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

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

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

Pericardial lesions are the most frequent complications of thoracic radiotherapy; they occur in 2% to 30% of the cases depending on the publications. Acute pericarditis, which is the most common form, develops early or late and usually has a favourable course. Chronic pericarditis is divided into chronic pericardial effusion, the incidence of which is underestimated as it produces few or no symptoms, and chronic constrictive pericarditis, itself divided into 2 subgroups of different prognosis depending on the presence (pure fibrous pericarditis) or absence (constrictive sero-fibrous pericarditis) of underlying myocardial lesions. The incidence of myocardial lesions ("myocarditis") varies from 4% to 13% in the literature. They have a minor clinical form characterized by arrhythmias or disorders of conduction and a major form as restrictive or congestive cardiomyopathy with or without cardiac failure. Lesions of the coronary vessels are probably underestimated in view of the results of recent necropsies. Radiation-induced vascular lesions and hyperlipidaemia seem to act synergetically in the genesis of atherosclerosis. Cardiac valve lesions are even less frequent, but here again their incidence seems to be underestimated by conventional diagnostic methods. Echocardiography, radionuclide angiography and exercise tests appear to be useful for the long-term monitoring of patients who had their chest irradiated.
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PMID:[Radiation-induced cardiopathies]. 294 May 28

We evaluated the preoperative and intraoperative general condition of 33 pediatric kidney recipients. Eighteen patients were anaesthetized with lumbar epidural anaesthesia. Ten patients were with nitrous oxide-oxygen-halothane, 5 cases were with NLA. Preoperatively many children had cardiovascular and metabolic complications. For example 39% of patients had history of hypertension. Sixty-seven percent of patients were found to have cardiomegaly (cardio-thoracic ratio > 50%) with chest X-ray film. Seven of 9 patients undergoing echocardiogram had abnormality of cardiac wall motion, valvular impairment, pericardial effusion. In forty-eight percent of patients, hyperlipidemia was found. During operation we could not maintain the cardiovascular stability following intratracheal intubation and manipulation of vena cava or abdominal aorta under NLA or nitrous oxide-oxygen-halothane anesthesia. Epidural analgesia inhibited the cardiovascular fluctuation following these surgical stresses. We concluded that epidural analgesia is the best anaesthesia for pediatric renal transplantation and phentolamine or PGE1 are useful to maintain cardiovascular stability and transplanted kidney function.
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PMID:[Anaesthetic management of pediatric renal transplantation for chronic renal failure]. 843 61

Most patients suffering from systemic lupus erythematosus develop secondary heart disease at some time during the course of the primary illness. The most common forms of this type of heart disease are acute fibrinous pericarditis and hypertension. By means of echocardiography, an increased incidence of pericardial effusion has been demonstrated. Although commonly noted at autopsy, myocarditis is often clinically silent. However, endomyocardial biopsy may confirm its presence during life. Libman-Sacks endocarditis, although encountered in 40 to 50% of hearts at autopsy, is rarely diagnosed during life. When significant valve dysfunction such as aortic insufficiency or mitral regurgitation develops during the course of systemic lupus erythematosus, then Libman-Sacks endocarditis should be strongly suspected. Cardiac arrhythmias, first degree AV block, and acquired complete heart block may develop either de novo or in association with lupus pericarditis, myocarditis, vasculitis, etc. Complete congenital heart block has been reported in newborns of mothers with systemic lupus erythematosus, particularly those who have an antibody to a soluble tissue ribonucleoprotein antigen called RO(SS-A). Coronary arteritis and premature coronary atherosclerosis manifesting in either angina pectoris or myocardial infarction in young adults, particularly women suffering from systemic lupus erythematosus, have received attention recently. The development of hypertension and hyperlipidemia while such patients are receiving prolonged corticosteroid therapy has been incriminated as the significant risk factor in premature coronary atherosclerosis. Longstanding hypertension and congestive heart failure have unfavorable prognoses. This report is based on a cumulative review of 50 patients with acute and chronic systemic lupus erythematosus seen at our institution and in private practice during the last 10 years.
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PMID:Heart disease in systemic lupus erythematosus: diagnosis and management. 1522 37

