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Query: UMLS:C0020473 (hyperlipidemia)
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Data from a health screening survey with over 18,000 adult participants were used to determine the relations between serum calcium concentration and the cardiovascular risk factors hypertension, hyperglycaemia, and hyperlipidaemia. Blood pressure and serum glucose and cholesterol concentrations were all positively related to each other independent of age, sex, kidney function, and obesity. Similar relations between the risk factors were found in subjects with hypertension or hyperglycaemia independent of the degree of overweight. These results suggested that there might be a metabolic syndrome of cardiovascular risk factors. Serum calcium concentration was positively related to systolic and diastolic blood pressures and serum glucose and cholesterol concentrations. Thus a common feature in the syndrome is an increased serum calcium concentration. The relations between serum calcium concentrations and the cardiovascular risk factors were not limited to the upper parts of the distribution, being seen over a wide range. Changes in calcium metabolism seem to be related to a metabolic syndrome of hypertension, impaired glucose tolerance, and hyperlipidaemia.
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PMID:Relation of serum calcium concentration to metabolic risk factors for cardiovascular disease. 314 67

Chylomicrons show calcium-dependent agglutination by C-reactive protein (CRP). This has been suggested as a mechanism by which fat embolism may occur in the absence of trauma. It may also play a role in the pathogenesis of acute pancreatitis in patients with types I and V hyperlipidaemia.
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PMID:Fat macroglobule formation from chylomicrons and non-traumatic fat embolism. 323 65

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

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.
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PMID:Metabolic changes with antihypertensive therapy of the salt-sensitive patient. 328 52

Dietary factors ingested in excess, deficient, or in imbalance have been implicated in the etiology, and corrected in the management of cardiovascular diseases, namely atherosclerosis and hypertension. Dietary factors include: calories; fats; cholesterol and other sterols; complex and simple carbohydrates; animal and vegetable protein; alcohol; and minerals. Atherogenesis from diets high in total and saturated fat and cholesterol may relate to increases in plasma total, low- or very low-density lipoprotein cholesterol or triglycerides, or decrease in high density lipoprotein cholesterol, or altered apolipoproteins. A variety of dietary manipulations can influence these lipid and lipoprotein levels and thereby reduce cardiovascular risk. Plasma lipid and lipoprotein levels in the population vary with age, gender, and race; cardiovascular risk is increased when cholesterol levels exceed the 75th or 90th percentile for healthy men and women for age. Abnormally high levels of plasma cholesterol or triglycerides in different lipoprotein carriers comprise the various hyperlipoproteinemias. The clinical presentations and dietary management of elevated LDL cholesterol, and/or VLDL/ and/or chylomicron triglycerides, or increased intermediate density lipoproteins are reviewed and discussed. Attention should be paid to family screening, and hyperlipidemias secondary to diseases or medication should be considered. Dietary counseling and management is advised for children at risk of hyperlipidemia and for adult patients up to 70 years of age. If lipids and lipoproteins are not normalized, then lipid-lowering drug therapy should be considered in adults. For control of hypertension, attention should be paid to calories and alcohol, and to calcium, potassium, and sodium.
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PMID:Why, what, and how to implement reduction of cardiovascular risk factors by diet. 332 Jan 54

We investigated the patients who underwent operation for cholelithiasis and the diabetic patients at our clinic in order to determine whether there was a significant relationship between the occurrence of cholesterol gallbladder stone and age, obesity, hyperlipidemia, diabetes mellitus and neuropathy. In 647 patients undergoing surgery, cholesterol gallstones were not highly associated with diabetes mellitus or hyperlipidemia, compared with calcium bilirubinate and black stones. Eighty-seven percent of the male operated patients and 88% of the female patients were over 40 years old of age. Of the female patients in whom gallstones were detected at surgery, 36% were obese. We found cholesterol gallbladder stone in 11.5% (males 11%, females 12%) of 208 diabetic patients at our clinic. All of them were over 40 years old. The prevalence of cholesterol gallbladder stones was related to the decrease in motor nerve conduction velocity in the male diabetic patients (p less than 0.05). We observed that method of treatment had no definite effect on the prevalence of gallbladder stones. Fifty-four percent of the diabetic patients was normolipidemic in both sexes. Obesity was present in 64% of the female cholesterol gallbladder stone patients. Our data suggest that age, obesity and poor contraction of the gallbladder could be high risk factors for cholesterol gallstone formation.
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PMID:The relationship between cholelithiasis and diabetes mellitus: discussion of age, obesity, hyperlipidemia and neuropathy. 336 60

