Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The risk for cardiovascular complications is already substantially increased in persons with borderline elevation of arterial pressure (141-159/90-94 mmHg and transiently below). It increases progressively with higher grades of hypertension. The main aim of treatment is thus a significant improvement in survival for the patient. Persons with raised blood pressure (BP) have often additional cardiovascular risk factors such as deranged carbohydrate metabolism, dyslipidemia, left ventricular hypertrophy, smoking and others. Treatment of hypertensive patients should thus not only normalize BP but should at the same time reduce associated risk factors or at least not increase them. Conventional antihypertensive treatment based on thiazides in high doses or beta-blocking agents led to marked reduction of strokes and heart failure, but did not satisfactorily reduce coronary heart disease or sudden cardiac death. It has been suspected that other cardiac risk factors are insufficiently influenced or eventually even deteriorated by conventional therapy, thus counteracting partly a beneficial effect of lowered BP. Beta-blockers however have at least a secondary preventive effect after myocardial infarction. Newer antihypertensive drugs such as ACE-inhibitors, calcium antagonists and alpha 1-blockers reduce left ventricular hypertrophy and are at least neutral with regard to metabolism of lipids and carbohydrates. The non-thiazide diuretic indapamide and the serotonin (S2-) blocker ketanserin likewise are neutral with regard to glucose and lipid metabolism. The efficacy of these new drugs regarding long term survival is as yet undetermined. Persisting borderline or established hypertension should as a rule always be approached with basic non-pharmacologic measures: loss of overweight, reduction of alcohol intake, exercise, avoidance of high salt foods, abstention from smoking and withdrawal of BP-raising drugs. If antihypertensive medication is indicated, potential first line drugs are ACE-inhibitors, calcium antagonists, beta-blockers, thiazides at low dose, indapamide, ketanserin, the alpha 1-blocker prazosin and others; initially as monotherapy, if needed in combinations of 2 or 3. Older patients or those will with additional disturbances such as diabetes, hypercholesterolemia, nephropathy, heart failure, ischemic heart disease, arrhythmias, claudication, asthma and others need problem-adjusted modifications of treatment.
 ...
PMID:[Antihypertensive therapy in the nineties]. 153 54

Cardiovascular disease, and in particular ischemic heart disease, is the principal cause of morbidity, functional disability, and mortality in patients with non-insulin-dependent (type II) diabetes. The main risk factors for the macrovascular complications of diabetes are dyslipidemia, hypertension, and cigarette smoking. Although degree of hyperglycemia is a risk factor for microvascular complications, it is not a prominent risk factor for macrovascular complications. Nevertheless, there are theoretical reasons for believing that glycemic control could lower cardiovascular risk. For example, glycemic control may both improve clearance and suppress hepatic overproduction of very-low-density lipoprotein. Moreover, there is direct empirical evidence that improved glycemic control can favorably alter lipid profiles in type II diabetic patients. Despite this, the only clinical trial that has assessed cardiovascular mortality as an end point in diabetic subjects (i.e., the University Group Diabetes Program) failed to demonstrate a benefit of glycemic control. In this study, the insulin-variable group, which achieved sustained glycemic control relative to the placebo group, had essentially the same cardiovascular mortality as the latter group. All of the conventional lipid-lowering agents have been shown to produce favorable changes in lipid profiles in diabetic subjects. However, the optimum regimen remains to be defined. Metabolic differences between diabetic and nondiabetic subjects mean that the optimum lipid-lowering regimens for the two categories of patients may differ. For example, nicotinic acid, which is a powerful lipid-altering drug, may worsen glucose intolerance. The characteristic lipid abnormalities in type II diabetic subjects are hypertriglyceridemia and low high-density lipoprotein cholesterol, not hypercholesterolemia. Although the role of hypertriglyceridemia as a cardiovascular risk factor in the general population has been questioned, there is evidence that this lipid abnormality may play a stronger role in diabetic subjects. For all of the above reasons, there is an urgent need for large-scale clinical trials assessing cardiovascular end points and testing various strategies of improving lipid profiles in diabetic subjects, particularly given the fact that all of the current generation of lipid-lowering trials have systematically excluded diabetic patients.
 ...
PMID:Dyslipidemia in type II diabetes. Implications for therapeutic intervention. 177 1

