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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)
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PMID:Diabetic dyslipidemia: a case for aggressive intervention in the absence of clinical trial and cost effectiveness data. 775 45

Two hundred and ninety one patients admitted with atrial fibrillation through the emergency room of a regional hospital in the year 1993 were reviewed to evaluate the presenting features and in-hospital treatment of patients with symptomatic atrial fibrillation. The incidence of atrial fibrillation increased with age (mean age was 73 +/- 12 years) and the ratio of female to male was 1.8:1. The commonest presenting features were palpitation (42.3%), dyspnoea (38.1%) and heart failure (16.4%). The most frequently associated cardiac conditions were hypertension (28.9%), atherosclerotic cardiovascular disease (24.7%) and rheumatic heart disease (17.5%). Pulmonary diseases (18.6%), diabetes mellitus (12.7%) and thyrotoxicosis (6.2%) were the principal associated non-cardiac conditions. Thromboembolic complications were found in 15 patients at presentation (5.2%). Cardiac enzyme assessment was investigated in two thirds of the patients (68.1%), while thyroid function test (59.5%) and echocardiography (29.6%) were less commonly investigated. Digoxin was still the most popular drug used for ventricular rate control, and cardioversion was performed in only 6.9% of patients. Antithrombotic therapy was used in 5.8% of patients only although it was clinically indicated in more than half of the patients (52%). Contraindications of anticoagulation were found in 23 patients (7.9%), including a history of gastrointestinal or cerebrovascular bleeding, active bleeding, chronic renal failure and poor drug compliance. The mean hospital stay was 5 +/- 4 days, compared to a mean stay of 2.7 days for other medical patients. Fourteen patients (4.8%) died during hospitalisation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Presentation and management of patients admitted with atrial fibrillation: a review of 291 cases in a regional hospital. 778 42

Important nutrition concepts will aid primary care/generalist physicians to implement practical aspects of health promotion and disease prevention in their practice, and improve the overall health of their patients. In today's society, chronic diseases that are related variably to overnutrition and dietary excesses or imbalances (obesity, diabetes mellitus, hypertension and atherosclerotic cardiovascular disease, some cancers) warrant knowledgeable diet modifications in high-risk individuals. However, serious nutritional deficiency diseases also still occur (as in alcoholic patients), and instituting appropriate diet and supplements will aid in preventing further morbidity and mortality. Nutrition knowledge changes with new scientific evidence, and the physician must be aware of reliable sources of continuing education and information appropriate for the practitioner and the patient.
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PMID:Nutrition concepts for the primary care/generalist physician. 783 65

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.
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PMID:Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics. 784 87

Atherosclerotic cardiovascular disease is a significant cause of morbidity and mortality in patients with chronic renal failure. It is unclear, however, if atherosclerosis in fact occurs at a higher incidence compared with the nonuremic population matched for age, hypertension, and diabetes mellitus or if it occurs at an accelerated rate following the onset of end-stage renal disease. The extent of true atherosclerotic lesions, versus clinically diagnosed "atherosclerosis," in patients with chronic renal failure is equally unclear. Potentially, the uremic state per se, the dialysis treatment, and factors unrelated to renal failure may participate in atherogenesis. The relative contribution of each of these factors is unknown. In this review, we discuss the pathology of "atherosclerotic" lesions in patients with chronic renal failure and the putative factors involved in atherogenesis in this population and describe the results of available studies examining the issue of accelerated atherosclerosis in uremia.
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PMID:Atherosclerosis in chronic renal failure. 792 27

Primary hypertension is a frequent polygenic disease with strong genetic and environmental components. During the last decade, evidence has been increasing that insulin resistance as a marker of increased risk for Type 2 diabetes and cardiovascular atherosclerotic disease is present not only in individuals with obesity, Type 2 diabetes and impaired glucose tolerance, but also in the majority of the hypertensive population. Insulin resistance describes a tissue- and pathway-specific defect of glucose metabolism present in the so called 'metabolic syndrome'. Hyperinsulinaemia compensates for insulin resistance, leading to a cluster of undesirable processes predisposing to diabetes, atheroma and, directly or indirectly, hypertension. Candidate mechanisms whereby this metabolic syndrome might lead to hypertension include renal sodium retention, vascular hyperresponsiveness, arteriolar smooth muscle cell proliferation, altered cellular electrolyte transport and composition, stimulation of sympatho-adrenergic activity and growth promoting effects. Insulin per se does not appear to be the cause of elevated blood pressure as frequently seen in insulin-resistant states, but it may act with other factors to promote hypertension and atherosclerotic cardiovascular disease.
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PMID:New aspects of insulin resistance in hypertension. 799 75