The National High Blood Pressure Education Program has released three Joint National Committee reports and a task force report on the detection, evaluation, and treatment of high blood pressure. Like its predecessors, the 1988 Joint National Committee report was developed using the consensus process; it is based on the latest scientific research and reflects the state of the art regarding hypertension management. This report updates findings of previous reports in several respects: it broadens the step-care approach to provide more flexibility for clinicians; encourages greater patient involvement in the treatment program; emphasizes a consideration of the quality of life in the management of patients; and addresses the cost of care. It also provides more emphasis on control of other risk factors for cardiovascular disease; includes a discussion of the new cholesterol guidelines; recommends a reduction in alcohol consumption; and discusses the use of calcium and fish oil supplementation. This document expands earlier reports on special populations, including blacks and other racial and ethnic minority groups, young and elderly patients, pregnant patients, surgical candidates, and hypertensive patients with cerebrovascular disease, coronary artery disease, left ventricular hypertrophy, congestive heart failure, peripheral vascular disease, renal disease, chronic obstructive pulmonary disease or bronchial asthma, gout, diabetes mellitus, and hyperlipidemia. The report also updates previous drug tables to include new drugs, revised recommended doses of some drugs, and drug interactions. Consideration of step-down therapy after blood pressure has been controlled is suggested. This report is intended as a guide for practicing physicians and other health professionals in their care of hypertensive patients and as a reference for those participating in the many community high blood pressure control programs throughout the country.
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PMID:The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. 256

Investigation of coronary heart disease manifesting as sudden death has highlighted the role of electrolyte disturbances in arrhythmogenesis. The identification of the 3 major cardiac risk factors--hyperlipidaemia, hypertension and smoking--does not fully explain sudden death in asymptomatic patients with an abnormal ECG. Sudden death is usually ascribed to cardiac arrhythmia whose pathogenesis has 3 possible mechanisms affecting the electrical properties of the heart. Thiazide diuretics are known to deplete potassium and magnesium in the body and while magnesium deficiency has been especially associated with cardiac rhythmicity, potassium levels modulate the cellular effects of calcium in the myocardium. In patients with ischaemic heart disease, both hypokalaemia and hypomagnesaemia correlate with the frequency of serious arrhythmias and even in ambulatory hypertensive patients on diuretics, it is important to preserve electrolyte homeostasis. There is, however evidence to suggest that some patients are more susceptible to diuretic-induced arrhythmias and in these patients even mild hypokalaemia can cause ventricular arrhythmias, and age may be a contributory factor. The risk of thiazide-induced arrhythmias has yet to be confirmed.
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PMID:Electrolyte abnormalities and ventricular arrhythmias. 352 91

The epidemiology and etiology, pathophysiology, diagnosis, clinical presentation, complications, and treatment of acute myocardial infarction (AMI) are reviewed. Major risk factors for AMI include age, sex (men greater than women), family history, race, hyperlipidemia, hypertension, cigarette smoking, diabetes mellitus, and diet. AMI occurs when there is a prolonged decrease in oxygen supply to the myocardium caused by coronary thrombosis or coronary vascular spasm. Traditional drug treatment of uncomplicated AMI includes oxygen, laxatives, and analgesics. For analgesia, narcotic agonists are generally preferred, although intravenous nitroglycerin is of value for both reducing infarct size and relieving pain. Fibrinolytic therapy is also indicated in these patients. Low-dose heparin should be initiated on admission to the hospital. Beta-adrenergic blocking agents have proven useful in reducing the incidence of ventricular fibrillation and sudden death. Antiplatelet agents may also be used to decrease long-term mortality. Recent studies have focused on reduction of infarct size using agents such as beta blockers, calcium-channel blockers, nitroglycerin, and thrombolytics. Revascularization procedures are required in some patients to re-establish adequate coronary perfusion. Most patients who survive AMI initially have a relatively uncomplicated clinical course. An increasing number of therapeutic interventions are available for acute and chronic treatment of AMI.
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PMID:Current concepts in clinical therapeutics: acute myocardial infarction. 352 26

The effects of calcium entry blockers on stimulated cholesteryl [3H]-oleate deposition in cultured macrophages were characterized in order to elucidate mechanisms underlying possible antiatherosclerotic effects. Stimulation of intracellular cholesteryl [3H]-oleate deposition was initiated by incubation of macrophages with beta-very low density lipoproteins (beta-VLDL). Nifedipine (Class I) markedly reduced cholesteryl [3H]-oleate deposition at all concentrations tested. However, Bay K 8644, a dihydropyridine which is known to stimulate calcium entry, also reduced cholesteryl [3H]-oleate deposition with a similar potency to nifedipine. The effects of three Class II calcium entry blockers were evaluated: verapamil, methoxyverapamil, and diltiazem. Verapamil inhibited cholesteryl [3H]-oleate deposition in a concentration-dependent manner. Similarly, methoxyverapamil reduced cholesteryl [3H]-oleate deposition in a concentration-dependent manner although the reduction was not as great as that produced by verapamil. In contrast, diltiazem at any concentration tested did not inhibit cholesteryl [3H]-oleate deposition. Flunarizine (a Class III calcium entry blocker) produced a modest stimulation of cholesteryl [3H]-oleate deposition at the lowest concentration used (10(-7)M) but marked depression at the highest concentration (10(-5)M). The results indicate calcium entry blockers may exert protective effects on the development of atherosclerosis in animal models of diet-induced hyperlipidaemia by inhibiting intracellular cholesteryl ester deposition, but this effect may not be related to their calcium entry-blocking effects.
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PMID:Inhibition of cholesteryl ester deposition in macrophages by calcium entry blockers: an effect dissociable from calcium entry blockade. 359 69


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