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

Untreated hypertension in age groups below 60 years has been shown to be associated with significant elevations in serum cholesterol and triglyceride levels. Drug therapy of hypertension has also been shown to have adverse effects on lipoproteins. We have investigated lipid and lipoprotein levels in a community-based sample of men and women 60 years and older belonging to one of the following groupings: (a) normal blood pressure (n = 1075); (b) untreated hypertension (n = 329); (c) drug-treated hypertension (n = 880). Serum lipid, lipoprotein, apolipoprotein or plasma glucose levels did not vary significantly between untreated hypertensives and normotensives of either sex. In a multiple regression model controlling for possible influences of age, overweight, alcohol and tobacco usage, and presence of coronary heart disease, anti-hypertensive drug therapy significantly predicted increased serum triglycerides (P less than 0.001) and reduced high density lipoprotein (HDL) cholesterol levels (P less than 0.01) in both sexes, reduced apolipoprotein A-I levels in males (P less than 0.001), and increased apolipoprotein B (P less than 0.01) and plasma glucose levels (P less than 0.001) in females. Adjusted triglycerides were 20% higher and HDL cholesterol was 7% lower in the presence of anti-hypertensive drug therapy. These effects were partially consistent with the known actions of thiazide diuretics and beta-blockers which were used by more than 50% and 40% of subjects, respectively.
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PMID:Dubbo Study of the elderly: hypertension and lipid levels. 134 82

The prevalence of abnormalities of lipoprotein cholesterol and apolipoproteins A-I and B and lipoprotein (a) [Lp(a)] was determined in 321 men (mean age 50 +/- 7 years) with angiographically documented coronary artery disease and compared with that in 901 control subjects from the Framingham Offspring Study (mean age 49 +/- 6 years) who were clinically free of coronary artery disease. After correction for sampling in hospital, beta-adrenergic medication use and effects of diet, patients had significantly higher cholesterol levels (224 +/- 53 vs. 214 +/- 36 mg/dl), triglycerides (189 +/- 95 vs. 141 +/- 104 mg/dl), low density lipoprotein (LDL) cholesterol (156 +/- 51 vs. 138 +/- 33 mg/dl), apolipoprotein B (131 +/- 37 vs. 108 +/- 33 mg/dl) and Lp(a) levels (19.9 +/- 19 vs. 14.9 +/- 17.5 mg/dl). They also had significantly lower high density lipoprotein (HDL) cholesterol (36 +/- 11 vs. 45 +/- 12 mg/dl) and apolipoprotein A-I levels (114 +/- 26 vs. 136 +/- 32 mg/dl) (all p less than 0.005). On the basis of Lipid Research Clinic 90th percentile values for triglycerides and LDL cholesterol and 10th percentile values for HDL cholesterol, the most frequent dyslipidemias were low HDL cholesterol alone (19.3% vs. 4.4%), elevated LDL cholesterol (12.1% vs. 9%), hypertriglyceridemia with low HDL cholesterol (9.7% vs. 4.2%), hypertriglyceridemia and elevated LDL cholesterol with low HDL cholesterol (3.4% vs. 0.2%) and Lp(a) excess (15.8% vs. 10%) in patients versus control subjects, respectively (p less than 0.05). Stepwise discriminant analysis indicates that smoking, hypertension, decreased apolipoprotein A-I, increased apolipoprotein B, increased Lp(a) and diabetes are all significant (p less than 0.05) factors in descending order of importance in distinguishing patients with coronary artery disease from normal control subjects. Not applying a correction for beta-adrenergic blocking agents, sampling bias and diet effects leads to a serious underestimation of the prevalence of LDL abnormalities and an overestimation of HDL abnormalities in patients with coronary artery disease. However, 35% of patients had a total cholesterol level less than 200 mg/dl after correction; of those patients, 73% had an HDL cholesterol level less than 35 mg/dl.
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PMID:Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. 153 90

We analyzed the serum concentrations of lipids and lipoproteins and the prevalence of other risk factors in a case-control study of 304 consecutive Chinese patients with acute stroke (classified as cerebral infarction, lacunar infarction, or intracerebral hemorrhage) and 304 age- and sex-matched controls. For all strokes we identified the following risk factors: a history of ischemic heart disease, diabetes mellitus, or hypertension; the presence of atrial fibrillation or left ventricular hypertrophy; a glycosylated hemoglobin A1 concentration of greater than 9.1%; a fasting plasma glucose concentration 3 months after stroke of greater than 6.0 mmol/l; a serum triglyceride concentration 3 months after stroke of greater than 2.1 mmol/l; and a serum lipoprotein(a) concentration of greater than 29.2 mg/dl. We found the following protective factors: a serum high density lipoprotein-cholesterol concentration of greater than 1.59 mmol/l and a serum apolipoprotein A-I concentration of greater than or equal to 106 mg/dl. The patterns of risk factors differed among the three stroke subtypes. When significant risk factors were entered into a multiple logistic regression model, we found a history of hypertension, a high serum lipoprotein(a) concentration, and a low apolipoprotein A-I concentration to be independent risk factors for all strokes. The attributable risk for hypertension was estimated to be 24% in patients aged greater than or equal to 60 years. In this population, in which cerebrovascular diseases are the third commonest cause of mortality, identification of risk factors will allow further studies in risk factor modification for the prevention of stroke.
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PMID:Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese. 192 51

