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

In order to determine the effect of obesity on the results of coronary artery bypass graft (CABG) surgery, we compared 250 obese patients undergoing CABG procedures between 1984 and 1987 with 250 age- and sex-matched controls of normal body mass index (BMI) undergoing CABG in the same period. The obese group had a greater incidence of diabetes mellitus (p less than 0.02), hypertension (p less than 0.05), hyperlipidaemia (p less than 0.05), and left main stem coronary artery disease (p less than 0.001). No differences were identified in the surgery performed, but obesity was associated with prolonged total bypass time (p less than 0.05). Operative mortality was 0.8% in both groups. Multivariate analysis demonstrated obesity to be an independent risk factor for perioperative morbidity (p less than 0.05). Univariate: respiratory (p less than 0.01); leg wound (p less than 0.001); myocardial infarction (p less than 0.02); arrhythmias (p less than 0.02); sternal dehiscence (p less than 0.02). At a mean follow-up time of 36.9 months obese patients exhibited a greater incidence of significant recurrent angina (p less than 0.01), which was associated with further weight gain (mean 12.2 kg; linear correlation: p less than 0.001, r = 0.891). Although in CABG surgery operative mortality is not increased in obese patients, aggressive pre- and postoperative weight control is indicated to reduce both perioperative morbidity and the incidence of recurrent angina.
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PMID:Influence of obesity on the early and long term results of surgery for coronary artery disease. 201 57

Regular drug treatment in mild hypertension (diastolic blood pressure 90-104 mm Hg) reduces death from stroke, and other non-coronary vascular events. The optimum strategy remains sequential monotherapy with the lowest effective dose, with drug combinations as an option. A beta-adrenoceptor blocker or low-dose thiazide is good value treatment for many patients. beta-Blockers are good for young (under 50 years), anxious non-smoking men, men after myocardial infarction, and renal failure patients. Older persons over about 65 years, women, smokers, stroke victims, and liver disease patients should generally take a thiazide or calcium ion-channel blocker. Pregnant women and untreated gouty patients should avoid diuretics. Calcium blockers and angiotensin-converting enzyme inhibitors are preferable in severe or insulin-dependent diabetes and renal failure, and angiotensin manipulators or thiazides in heart failure or peripheral vessel disease. Hyperlipidaemia should not generally exclude thiazides or beta-blockers. Some hypertensive stroke patients without encephalopathy may not need antihypertensive drug treatment for the first 24-48 hours. Drug treatment should be tailored to individuals according to their general condition, physiological age, and any concurrent disease or medication. Unwanted drug reactions should not deter patients from fulfilling social and economic goals. The desired treatment end-point is a diastolic pressure of 85-89 mm Hg, but a compromise is usual in poorly motivated young men, and the elderly.
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PMID:Optimising drug management of individuals with cryptogenic hypertension. 202 55

More than a decade has passed since the introduction of the concept that inhibition of platelet function may be helpful in preventing the initiation of thrombus formation. Aspirin has been recognized as inhibiting normal platelet function and the mechanism has been clearly delineated. Legions of patients have been studied to answer the question of whether aspirin is efficacious in the primary prevention of acute myocardial infarction. At the present time, however, a solid, clear answer is not available and firm recommendations cannot be made. A large number of studies evaluating aspirin and other antiplatelet agents in the prevention or delay of recurrent myocardial infarction (secondary prevention) have been completed and those studies reporting a favorable beneficial effect are in the minority. In these secondary prevention studies reporting success, the doses of aspirin employed were large enough to inhibit both the cyclo-oxygenase system and thromboxane A2 production as well as the synthesis of prostacyclin. Thus, in these studies if aspirin is effective in reducing adverse cardiovascular events, its efficacy is being mediated by an unknown mechanism. If the reader of the few studies that report positive results is convinced of the benefit of aspirin, it must be emphasized that thoughtful, cautious patient selection based upon the individual's cardiovascular risk profile must be exercised. Individual variation may exist with respect to aspirin's beneficial effect. It must be absolutely recognized that aspirin or any antiplatelet agent does not in any way substitute for the removal or treatment of coexisting risk factors such as tobacco, obesity, hypercholesterolemia, hyperlipidemia, hypertension, and metabolic disease. In contrast to aspirin, control of the above risk factors has been established as beneficial. Aspirin is not free of undesirable side-effects; fatalities secondary to hemorrhage have been reported, and these must be known in detail and understood by both physician and patient before this agent is prescribed in the prophylactic treatment of cardiovascular disease.
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PMID:Aspirin in the prevention of thrombosis. 203 Jun 40