Reasons for the current emphasis on cholesterol as coronary risk factor are multiple. On one hand current studies have shown that primary as well as secondary prevention of ischemic heart disease is a realistic possibility with lipid lowering measures. On the other hand new drugs are actually available which permit a potent and adapted therapy of hyperlipidemias. According to new guidelines of the Swiss "lipid task force" screening for hypercholesterolemia is recommended. A cholesterol value greater than 6.5 mmol/l should be investigated and treated. Because a great proportion of adult Swiss fall into this category (approximately 1/3) it is essential that all those are efficiently treated that have markedly abnormal cholesterol values or present with other risk factors such as smoking and hypertension or have a personal or familiar history of ischemic heart disease. Because progression is likely in patients with or after manifest ischemic heart disease even when hypercholesterolemia is mild (over 5.2 mmol/l) all patients presenting with an infarct should be investigated for dyslipidemia. Cholesterol, triglycerides and HDL should be determined. Dietary measures are the basis of every attempt to reduce hyperlipidemia. Most importantly intake of saturated fats prevailing in animal products should be restricted. The next important step is reduction of dietary cholesterol and in obese patients also caloric restriction. Lipid lowering agents are recommended in patients at risk who do not respond to or comply with dietary regimens. According to type of dyslipidemia bile-acid-binding resins, fibrates, nicotinic acid or HMG-CoA reductase inhibitors are available.
 ...
PMID:[Lipid-lowering therapy in the prevention of coronary heart disease]. 221 47

56 cerebral ischemia patients up to the age of 40 were investigated using a strict clinical and instrumental protocol in order to elicit the relative importance of the various iatrogenic factors involved. In addition to atherosclerosis risk factors (smoking, hypertension, ischemic heart disease, diabetes, dyslipidemia) other possible causes of cerebral ischemia were sought (arteritis, migraine, head injury, oral contraceptives, coagulation disorders, cardiogenic embolism, etc.). 50% of the patients examined had at least two atherosclerosis risk factors and 55% had other causes singly or in association with atherosclerosis.
 ...
PMID:Cerebral ischemia in young adults. 733 59

Microalbuminuria in diabetic patients is associated with ischemic heart disease and insulin resistance. We previously found a 9% prevalence of microalbuminuria in a nondiabetic population that we have reassessed, investigating associations of microalbuminuria with hypertension, dyslipidemia, hyperinsulinemia, and sodium-lithium countertransport. Of 125 subjects reexamined, 42 had been microalbuminuric 3 years previously. Twelve of these (29%) were microalbuminuric on at least one sample at follow-up, and 30 (76%) were normoalbuminuric on two. Of the 79 previously normoalbuminuric subjects, 12 (15%) became microalbuminuric on one sample, while 67 (85%) remained normoalbuminuric. Subjects who were microalbuminuric at both screening and recall were older (mean +/- SD, 65.9 +/- 11 versus 59.1 +/- 10.2 years, P = .04), with a higher waist-to-hip ratio (0.93 +/- 0.09 versus 0.86 +/- 0.08, P = .008) and at recall, on univariate analysis, had higher specific insulin (44.2 [range, 16.9 to 157.0] versus 28.4 [7.4 to 129.0] pmol/L, P = .005), intact proinsulin (5.1 [1.5 to 11.0] versus 3.0 [0.8 to 14.6] pmol/L, P = .003), and des-31,32-proinsulin (5.0 [0.5 to 9.8] versus 1.0 [0.5 to 12.2] pmol/L, P = .004) concentrations. There was also a significant difference in des-31,32-proinsulin concentration, after adjustment for covariates (P = .013), between subjects classified either as microalbuminuric or as normoalbuminuric at screening. There was no difference in body mass index; fasting blood glucose; systolic or diastolic blood pressure; total, HDL, or LDL cholesterol; triglycerides; plasminogen activator inhibitor-1; or sodium-lithium countertransport activity between consistently normoalbuminuric and persistently microalbuminuric subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Longitudinal study of associations of microalbuminuria with the insulin resistance syndrome and sodium-lithium countertransport in nondiabetic subjects. 767 Sep 46

