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

Recent evidence suggests that metabolic changes that occur with antihypertensive agents may influence cardiovascular risk. Diuretic therapy is particularly appropriate for the salt-sensitive hypertensive patient. However, diuretic-induced electrolyte abnormalities may lead to ventricular arrhythmias, even in patients with uncomplicated essential hypertension. Antihypertensive drugs may change circulating lipoprotein levels, which may influence the development of atherosclerosis. Therefore, serum cholesterol and triglyceride levels should be monitored when antihypertensive drugs are administered that can cause hyperlipidemia. Weight reduction and diet therapy should be used because these may have a greater effect on reducing hyperlipidemia, though choice of antihypertensive agents is important. In addition, glucose tolerance may worsen with thiazide therapy, perhaps because newer evidence suggests that insulin resistance is common in essential hypertension. This glucose intolerance may be corrected with potassium repletion or substitution of bumetanide for thiazide. The calcium antagonists may be substituted for diuretic therapy, or other classes of antihypertensive drugs may be used with a reduced dose of diuretic drug if these metabolic changes persist. Thus, attention to metabolic changes may be as important as blood pressure reduction in treatment of the salt-sensitive hypertensive patient.
Am J Cardiol 1988 Jun 15
PMID:Metabolic changes with antihypertensive therapy of the salt-sensitive patient. 328 52

A treadmill exercise test response may become positive because a diagnostic electrocardiographic ST-segment shift occurred during exercise, or, less often, because it occurred only during the recovery period after exercise had been completed. Factors that may be related to these 2 different responses in subjects enrolled in the Program of Surgical Control of Hyperlipidemia were investigated. No differences were found with regard to age, sex, level or location of Minnesota electrocardiographic Q-QS codes, number of narrowed coronary arteries, presence of collateral coronary artery circulation, ejection fraction, number of abnormally moving left ventricular wall segments, heart rate, systolic and diastolic blood pressure, double product, total exercise time, exercise-induced angina, or maximally achieved exercise heart rate or double product. Thus, the same significance should be attributed to a recovery-positive as to an exercise-positive treadmill test, and electrocardiographic, hemodynamic and angiocardiographic variables do not distinguish between subjects who exhibit these 2 different responses.
Am J Cardiol 1987 Sep 01
PMID:Comparison of exercise-positive with recovery-positive treadmill graded exercise tests. 330 68

Dietary fats play a critical role in atherogenesis and thrombosis. Both the amount of fat consumed and its composition affect various events associated with coronary artery disease. Dietary unsaturated fatty acids appear to reduce the incidence of these events, in particular polyunsaturated fatty acids (PUFAs), which exert markedly different effects on risk factors related to heart disease. The omega-3 (n-3) PUFAs, at high levels of dietary intake, significantly reduce hyperlipidemia and the production of the prothrombotic substance thromboxane, and they enhance the production of the platelet-antiaggregatory substance prostacyclin. Data from clinical trials indicate a significant reduction of levels of very low density lipoprotein (VLDL). The n-3 PUFAs also depress hepatic fatty acid and triglyceride synthesis and VLDL secretion. The n-3 PUFAs of fish oils displace arachidonic acid from tissue phospholipids and concomitantly increase n-3 PUFA levels, which inhibit thromboxane synthesis. Most significantly, in human subjects the antiaggregatory prostacyclin PGI3 is also synthesized and the net effect is enhanced antiaggregatory/antiadhesive activity. In addition, the chemotactic platelet adhesion-promoting substance leukotriene B4 is suppressed. These composite effects reduce atherogenesis and thrombosis. Fish oil n-3 PUFAs may also reduce blood pressure and blood viscosity. Through the combined vasodilatory effects via prostacyclin (PGI2 and PGI3), fish oils may improve peripheral circulation and thereby facilitate VLDL removal. The n-3 PUFAs of fish oils, by altering membrane fluidity in a specific manner, alter the activities of membrane-bound enzymes and may change receptor activity, specificity and signal transduction. Overall, these data indicate a beneficial role for n-3 PUFAs as part of a dietary approach to minimizing coronary artery disease.
Am J Cardiol 1987 Oct 30
PMID:Effects of polyunsaturated fatty acids on factors related to cardiovascular disease. 331 46

