response to stress, while in contrast, dihydropyridine calcium antagonists such as nifedipine may cause reflex increases in heart rate. These differences may be of importance in light of epidemiologic evidence that lower heart rates are associated with a reduced long-term risk of cardiovascular mortality, and experimental data showing that a lower heart rate may protect against the development of atherosclerosis. Calcium antagonists also inhibit platelet aggregation and thrombus formation which may contribute to their anti-ischaemic effects. Clinical trial data suggest that calcium antagonists may stay the progression of atherosclerosis. Mechanisms underlying an anti-atherosclerotic effect may include attenuation of endothelial dysfunction, prevention of LDL, peroxidation, stimulation of LDL receptor activity, inhibition of superoxide radical generation, and inhibition of vascular smooth muscle cell growth. Heart-rate-controlling calcium antagonists, such as verapamil and diltiazem, may reduce reinfarction rates following acute myocardial infarction and thus may have a role in post-infarction patients who do not show evidence of heart failure. Their use in heart failure patients receiving an angiotension-converting enzyme inhibitor (ACE-I) is under investigation in several large trials. Because calcium antagonists have a mechanism of action different from ACE-I, the pairing of a heart-rate-controlling calcium antagonist with an ACE-I might be expected to offer additive cardioprotective and vascular protective effects.
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PMID:The role of calcium antagonists in ischaemic heart disease. 884 1

Treatment of hypercholesterolemia with HMG-CoA-reductase inhibitors has revolutionized medical intervention towards the prevention of coronary artery disease. There is a wide sprectrum of patients with diverse underlying clinical conditions that may benefit from treatment using these agents. These include patients with multiple risk factors, individuals following major vascular events, and those with special conditions that are associated with accelerated atherosclerosis. The latter include patients with severe, dominantly inherited hypercholesterolemia, patients with major organ dysfunction such as chronic renal failure, and individuals after transplantation. Multimodality intervention includes behavior modification and mechanical as well as pharmacological treatment. It is aimed at several important targets: cholesterol reduction, control of hypertension and diabetes, improvement of myocardial contractility, reduction of infarct size, and control of hemostasis. Most of these patients require multiple drugs, which may interact at the pharmacodynamic (efficacy and safety) as well as pharmacokinetic levels. These potential interactions should be considered while planning and implementing preventive measures for an individual as well as for the community. The beneficial effects and the potential hazardous interactions between HMG-CoA reductase inhibitors and other medications are presented and discussed using two models: heterozygous familial hypercholesterolemia and major organ transplantation. Although there is a partial overlap in the medications used for the treatment of these two conditions, some of them differ. The interaction between HMG-CoA reductase inhibitors and other cholesterol-lowering agents, mainly fibrates, is discussed in the first model summarizing data from controlled clinical trials. The interaction with cyclosporin A is presented using the second model. A potential benefit of fluvastatin, as compared with other currently available HMG-CoA reductase inhibitors, which may be related to its relatively short plasma half-life and low systemic exposure, is discussed.
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PMID:Targeted prevention of coronary artery disease: pharmacological considerations in multimodality treatment. 890 72

Plasma lipoprotein cholesterol abnormalities, diabetes, hypertension and smoking have all been identified as independent predictors of cardiovascular events. Clustering of multiple risk factors suggests a common metabolic link among high blood pressure, insulin resistance, plasma lipoprotein abnormalities and obesity. New guidelines for the management of dyslipidemias target patients with established coronary artery disease (CAD), and high risk patients with multiple risk factors and severe genetic lipoprotein disorders, such as familial hypercholesterolemia. To determine the prevalence of lipoprotein, apolipoprotein and metabolic disorders in premature CAD, 243 men and 61 women with premature CAD (occurring before age 60 years) and 203 age- and sex-matched controls (152 men, 61 women) were studied. After correcting for beta-blocker use (40% of men and 54% of women), hypertension and diabetes were seen more frequently in CAD patients than in controls. In men and women, cholesterol, triglycerides, low density lipoprotein (LDL) cholesterol, apolipoprotein B and lipoprotein (a) were significantly higher, and high density lipoprotein (HDL) cholesterol was lower, in CAD patients than in controls. By stratifying patients according to LDL cholesterol: HDL cholesterol ratio (5 or less, or greater than 5) and by triglyceride levels (less than 2.3 mmol/L, or 2.3 mmol/L or greater), significantly more men and women with CAD were found to have an elevated LDL cholesterol:HDL cholesterol ratio and elevated triglycerides (13.8% versus 1.9%, men and women combined, CAD versus controls, P < 0.0001). A metabolic factor index was devised, assigning a score of 1 each for presence of hypertension, lipoprotein abnormalities, diabetes or fasting blood glucose above 7.0 mmol/L, and a body mass index of 27 or greater. The prevalence of a metabolic factor index of 3 or more was 29.2% in CAD men versus 6.7% in controls (P < 0.0001) and 38.3% in CAD women versus 11.7% in controls (P < 0.01). Familial hypercholesterolemia was seen in fewer than 5% of patients with premature CAD and type III dyslipoproteinemia in one of 343 CAD patients. The distribution of apolipoprotein E phenotypes was the same in CAD patients and controls. Multivariate analysis revealed that in men, HDL cholesterol, lipoprotein (a) levels and smoking were the best predictors of risk. In men, plasma levels of LDL cholesterol, triglycerides or body mass index did not enter the model at the P < 0.05 level. In women, low HDL cholesterol, lipoprotein (a), the presence of diabetes, smoking and apolipoprotein B levels were all predictors of risk (P < 0.05). However, the clustering of risk factors may be the best predictor of risk. In this selected population, HDL and lipoprotein (a) are the best metabolic markers of premature CAD; metabolic factor clustering is common in patients with premature CAD.
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PMID:Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians. 911 13

Hypertension is an important risk factor for the development of atherosclerosis. Traditional antihypertensive therapy is not fully effective in prevention of cardiovascular abnormalities of hypertension. Two classes of hypotensive drugs, calcium antagonists and angiotensin-converting enzyme (ACE) inhibitors, reduce atherosclerosis in several experimental models in animals. Anti-atherosclerotic effects of calcium antagonists include attenuation of endothelial dysfunction, prevention of LDL modification, stimulation of LDL receptor activity, inhibition of superoxide radical generation and inhibition of vascular smooth muscle cells proliferation and migration. In large angiographic trials calcium antagonists reduced the development of new atherosclerotic plaques. ACE inhibitors also lead to the lower incidence of atherosclerosis in experimental animals. They inhibit migration and proliferation of vascular smooth muscle cells, reduce macrophage-derived foam cell accumulation, preserve protective endothelium function, reduce LDL modification and increase fibrinolytic activity. It depends on reduced angiotensin II synthesis, increased concentration of kinins, substance P and angiotensin-(1-7), inhibition of leukotriene B4 formation and improvement of insulin action. In some studies they also reduce plasma lipids concentration, including lipoprotein (a). ACE inhibitors were found to be ineffective in prevention of restenosis after PTCA in human but data derived from large, multicenter trials indicate that they are effective in the secondary prevention of myocardial infarction.
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PMID:[Anti-atherosclerotic action of hypotensive drugs]. 924 14

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