The development of advanced coronary atherosclerosis was studied in the FHC swine. This model exhibits spontaneous elevations in plasma cholesterol, LDL, and apo B while fed a low-cholesterol, low-fat diet. Hypercholesterolemic animals bearing the apo B genotypes Lpb2/3, 3/3, 3/5, 5/5 and 3/8 developed stenotic coronary lesions containing necrotic cores, fibrous caps, calcification, neovascularization, hemorrhage, and fissuring. Myocardial infarction and myocardial ischemia were also observed. The complicated atherosclerotic plaques observed in this swine model closely resemble advanced coronary artery disease (CAD) found in humans. While coronary atherosclerosis was not observed in the absence of hypercholesterolemia, neither the apo B genotype nor the level of hypercholesterolemia was found to predict the extent of lesion formation. Similar to the case in humans, the familial dyslipidemia associated with the development of CAD in the FHC swine appears to be polygenic.
 ...
PMID:Familial hypercholesterolemia associated with coronary atherosclerosis in swine bearing different alleles for apolipoprotein B. 769 72

Risk factor profile of 142 patients with normal epicardial coronary arteries (86 males, 56 females, mean age 47 +/- 11 years) out of 1,508 consecutive patients undergoing coronary angiography was analysed. The mode of presentation in these patients was old or recent myocardial infarction (16.1%), unstable angina (12.0%), angina on effort (43.7%), atypical chest pain (8.5%), and anginal equivalent (19.7%). One or more stress test was positive in the majority (88%) of patients. Though the majority (39.5%) of patients had one risk factor, multiple (two or more) risk factors were not uncommon. Risk factor profile in patients with normal coronaries included hypertension (45.7%), dyslipidemia (33.8%), obesity (19.7%), positive family history of coronary artery disease (18.3%), cigarette smoking (16.1%), and minor risk factors (hyperuricemia, sedentary life style, Type A personality, oral contraceptive intake -15.4%). The mechanism of myocardial ischemia in patients with normal coronary arteries is not fully understood. We conclude that approximately one tenth of patients with clinically manifest coronary artery disease and one or more conventional risk factors do not have atherosclerotic changes in their epicardial coronary arteries as seen on coronary angiography.
 ...
PMID:Profile of coronary risk factors in patients with manifest ischaemia and normal coronary arteries. 779 18

The relationship of dyslipidemia, particularly hypercholesterolemia to coronary heart disease is now well established. Although ischemic heart disease and stroke share many of the same risk factors, the relationship of cholesterol to stroke remains controversial. The 6-year and 12-year follow-up of the MRFIT study showed that elevated cholesterol significantly increased the risk for fatal nonhemorrhagic stroke. Atkins found no evidence that lowering plasma cholesterol influenced the incidence of fatal or nonfatal stroke and regression analysis showed no statistical association between the magnitude of cholesterol reduction and the risk for fatal stroke. We cannot preclude the possibility that more effective cholesterol lowering over a longer period of time might be effective. Hypertension is the most powerful risk factor for stroke. The San Antonio Heart Study reported a clustering of cardiovascular risk factors in individuals who developed hypertension during an eight-year follow-up period (higher levels of BP, fasting TC and LDLC, TG, glucose and insulin, and BMI, less favourable fat deposition, and lower HDL). Insulin resistance may be the unifying factor that results in those phenomena, the so-called syndrome X. The important factor underlying syndrome X may be central or visceral obesity, suggesting that maintenance or attainment of ideal weight would be a powerful preventive factor against both CHD and nonhemorrhagic stroke. There is evidence from the Treatment of Mild Hypertension Study that nutritional/hygienic measures can reduce the syndrome X risk factors and hence the risk of coronary heart disease and stroke.
 ...
PMID:Dyslipidemia and metabolic factors in the genesis of heart attack and stroke. 791 92