Recent experimental and epidemiologic evidence has dispelled all doubts about the need to treat patients with hyperlipidemia. Therapy should focus on 3 areas: control of concomitant risk factors for atherosclerosis, reduction of lipid levels through diet and, if response to diet proves inadequate, administration of lipid-lowering agents. There are 4 categories of first-line drugs: resins, fibrates, nicotinic acid and probucol. Probucol has a sustained effect, additive to that of a lipid-lowering diet; it can reduce total serum cholesterol and cause xanthoma regression even in patients with receptor-defective homozygous familial hypercholesterolemia. It is effective when used alone and has an additive effect when combined with resins or nicotinic acid. Compared with many other lipid-lowering medications, it is well tolerated. Although the combination of probucol and clofibrate may cause a significant decrease in high density lipoproteins, there is no evidence that this decrease carries any adverse consequences for the underlying disease process.
Am J Cardiol 1986 Jun 27
PMID:Medical management of hyperlipidemia and the role of probucol. 346 Mar 20

Late changes are frequent in saphenous vein grafts. About 10 to 12 years after bypass, about one-third are occluded, one-third have wall irregularities and narrowings attributed to atherosclerosis and one-third are seemingly intact. These changes are associated with recurrence of angina and other deleterious clinical events such as unstable angina, acute myocardial infarction, heart failure and death. Intimal fibrous hyperplasia may be a precursor of these changes, which could be minimized by appropriate surgical technologies and perhaps antiplatelet therapy. These late changes appear related to serum hyperlipidemia and smoking. Optimal control of these risk factors may retard their development and subsequent clinical deterioration. Although internal mammary artery (IMA) graft is the conduit of choice because of its apparent immunity to premature atherosclerosis, and hence its longer durability, saphenous vein grafts are still placed in many old patients and others, when a short operation time is a priority, and above all in combination with IMA grafts in order to obtain complete revascularization.
Can J Cardiol 1987 Nov
PMID:Late changes in saphenous vein coronary artery bypass grafts and their implications in clinical practice. 350 31

A variety of treatments to lower elevated plasma lipid levels in patients with hyperlipidemia are available. Adverse side effects ranging from mere annoyances to uncommon serious consequences may be associated with dietary modification, recreational physical exercise, and drug intervention. As in other clinical circumstances, risk-to-benefit ratios must be taken into consideration in the management of hyperlipidemia.
Cardiol Clin 1986 Feb
PMID:Adverse effects of the treatment for hyperlipidemia. 351 36

Atherosclerosis, the most frequent complication of diabetes, could be the result of hyperlipidemia, among other factors. Mounting evidence suggests that reducing the concentration of triglyceride-rich lipoprotein, which influences the production of the possibly atherogenic intermediate density lipoprotein (IDL), might diminish the circulating level of potentially atherogenic lipoproteins. Hypertriglyceridemia, even in the absence of obesity, is associated with insulin resistance. To compensate, pancreatic B cells respond to glucose challenge by producing hyperinsulinemia. If the B cells cannot respond adequately, carbohydrate intolerance ensues. Insulin-treated diabetics may also become hyperinsulinemic because routine insulin injection may not reflect physiologic need and because the insulin is administered peripherally rather than portally. Hyperinsulinemia increases the production of circulating triglyceride. It appears to do this in rats by causing the production of more triglyceride-rich lipoprotein particles rather than by increasing the triglyceride content of each particle. Further, at least in rats, the insulin-induced increase in triglyceride production requires the presence of supplementary dietary fructose. Hyperinsulinemia also increases the activity of adipose tissue lipoprotein lipase and the degradation of very low density lipoprotein (VLDL). The concentration of VLDL depends on balance of production and degradation. Accelerated VLDL degradation leads to an increase in IDL production. Because there is mounting evidence that IDL may be atherogenic, this cycle could accelerate atherogenesis. As such, it is reasonable to postulate that reducing the concentration of triglyceride-rich lipoproteins would break this cycle and would diminish the circulating level of potentially atherogenic lipoproteins.
Am J Cardiol 1986 May 30
PMID:Hypertriglyceridemia and carbohydrate intolerance: interrelations and therapeutic implications. 352 Dec 48

