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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A choice of many antihypertensive strategies is now offered for the treatment of the hypertensive patient with renal insufficiency. Angiotensin-converting enzyme (ACE) inhibitors appear to be the drugs of choice since they not only lower blood pressure but also reduce some important risk factors that may cause progressive loss of renal function, such as intraglomerular hypertension, angiotensin II (Ang II)-induced glomerular growth, proteinuria and hyperlipidemia. Indeed, several clinical studies now show that ACE inhibitors offer renal protection beyond the lowering of systemic blood pressure. The new class of Ang II receptor antagonists and its first representative losartan has not yet been tested clinically for its renal protective efficacy. The first signs, however, look promising, since losartan appears to induce changes in several identified risk factors to the same extent as ACE inhibitors, such as renal vasodilation, and a fall in proteinuria and serum lipids. The challenge will be to discover the differences between ACE inhibitors and Ang II receptor antagonists and to use them to the future advantage of the renal patient.
Can J Cardiol 1995 Aug
PMID:Losartan in patients with renal insufficiency. 766 17

The significance of silent myocardial ischemia detected by dipyridamole perfusion scintigraphy was evaluated in 80 patients with stable angina and reversible defects (RD) but no infarction. The patients were divided into two groups: 26 patients with silent RD (62 +/- 7 years) and 54 patients with painful RD (65 +/- 7 years). Coronary risk factors, extent of coronary lesions, localization and degree of RD, and prognosis were compared. There was no significant difference in the incidence of coronary risk factors between these two groups, except for hyperlipidemia which was less frequently observed in patients with silent RD than in those with painful RD (8% vs 41%, p < 0.01). Coronary angiography revealed a higher prevalence of insignificant lesions or single vessel disease in patients with silent RD than in those with painful RD (73% vs 39%, p < 0.05). Dipyridamole perfusion scintigraphy revealed a lower degree of RD in patients with silent RD than in those with painful RD (4.4 +/- 3.3 vs 9.0 +/- 4.1 segments, p < 0.05), though there was no significant difference in the localization of RD between these two groups. Treadmill stress testing revealed a lower incidence of chest pain in patients with silent RD than in those with painful RD (26% vs 65%, p < 0.05), despite the mean exercise-duration being significantly longer in the former than in the latter (5.5 +/- 1.7 vs 3.9 +/- 1.7 min, p < 0.05). There was no significant correlation between the late peak serum ML-1 level and LV volume, and the size and motion of infarcted areas in group B.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiol 1995 Jul
PMID:[Significance of silent ischemia in dipyridamole perfusion scintigraphy: evaluation in patients with angina]. 766 46

This study defined the patterns of investigation and treatment of serum lipids and other modifiable risk factors for atherosclerosis among 3,304 hospitalized patients at high risk for future cardiovascular events. There were 2,161 men and 1,143 women; 1,955 were aged < 70 years, and 1,349 were aged > or = 70 years. Acute (61%) and chronic (65%) cardiac ischemia was the most prevalent reason for high-risk status, followed by cardiac revascularization (46%) and diabetes (28%). Only 28% of patients had lipid measurements recorded during their hospital stay, or recorded at any time between 1988 and 1993. A lipid-lowering diet or drugs were prescribed for 22% and 8% of all patients, respectively, and an adjustment in lifestyle in only 5% of all patients. Moreover, measurement and therapy of lipid risk were recorded less frequently in older patients (p < 0.01), and less often in women (p < 0.01). Logistic regression analysis revealed admission for revascularization, preadmission lipid-lowering or lifestyle therapies, and history of hyperlipidemia or diabetes to be associated with increased likelihood of in-hospital lipid measurement; age > or = 70 years was associated with reduced likelihood of lipid determinations (p < 0.01). The overall investigation and therapy of serum lipids and other risk factors in acute care patients at high risk for cardiovascular events appear less than optimal. Moreover, there is significantly fewer measurements and less treatment of risk factors in women and older patients. Improvement in these practice patterns would improve patient outcomes for the most important diseases in society.
Am J Cardiol 1995 Sep 15
PMID:Low incidence of assessment and modification of risk factors in acute care patients at high risk for cardiovascular events, particularly among females and the elderly. The Clinical Quality Improvement Network (CQIN) Investigators. 767 79