The left ventricular contractility was evaluated in patients with hyperlipidemia or uncomplicated Functional Class I-III angina by using echocardiography at rest and during bicycle ergometric tests. A total of 47 males under 60 years were examined, who were divided into 4 groups: 1) 10 healthy subjects; 2) 14 hyperlipidemic subjects without signs of coronary heart disease; 3) 10 patients with Functional Class I-III angina who showed no ischemic response to bicycle ergometry; and 4) 13 patients with angina pectoris who showed an ischemic response to exercise. The patients had no history of myocardial infarction. The patients from Groups 2-4 displayed a lower overall left ventricular contractility as manifested by no decrease in left ventricular end systolic volume after exercise and other parameters. They also exhibited a segment asynergy in myocardial performance.
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PMID:[Myocardial contractility in subjects with hyperlipidemia and patients with angina pectoris according to findings of bicycle ergometry echocardiography]. 204 Dec 83

Atherosclerosis frequently develops in SVGs during the first 10 years. This process appears related to coronary risk factors. Several studies have found an association between hyperlipidemia and atherosclerosis documented at pathology. Late changes attributed to atherosclerosis that were observed at angiography were also significantly related to elevated serum levels of total cholesterol and triglycerides. They also were found in association with diabetes, systemic hypertension, and smoking in some studies. Several clinical studies have documented an association of one or several coronary risk factors with postoperative clinical events, including recurrence of angina, myocardial infarction, heart failure, reoperation because of clinical deterioration, and survival. These factors have been shown to act alone or in combination. The most important is an abnormal lipid profile and diabetes. Smoking and hypertension were seldom found to be significant predictors when considered separately, but appear to play an important role in association with the others. Control of coronary risk factors, particularly hyperlipidemia and smoking, seems mandatory in order to prevent SVG atherosclerosis and progression of the disease in the native coronary arteries.
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PMID:Coronary risk factors and the postbypass patient. 204 86

A study is presented of 103 patients with myocardial infarction (age: from 23 to 41 years) and 100 patients over 55 years-old. The younger patients showed rarely stenocardia in the preinfarction period, macrofocal lesions prevailed, more pronounced were leucocytosis, hyperenzymemia, hyperlipidemia and hyperthermia, rarely cardiogenic shock, cardiac asthma, pulmonary edema and complex rhythm disorders. Diagnostic errors were observed in 48.5% at the prehospital stage in the younger patients. The most frequent causes of errors were awareness of the physician for coronary pathology in the young, inadequate anamnesis screening and examination of patients.
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PMID:[The diagnosis of myocardial infarct at a young age in the prehospital stage]. 208 89

The authors report the case of a 18 year old man with a chronic corticosteroid-refractory nephrotic syndrome complicated by carotid artery thrombosis and myocardial infarction. Thromboembolism is one of the most serious complications of the nephrotic syndrome. Serious clotting factor disturbances are observed: changes in platelet function (hyperaggregability) increased plasma zymogens and cofactors, increased plasma fibrinogen, abnormalities of the fibrinolytic system and acquired deficiencies of coagulation inhibitors. The respective role of each of these abnormalities have not been clearly established, but it is likely that increased platelet aggregation and antithrombin III deficiency are important factors in producing a hypercoagulable state in the nephrotic syndrome. Hyperlipidemia is also a characteristic feature of the nephrotic syndrome: these is a wide spectrum of lipoprotein patterns with increased low density lipoproteins (LDL) or very low density lipoproteins (VLDL) or both; contradictory results have been reported with respect to the high density lipoproteins (HDL): decreased, normal or even increased plasma levels have been observed. In addition, changes in the distribution and composition of LDL and VLDL subclasses have been detected. Most of these changes have an atherogenic potential but controversy still surrounds the question of the prevalence of ischaemic heart disease in the nephrotic syndrome; it is unlikely that nephrotic syndromes of short duration have any influence on the incidence of coronary events, but patients with chronic heavy protein urea and long-term exposure to abnormalities of haemostasis and lipid profiles appear to have a significant risk of developing cardiovascular disease and may require long-term anticoagulant therapy.
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PMID:[Carotid artery thrombosis and myocardial infarction in nephrotic syndrome]. 210 97