Lipoprotein (a) [Lp(a)] is composed of 1 low-density lipoprotein (LDL) particle, to which 1 molecule of apolipoprotein (a) is covalently linked. Elevated levels of Lp(a) have been associated with coronary artery disease (CAD) and Lp(a) has been shown to be highly heritable. Our purpose was to determine the prevalence of familial Lp(a) excess in patients with CAD. We determined plasma levels of Lp(a) in 180 patients (150 men and 30 women) with angiographically documented CAD before age 60 years, and in 459 control subjects (276 men and 183 women) clinically free of cardiovascular disease. In addition, Lp(a) levels were determined in families of 102 of the CAD probands (87 men and 15 women). No gender differences in Lp(a) levels were observed between men and women (patients or control subjects). Patients with CAD had higher Lp(a) levels than did control subjects (19 +/- 21 vs 13 +/- 15 mg/dl, p less than 0.001). The prevalence of Lp(a) excess (defined as greater than 90th percentile of controls) was 17% in patients with CAD (p less than 0.05). Lp(a) levels were not correlated with cholesterol, LDL cholesterol, high-density lipoprotein (HDL) cholesterol or apolipoproteins A-I or B. There was a weak correlation between Lp(a) and triglycerides (r = 0.166, p less than 0.05) in patients and control subjects. Stepwise discriminant analysis revealed that Lp(a) was a risk factor for the presence of CAD in men, independent of smoking, hypertension, diabetes, LDL and HDL cholesterol, or apolipoprotein A-I and B levels. Family studies revealed that Lp(a) levels are strongly genetically determined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of lipoprotein (a) [Lp(a)] excess in coronary artery disease. 182 34

The effect of cigarette smoking on intracranial internal carotid artery atherosclerosis (ICAS) was studied by obtaining cigarette smoking histories and data on other potential predictors, including serum lipid estimations, for consecutive patients undergoing carotid arteriography. The duration of cigarette smoking was the most significant independent predictor of the presence of ICAS. Other independently significant predictors of ICAS were hypertension, diabetes mellitus, and current systolic blood pressure. The interaction of diabetes and duration of smoking was a significant negative predictor. In patients for whom serum lipid values were available, lower levels of apolipoprotein A-I were associated with a higher risk of having ICAS. However, the effect of apolipoprotein A-I as a predictor of the presence of ICAS was far outweighted by the effects of duration of smoking and hypertension.
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PMID:Predictors of intracranial carotid artery atherosclerosis. Duration of cigarette smoking and hypertension are more powerful than serum lipid levels. 185 94

An open-label study was conducted to evaluate the clinical safety and efficacy of transdermal clonidine as an adjunct to sustained-release (SR) diltiazem (90 mg twice daily) in mild-to-moderate hypertension. Ninety patients with a mean baseline sitting blood pressure of 154/102 mmHg were given 90 mg of diltiazem SR twice daily and transdermal placebo. After four weeks of therapy, 21 patients (23%) had trough sitting diastolic blood pressures (DBP) less than 90 mmHg and were withdrawn. Of the remaining 69 patients (DBP greater than or equal to 90 mmHg), 60 (mean blood pressure 149/98 mmHg) continued to receive 90 mg of diltiazem SR twice daily, to which was added transdermal clonidine, titrated as needed (3.5 cm2, 7.0 cm2, or 10.5 cm2) to achieve blood pressure control. During titration, 58 patients achieved DBP less than 90 mmHg, with a mean blood pressure of 133/84 mmHg. Of these patients, 54 completed an eight-week maintenance period, during which their mean blood pressure was 137/84 mmHg. No significant decrease in pulse or change from baseline in lipid profiles (high-density lipoprotein, low-density lipoprotein, apolipoprotein A-I, apolipoprotein B) was observed with combination therapy. The most frequently reported side effect during maintenance therapy was mild skin irritation at the transdermal application site. One patient was withdrawn because of contact dermatitis. Compliance with the oral twice-daily regimen was variable, with 83% of patients failing to take diltiazem SR at the prescribed dosing intervals 80% to 100% of the time. Transdermal clonidine was worn as directed by 97% of patients. It is concluded that transdermal clonidine in combination with diltiazem SR is safe and effective in the treatment of mild-to-moderate hypertension.
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PMID:Transdermal clonidine as an adjunct to sustained-release diltiazem in the treatment of mild-to-moderate hypertension. 193 99