Recently, the prevalence of acute myocardial infarction (AMI) in the elderly patients has increased. The clinical features have not been extensively studied, so this study attempted to clarify the clinical course and prognosis of elderly patients with AMI. The patients were divided into two groups, those over 80 years old and those between 60 and 79 years old. The clinical symptoms, electrocardiographic findings, complications, and short-term prognosis were compared. The serum lipid levels were compared between the AMI groups and age-matched control groups consisting of subjects without sclerotic heart disease. There was no significant difference in clinical symptoms between the two groups, electrocardiographic findings, incidence of complications, and mortality. The total cholesterol and LDL cholesterol levels, and atherogenic index were significantly higher in the 60-79 years old AMI group, but no significant difference was observed in the 80 years and over AMI group compared to the control group. The HDL cholesterol level of the 60-79 years old AMI group was significantly lower, but no significant difference was observed in the 80 years and over group. There was no significant difference in triglyceride level in either AMI group. Therefore, in patients aged 60-79 years hyperlipidemia is a risk factor for ischemic heart disease, but the relationship between serum lipid and AMI is not positively established in patients older than 80 years. These results suggest that the significance of hyperlipidemia in patients over 80 years old should be reconsidered.
J Cardiol 1995 Mar
PMID:[Serum lipid states in elderly patients with acute myocardial infarction: comparison between patients aged 60 to 79 and 80 years and over]. 772 71

Expression of the tissue factor (TF) and the plasminogen activator inhibitor-II were induced in cultured human monocytes-macrophages by incubation with lipoproteins. Very low-density lipoprotein (VLDL) augmented the TF and PAI-II expression the most, followed by low-density lipoprotein (LDL) and a very weak effect by high-density lipoprotein (HDL). In macrophages pre-cultured for 3 days, oxidized LDL augmented the expression of TF activity in the macrophages to a greater extent than native LDL. These findings indicate that lipoproteins affect both monocytes and macrophages, and that they induce a hypercoagulable-hypofibrinolytic state. Thus hyperlipidemia may be a direct risk factor for thrombotic disease.
Int J Cardiol 1994 Dec
PMID:Effect of lipoproteins on tissue factor activity and PAI-II antigen in human monocytes and macrophages. 773 48

Patients with diabetes mellitus have a two- to fourfold increase in clinical manifestations of atherosclerotic cardiovascular disease (ASCVD). Traditional risk factors such as age, hypertension, left ventricular hypertrophy, hyperlipidemia and smoking are still operative in diabetes but do not account for the total increase in ASCVD risk associated with diabetes. The most common lipid abnormalities in noninsulin-dependent diabetes mellitus and poorly controlled insulin-dependent diabetes mellitus are hypertriglyceridemia and low high density lipoprotein cholesterol. Evidence is presented to support the hypothesis that these lipid abnormalities are atherogenic in diabetes. Treatment of diabetic dyslipidemia with conservative measures (diet, weight loss, aerobic exercise, improved glycemic control) and pharmacological management have been shown to be highly effective in normalizing the lipid abnormalities. However, few trials of lipid lowering therapy have included patients with known diabetes mellitus and, to date, there have been no well-controlled prospective trials of lipid lowering therapy in diabetes. There is therefore no definitive proof regarding the benefit of lipid lowering therapy in diabetes mellitus. There are also no data regarding the cost effectiveness of lipid lowering therapy in reducing ASCVD complications in diabetes. There are data, however, showing that complications of ASCVD in patients with diabetes account for a large percentage of total health care expenditures. The overwhelming evidence that patients with diabetes have a high rate of ASCVD, that traditional risk factors for ASCVD are operative in diabetes and that the dyslipidemia of diabetes is highly prevalent and proatherogenic, predicts that the treatment of ASVD risk factors, including dyslipidemia, will be associated with a substantial reduction in ASCVD complications.(ABSTRACT TRUNCATED AT 250 WORDS)
Can J Cardiol 1995 May
PMID:Diabetic dyslipidemia: a case for aggressive intervention in the absence of clinical trial and cost effectiveness data. 775 45