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called uremic heart diseases]. 210 35

Decisions to resect small aortic aneurysms or employ non-operative treatment for aorto-iliac occlusive disease must depend on current rather than historical surgical results. To assess current morbidity and mortality, we reviewed 200 consecutive aortic resections in two groups of patients treated from 1981 to 1989: those undergoing elective aortofemoral bypass for occlusive disease (AFB, no. 100) or resection of infrarenal abdominal aortic aneurysms (AAA, no. 100). Indications for AFB included claudication (54%), rest pain (32%), and gangrene (13%). AAA size ranged from 3 to 14 cm (mean 6.5 +/- 2.4 cm); 45% presented with abdominal or back pain. Patients undergoing AFB were younger (AFB 61.5 +/- 10 years vs AAA 68.7 +/- 8.9 years) with a higher incidence of some atherosclerotic risk factors, diabetes mellitus 30% vs 10%, tobacco use 77% vs 49%, hyperlipidemia 21% vs 7%; p less than 0.001). Coronary artery disease (CAD) was more prevalent in AAA patients (49% vs 34%; p less than 0.001). Postoperative mortality was not different in occlusive or aneurysmal disease (3% AFB vs 2% AAA), nor was the occurrence of serious complications such as myocardial infarction (2% vs 1%) or pulmonary embolism (2% vs 3%). Improvements in patient selection, perioperative care and surgical technique have lowered the mortality of elective aortic surgery. Given the current standard of care, an aggressive approach to AAA even in high risk patients is appropriate. The low morbidity of AFB for occlusive disease mandates a critical appraisal of less effective nonoperative therapies.
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PMID:Current results of elective aortic reconstruction for aneurysmal and occlusive disease. 221 95

A male to female ration of coronary disease of 2:1 has been a consistent finding. This differential persists event when the classic risk factors for coronary disease--hypertension, smoking, obesity, diabetes, and hyperlipidemia--are controlled for gender. The most likely ultimate cause of this phenomenon is male-female differences in sex hormone patterns. Clinical studies in this area have either compared the sex hormone profiles of men and women with and without coronary disease or computed the relative prevalence of disease in populations that differ in their sex hormone patterns. In general, research findings have disputed the hypothesis that persons with coronary disease have low levels of a protective factor such as estrogen or progesterone and high levels of testosterone. Coronary disease patients actually have elevated estrogen levels and low testosterone levels; endogenous progesterone levels are normal before infarction but show a stress-mediated increase in the immediate postinfarction period. Findings of a low prevalence of coronary disease in premenopausal women, a loss of protection after menopause, and a low prevalence of coronary disease in men with cirrhosis-related hyperestrogenemia suggest that natural estrogens are antiatherogenic. The protective effect of pregnancy against myocardial infarction, despite concomitant potentially thrombogenic levels of estrogen at the time, seems to indicate that progesterone, whose levels are also extremely high during pregnancy, plays a major anti-infarction protective effect distinct from that of estrogen. Studies of women oral contraceptive (OC) users and men taking estrogens for brief periods have found that these exogenous hormones produce coronary thrombosis but not atherosclerosis. Finally, the finding of increased coronary disease risk in long-term OC users indicates that synthetic estrogens favor coronary atherosclerosis by suppressing natural estrogen and progesterone production.
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PMID:Sex hormones and coronary disease: a review of the clinical studies. 223 42


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