HDL cholesterol and apolipoprotein A-I are associated with the development of coronary artery disease (CAD). The presence of a PstI site polymorphism adjacent to the gene encoding apo A-I (known as P2) has also been shown to be associated with CAD but this relationship is controversial. A case control study was conducted in an Australian population to re-examine whether the rare P2 allele is associated with CAD. Data were derived from 159 cases of angiographically confirmed CAD and 99 healthy controls. The proportion of CAD cases carrying the P2 allele did not differ significantly from controls (11% versus 9%). In a multiple logistic regression model controlling for the effects of age, country of birth, hypertension and hypotensive drugs, body mass index and lipid variables, the P2 allele failed to predict significantly the presence of CAD (odds ratio 1.83; 95% confidence interval 0.65-5.19).
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PMID:High density lipoproteins, genetic polymorphism for apo A-I and coronary artery disease. 195 6

The effect of serum lipids and lipoproteins on extracranial carotid artery atherosclerosis (CAS) was studied in patients who underwent carotid arteriography. Serum lipid and lipoprotein values along with data on other potential predictors of extracranial CAS were determined in 240 patients who had at least one extracranial carotid artery visualized. In a multiple logistic regression analysis, the independently significant predictors of the presence of extracranial CAS were, in decreasing order of significance, duration of smoking of cigarettes, hypertension, age, and low-density lipoprotein cholesterol. Serum cholesterol, triglycerides, high-density lipoprotein cholesterol, and apolipoprotein A-I did not show an independent effect. Although low-density lipoprotein cholesterol was an independent predictor of the presence of extracranial CAS, its effect as a predictor was far outweighed by the effects of the duration of smoking of cigarettes and a history of hypertension.
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PMID:Serum lipids and lipoproteins are less powerful predictors of extracranial carotid artery atherosclerosis than are cigarette smoking and hypertension. 200 93

Cardiovascular disease is a frequent complication of insulin-dependent diabetes mellitus (IDDM), but the prevalence, interrelations, and risk factors of its principal components (coronary, cerebrovascular, and lower-extremity arterial disease) and of medial arterial wall calcification are not well understood. To address these issues, data from the Epidemiology of Diabetes Complications Study (n = 657) baseline examination were examined. The term coronary heart disease (CHD) was applied to those with myocardial infarction or angina, whereas lower-extremity arterial disease (LEAD) was applied to those who had undergone amputation of a lower limb or who had an ankle to arm blood pressure ratio less than 0.8 at rest or after exercise. Calcification of the lower-extremity arteries was considered to be present if ankle pressure was more than 100 mm Hg higher than brachial pressure. Although the prevalence of CHD was low, LEAD was significantly more common in women than in men (p less than 0.01), whereas calcification was more frequent in men than in women (p less than 0.01). Ten percent of those with LEAD also had CHD, and 8% with LEAD had calcification. Modeling of potential risk factors (e.g., diabetes duration and glycosylated hemoglobin) revealed that duration, female gender, fibrinogen, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and high density lipoprotein cholesterol to apolipoprotein A-I ratio were independent predictors of LEAD, whereas for CHD only, diabetes duration and hypertension contributed to CHD. Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. The results suggest that although LEAD, CHD, and calcification often coexist, their risk factor profiles differ.
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PMID:Cardiovascular disease and arterial calcification in insulin-dependent diabetes mellitus: interrelations and risk factor profiles. Pittsburgh Epidemiology of Diabetes Complications Study-V. 206 46

The association between angiographically defined coronary artery disease (CAD) and serum lipids, lipoproteins, and apolipoproteins was evaluated in 151 black men and 245 black women. Patients with 70% or greater narrowing of at least one coronary artery or greater than or equal to 50% stenosis of the left main coronary artery (n = 179) were compared to those with lesions of less than 50% stenosis (n = 217) for total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), LDL-C/HDL-C, triglycerides, apolipoprotein A-I, apolipoprotein B, and apolipoprotein A-I/B. A consistently more atherogenic pattern of lipids, lipoproteins, and apolipoproteins occurred only among the women. Using stepwise selection multiple logistic regression analysis, the ratio of apolipoprotein A-I/B (odds ratio = 0.38, 95% confidence limits 0.24-0.61) was the only statistically significant association of CAD in women, after adjusting for the effects of age, body mass index, and histories of smoking, hypercholesterolemia, hypertension, and diabetes. When stratified by median of total cholesterol, the ratio of apolipoprotein A-I/B was the most strongly associated with the presence of CAD in the lower half of the total cholesterol distribution (less than 208 mg/dl), whereas in the upper half of the total cholesterol distribution the total cholesterol/HDL-C ratio was more strongly associated with CAD. None of the variables studied was associated with CAD in men. These results support other studies suggesting that apolipoproteins may be better predictors of CAD.
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PMID:Serum lipids, lipoproteins and apolipoproteins in black patients with angiographically defined coronary artery disease. 210 48


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