In the Program of Surgical Control of Hyperlipidemia, the relation of the Minnesota Q-QS codes for rest electrocardiograms to left ventricular (LV) function was studied in patients with healed myocardial infarction (MI). Of 838 subjects enrolled in the study, 477 (57%) had codable Q-QS patterns at the time of randomization. There was an extremely high correlation between the level of the Minnesota code and concurrent LV function, the latter being determined on left ventriculography by both ejection fraction and the number of segmental wall motion abnormalities. Subjects without a Q-QS code had less myocardial damage than did those with a code present in a single cardiac area. Extent of LV damage correlated with the level of significance of the Q-QS code, and when the code was present in only 1 cardiac location damage was greatest if the anteroseptal area was involved. Q-QS codes present in 2 rather than 1 cardiac area were associated with an even greater degree of LV damage. A previous study has shown a strong correlation between LV function and the Minnesota codes when the latter were recorded 0.5 to 5 years (mean 2.2) earlier at the time of the acute MI. The present data show that the relation between LV function and the Minnesota codes after an acute MI persists over time and is even stronger when both are determined in the healed state at a time remote from the acute event.
Am J Cardiol 1986 Sep 01
PMID:Relation between Q-QS changes on the rest electrocardiogram and left ventricular function with healed myocardial infarction. 375 7

The clinical features and course of 30 patients (26 men and 4 women) under 30 years of age (mean age 27.3 years) with an acute myocardial infarction (MI) are described. The most common risk factor among this group of patients was smoking in 20 patients (66%). The prevalence of the other risk factors was low: hyperlipidemia in four patients and family history of ischemic disease in another four patients, diabetes mellitus, hypertension, and obesity each in one patient. Seven patients (23%) had none of the conventional risk factors. Three patients were exerting themselves prior to the onset of their MI pain; all of them had normal coronaries. Five patients experienced chest pain prior to MI, among them only two experienced classical angina pectoris. Eighteen patients underwent uncomplicated MI. The complications in the other 12 during the acute MI were rhythm disturbances in eight and congestive heart failure in four. Cardiac catheterization was performed in 25 patients. The occurrence of zero, one, or multivessel disease was equal. The 30 patients were followed up from six months to 15 years (mean 7 years). In 18 patients circulating aggregated platelets were measured one year after the MI. Elevated values were found in all of them (mean +/- SD 34.9 +/- 9.1%). In 6 of the 18, all heavy smokers, extreme values were found in the range of 39-55%. Three out of the 30 patients died within five years after their first MI. The other 15 patients developed complications, most of them angina pectoris. Five patients were hospitalized for reinfarction. None of the 30 underwent aortocoronary bypass operation.(ABSTRACT TRUNCATED AT 250 WORDS)
Clin Cardiol 1987 Jan
PMID:Myocardial infarction in young adults under 30 years: risk factors and clinical course. 381 21

A prospective randomised trial was performed on 100 patients undergoing coronary artery bypass grafting without concomitant procedure. The study group commenced oral verapamil 40 mg three times daily on the first post-operative day while the control group received no antiarrhythmic agents. The pre-operative characteristics of both groups were similar with the exception of the incidence of hyperlipidemia which was greater in the verapamil group (P = 0.04). Myocardial protection was achieved with cold crystalloid cardioplegia. Cardiopulmonary bypass times, aortic cross clamp times and graft numbers were similar for both groups. Nine patients were excluded on the first post-operative day; the remainder were studied for 8 days. Supraventricular tachyarrhythmias (atrial fibrillation, atrial flutter or paroxysmal supraventricular tachycardia) were detected in 8 patients in the study group (n = 44) and in 5 patients in the control group (n = 47). The difference was not significant (P = 0.3). The ventricular rate in patients taking verapamil who developed supraventricular tachycardia was 138 +/- 14.9 compared with 156.8 +/- 17.9 in the control group, but the difference failed to reach significant levels (P = 0.065). In conclusion, prophylactic oral verapamil 40 mg given three times daily after coronary artery surgery failed to decrease the incidence of post-operative supraventricular tachycardia or to significantly influence the ventricular rate if tachycardia developed.
Int J Cardiol 1985 Sep
PMID:Oral verapamil fails to prevent supraventricular tachycardia following coronary artery surgery. 389 51


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