The aim of this study was to determine the effect of gemfibrozil, compared with lovastatin, in patients with high levels of lipoprotein(a) and on plasma lipid profile. Twenty-seven nondiabetic patients with high levels of plasma lipids and lipoprotein(a), 19 male and eight female, aged 37-68 (mean +/- S.D. 54.2 +/- 7.5) years, were randomly assigned to 2 weeks of treatment with gemfibrozil 600 mg twice daily (14 pts.) or lovastatin 40-80 mg once daily (13 pts.). Patients had fasting plasma total cholesterol levels > or = 6.2 mmol/l, low-density lipoprotein > 4.14 mmol/l and lipoprotein(a) > 0.62 mmol/l. All patients but one had triglycerides > 2.82 mmol/l. There were no statistical differences between both groups in terms of age, sex, clinical diagnosis and previous medication. After 3 months of treatment, gemfibrozil reduced triglycerides (47.9% vs. 24.5%; P < 0.001), very low density lipoprotein (43.9% vs. 24.6%; P < 0.05), lipoprotein(a) (25.3% vs. 4.9%; P < 0.05) and increased high-density lipoprotein (34.4% vs. 11%; P < 0.01) more than lovastatin. Gemfibrozil and lovastatin reduced comparably total cholesterol (21.4% vs. 29.0%; P = NS) and low-density lipoprotein (26.5% vs. 37.3%; P = NS). The plasma levels of high-density lipoprotein and lipoprotein(a) were unchanged significantly by lovastatin. In conclusion, besides well-known efficacy in hyperlipidemia treatment, gemfibrozil also increased high-density lipoprotein and reduced lipoprotein(a), which may have important epidemiologic implications.
Int J Cardiol 1995 Feb
PMID:Effect of gemfibrozil versus lovastatin on increased serum lipoprotein(a) levels of patients with hypercholesterolemia. 777 89

Long-term survival of heart transplant recipients is now commonplace, due to improved perioperative care. It is thus appropriate to review recent studies concerning immunosuppression-related clinical problems in heart transplant recipients, including infections, malignancies, hypertension, hyperlipidemia, and osteoporosis. Hormonal and peripheral vascular responses of the denervated heart, exercise tolerance, pulmonary function, and parenting are also discussed.
Curr Opin Cardiol 1995 Mar
PMID:Clinical follow-up of the heart transplant recipient. 778 85

In 482 patients sequentially referred for diagnosis and therapy of hyperlipidemia, our specific aim was to determine the prevalence of homocysteinemia, to assess whether it was independently associated with atherosclerotic vascular disease, and to determine how effectively high homocysteine could be treated with folic acid and pyridoxine. Of the 482 patients, 18 (3.7%) had high homocysteine (> or = 16.2 mumol/L, median = 19), 31 had high cystathionine (> or = 342 nmol/L) with normal homocysteine (median = 12), and 433 had normal cystathionine and homocysteine (median = 9). Of the 18 patients with high homocysteine, 13 (72%) had atherosclerotic vascular disease, much higher than the 44% (192 of 433 patients) with normal homocysteine (chi-square = 5.4, p = 0.02). In the 18 kindreds with a homocysteinemic proband, 14 (78%) had > or = 1 first-degree relatives with atherosclerotic vascular disease before age 65, compared with 50% (215 of 433) of the families where the proband had normal homocysteine (chi-square = 5.5, p = 0.02). In the 482 patients already at high risk for atherosclerotic vascular disease by virtue of hyperlipidemia, when assessed by logistic regression, homocysteine was an independent positive predictor of atherosclerotic vascular disease (p = 0.007); relative risk for atherosclerotic events was 2.8 times higher (p = 0.0004) in patients with top (> or = 11.4 mumol/L) than with bottom (< 6.9 mumol/L) quintile homocysteine. After 15 weeks of folic acid (5 mg/day) and pyridoxine (100 mg/day) therapy in 10 patients with high homocysteine, median homocysteine normalized, decreasing from 18 to 11 mumol/L (p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1995 Jan 15
PMID:Evidence that homocysteine is an independent risk factor for atherosclerosis in hyperlipidemic patients. 781 Apr 87

Each hyperlipidemia patient requires individual management. Treatment choices are thus made for each patient on the basis of evaluation of their overall cardiovascular risk. This evaluation involves four types of characteristics: those which cannot be changed (age, gender), classical lipid and non-lipid risk factors, and finally cardiovascular status with two types of evaluation (clinical status and sub-clinical, atherosclerosis). Three examples are presented here, enabling more precise assessment of lipid risk: syndrome X which shows to what extent risk factors are often associated, combined familial hyperlipidemia which emphasises the importance of family history, and lipoprotein (a). The latter is a risk factor relatively inaccessible to treatment but which enables better evaluation of the risk of the patient and choice of a stricter treatment goal when it is very high.
Ann Cardiol Angeiol (Paris) 1994 Oct
PMID:[New lipid factors of cardiovascular risk]. 782 48


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