Uric acid is formed by catabolism of purine nucleotides. Approximately 25% is excreted through the intestines and the rest through the kidneys. A little less than 5% of the population in western industrialised countries have hyperuricaemia, primarily men and postmenopausal women. Hyperuricaemia is in most cases caused by reduced renal excretion, which may be idiopathic with otherwise normal renal function. But the condition is often associated with hypertension, nephropathy and treatment with diuretics and certain other drugs. Hyperuricaemia due to increased purine metabolism is seen in malignant haematological diseases, other conditions with increased cellular turnover and during initiation of chemotherapy in malignant diseases. Moreover hyperuricaemia is associated with some metabolic disturbances and risk factors of atherosclerotic cardiovascular disease including hypertension, overweight, insulin resistance and hyperlipidaemia. Hyperuricaemia is rarely caused by constitutional enzymatic abnormalities influencing purine metabolism. In most cases hyperuricaemia is asymptomatic. It may though be complicated by gout, urolithiasis and possibly gouty nephropathy. The risk of complications is correlated to the degree and duration of hyperuricemia. Consequently, measures to affect predisposing and associated conditions should be taken including weight reduction, physical exercise and diet guidance, treatment of hypertension and possibly changes in medication. Urate lowering drug treatment is normally not indicated in asymptomatic hyperuricaemic individuals.
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PMID:[Hyperuricemia]. 800 1

Hypertension and atherosclerotic cardiovascular disease represent major global health problems. Practising physicians are challenged daily by patients suffering adverse cardiovascular events, such as myocardial infarction, stroke, heart failure and sudden cardiac death. Major risk factors have been identified of which the most important is left ventricular hypertrophy. In recent years, growth factors, regulatory peptides and effector hormones of the renin-angiotensin-aldosterone system have been identified as important modulators of cell growth and behaviour. It therefore follows that a major emphasis has been placed on the importance of abnormalities in organ structure as the primary basis for impaired function of the heart and vasculature, including large and medium sized arteries and resistance vessels, or arterioles. The concept of reparation recognizes the importance of abnormalities in tissue structure to the functional basis of disease. It suggests that the structurally remodelled heart and vasculature can be restored to, or toward, normal structure and function by suitable therapy. Experimental and clinical trials which address this premise are reviewed herein.
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PMID:Cardioreparation and the concept of modulating cardiovascular structure and function. 819 34

Hyperinsulinemia is very much in the spotlight. Debate rages as to its significance and role in the etiology not only of NIDDM, but also other morphological and metabolic risk factors for atherosclerotic cardiovascular disease, including upper-body obesity, dyslipidemia, hypertension, and hyperuricemia. Epidemiological data support a key role for hyperinsulinemia in these disorders but it is far from conclusive except for the fact that hyperinsulinemia and insulin resistance may be present many years before the onset of impaired glucose tolerance and NIDDM, and clearly play a role in their etiology. The thrifty genotype hypothesis provides a plausible basis for a better understanding of how hyperinsulinemia and insulin resistance could lead to glucose intolerance and atherosclerotic cardiovascular disease, but the detailed biochemical mechanisms remain elusive. A role for increased sympathetic nervous system activity, resulting from hypothalamic stimulation as a primary event causing hyperinsulinemia, cannot be excluded as a cause of hyperinsulinemia. The current focus on hyperinsulinemia also has resulted in closer examination of the therapy of diabetes and hypertension, emphasizing the need to avoid hyperinsulinemia in both IDDM and NIDDM individuals because of the putative risk of atherosclerotic cardiovascular disease and hypertension. There is still a paucity of epidemiological data to support a role for hyperinsulinemia in the etiology of hypertension. However, clinical practice already is being influenced by the fact that ACE inhibitors have been shown to reduce insulin resistance in clinical research studies. The research reviewed here, particularly that relating to hyperinsulinemia, insulin resistance, and cardiovascular disease risk factors, has opened new vistas for the treatment and prevention of NIDDM and atherosclerotic cardiovascular disease. Appropriate exercise clearly is associated with improved insulin sensitivity, modification of CVD risk factors, and lower prevalence of NIDDM. Upper-body obesity, the latest culprit in the field, can also be reduced by exercise. Hyperinsulinemia and insulin resistance can be detected in children, adolescents, and young adults. NIDDM can be prevented, but clearly, intervention needs to commence in childhood, and intensive risk factor intervention in subjects with NIDDM can reduce the risk of atherosclerotic cardiovascular disease. It seems paradoxical that prevention of NIDDM and atherosclerotic cardiovascular disease are now possible even though the biochemical and molecular basis of these disorders is not fully understood.
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PMID:Hyperinsulinemia--how innocent a bystander? 829 79

Hypertension and diabetes mellitus are interrelated diseases that, if untreated, strongly predispose to atherosclerotic cardiovascular disease and renal disease. More than 3 million Americans have both hypertension and diabetes, which are particularly prevalent in the socioeconomically disadvantaged. Hypertension contributes substantially to morbidity and mortality in people with diabetes. This report is an update of the 1987 working group report on hypertension and diabetes and includes important new information on the management of hypertension in people with diabetes. Although treatment of hypertension in most people with diabetes does not differ from that in people who do not have diabetes, this report outlines some special considerations relevant to the presence of both diseases. Lifestyle modification is considered as an initial treatment modality or as an adjunct to pharmacologic measures. This report also includes a discussion of the treatment of hypertension and diabetes in children, an expanded review of sexual dysfunction, and an increased emphasis on the effect of hypertension and diabetes on target organs. A treatment algorithm represents a practical guideline for the physician. Since the previous report, there has been an increased awareness, through clinical trials and pharmacologic research, of the importance of flexibility in the use of antihypertensive drugs as well as a refinement of nonpharmacologic approaches in treating people with both hypertension and diabetes.
Hypertension 1994 Feb
PMID:National High Blood Pressure Education Program Working Group report on hypertension in diabetes. 830 22


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