Asymptomatic or silent myocardial ischemia (SI) is frequent in coronary heart disease and its prognostic value is controversial. The aim of our study is to compare coronary atherosclerosis, left ventricular function and clinical out come of 110 patients with S.I. (A group) and 210 patients with stable angina (B group). The 320 patients were submitted: to symptom limited exercise stress-test with permanent electrocardiographic control by a Case 12-15 digitalized system with ST segment depression interpretation. A test was considered positive for ischemia if there was ST depression of > 1 mv in magnitude from baseline, persisting for 0.08 sec or exercise angina and ischemia: to selective coronarography by Seldinger technic, with left ventricular cineangiography in 2 incidences. A significant coronary stenosis was defined as > 50% reduction of luminal diameter; to medical treatment with betablockers (87.5% of patients), calcium inhibitors (12.5%), aspirin (90%) and nitrates; to regular medical surveillance. During the follow-up (42.4 +/- 5 months in mean) the number of deaths, myocardial infarctions, heart failure, unstable angina and revascularizations were analyzed. Patients of A group with S.I. had a high percentage of risks factors (diabetes mellitus 55%, nicotinism 85%, dyslipidemia 22.5%) and history of previous myocardial infarction in 33% of cases. There are not significant differences between severity and extension of coronary disease, or ventricular dysfunction in patients of A group or B. The percentages of deaths (2.10 versus 3%), acute myocardial infarctions (9.5 versus 8.5%), heart failures (2.72 versus 3%), surgical indications (14.7 versus 15.7%) are not significantly different between the 2 groups. In A group, 34% of patients were treated by angioplasty versus 40% of patients in group B (p < 0.02). S.I. has a bad prognostic and the clinical out come of coronary heart disease is not dependent of presence of angina during exercise testing and daily activities.
 ...
PMID:[Prognosis of silent myocardial ischemia]. 803 89

From a survey on 8,000 coronary angiographic studies performed in our Institute between January 1980 and June 1990, 105 patients were identified as having angiographically normal coronary arteries and myocardial infarction (MI). Coronary arteries considered as normal were subdivided in completely normal (Group I), or slightly abnormal, with minimal lesions resulting in less than 30% narrowing of a major artery, defined as mild coronarosclerosis (Group II). Thirty-five patients were excluded from the study, because of the lack of complete follow-up data; the remaining 70 patients represent the study group we examined. The following parameters were examined: sex, age at the time of acute MI, family of ischemic heart disease, hypertension, dyslipidemia, diabetes, smoking, stable or unstable angina before MI, location of the MI, ejection fraction (EF), presence of completely normal coronary arteries or mild coronarosclerosis. Follow-up was obtained by contacting the patients or their families; post infarction angina, reinfarction, sudden death or cardiac death were noted. The subjects were divided in 2 groups, according to the coronary anatomy; Group I consisted of 41 patients with completely normal coronary arteries and Group II consisted of 29 patients with mild coronarosclerosis. No significant statistical difference was noted between the 2 groups regarding age, sex and coronary risk factors (except for dyslipidemia which was significantly more prevalent in the subjects with mild coronarosclerosis). Prevalence of left ventricular impairment (EF < 45%) and coronary events (angina, reinfarction and death) were significantly higher in Group II. There was no significant difference in age or clinical risk factor prevalence between patients with complicated and non complicated clinical course.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Prognosis in patients with myocardial infarction and angiographically normal coronaries]. 806 93


1 2 3 4 5 6 7 8 9 10 Next >>