HIV infection is a global public health issue that is frequently associated with cardiovascular involvement. These HIV-associated cardiovascular manifestations are often clinically occult or attributed incorrectly to other non-cardiac disease processes. A heightened awareness and routine screening for cardiovascular involvement in HIV-infected patients leads to earlier detection and the hope for a reduction in associated morbidity and mortality. Left ventricular dysfunction, an independent predictor of mortality in HIV-infected patients, is the result of many causes in this population and may result in dilated cardiomyopathy and congestive heart failure in about 10% of patients. Other HIV-associated cardiovascular problems include infective endocarditis, cardiovascular malignancy, pulmonary arterial hypertension, vasculitis, pericardial effusion, premature atherosclerosis, and arrhythmias. HIV-associated cardiovascular emergencies include congestive heart failure, pulmonary edema, supraventricular and ventricular arrhythmias, endocarditis, and tamponade. Anti-infective and immunomodulatory therapies may be particularly helpful in this population to reduce associated cardiovascular disease. Highly active antiretroviral therapy may result in lipodystrophy, hyperlipidemia, truncal adiposity, and insulin resistance that can be improved by physical activity and training programs. Cardiovascular complications of therapeutic drugs in HIV-infected patients include torsade de pointes, congestive heart failure, dyslipidemia, accelerated atherosclerosis, and myocardial infarction. In summary, cardiovascular complications are important contributors to morbidity and mortality in HIV-infected patients that can be detected early in many cases and treated effectively.
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PMID:HIV-related cardiovascular disease and drug interactions. 1544 73

Cardiovascular manifestations of HIV vary according to disease stage, treatment regimen and geographical location. Common cardiac complications of HIV disease in patients off highly active antiretroviral therapy (HAART) include dilated cardiomyopathy, myocarditis, pericardial effusion, endocarditis, pulmonary hypertension and non-antiretroviral drug-related cardiotoxicity. However, with the introduction of HAART that has substantially modified the course of HIV disease by lengthening survival, additional cardiovascular consequences are a result of the metabolic syndrome with a propensity toward hyperlipidaemia and atherosclerotic heart disease. Because most of the world's HIV-infected patients have not been treated with HAART, the principal HIV-associated cardiovascular manifestations of patients off HAART are reviewed and new knowledge about the prevalence, pathogenesis and treatment in the HAART era are emphasised in this review. Exercise, a nonpharmacological approach to treating HAART-associated metabolic syndrome, is also discussed.
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PMID:Cardiovascular disease and toxicities related to HIV infection and its therapies. 1625 61

The survival of patients with HIV infection who have access to highly active antiretroviral therapy has dramatically increased. In HIV-infected persons, cardiovascular disease can be associated with HIV infection, opportunistic infections or neoplasias, use of antiretroviral drugs or treatment of opportunistic complications, mode of HIV acquisition (such as intravenous drug use), or with the classic non-HIV-related cardiovascular risk factors (such as smoking or age). Diseases of the heart associated with HIV infection or its opportunistic complications include pericarditis and myocarditis. Pericarditis may lead to pericardial effusion rarely causing tamponade. Cardiomyopathy is often clinically silent with asymptomatic left ventricular systolic dysfunction. Endocarditis is mainly the consequence of intravenous drug abuse, possibly leading to life-threatening valvular insufficiency with the need for cardiac surgery. A further serious condition associated with HIV infection is pulmonary hypertension potentially leading to right heart failure. The cardiovascular complications of HIV infection such as cardiomyopathy and pericarditis have been reduced by highly active antiretroviral therapy, but premature coronary atherosclerosis is now a growing problem because antiretroviral drugs can lead to serious metabolic disturbances resembling those in the metabolic syndrome. Lipodystrophy, a clinical syndrome of peripheral fat wasting, central adiposity, dyslipidemia, and insulin resistance, is most prevalent among patients treated with protease inhibitors. These patients should thus be screened for hyperlipidemia, hyperglycemia, and hypertension, and they may be candidates for lipid-lowering therapies. When initiating lipid-lowering therapy, interactions between statins and HIV protease inhibitors affecting cytochrome P450 function must be considered. Restenosis rate after percutaneous coronary intervention may be unexpectedly high.
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PMID:Cardiovascular disease in HIV infection. 1678 Dec 13

Tuberculous pericarditis is an exceedingly rare but a well-described extra-pulmonary manifestation of tuberculosis (TB) infection in Hong Kong. An 82-year-old woman with a known history of diabetes mellitus, hypertension and hyperlipidaemia was admitted for congestive heart failure. Routine echocardiographic study during admission revealed a massive pericardial effusion (~4 cm in thickness) but with no tamponade effect. Pericardiocentesis was performed and 1.6 L of heavily blood stained fluid was drained. All tumour and auto-immune markers were unremarkable. A whole body positron emission tomography-computer tomography (PET-CT) scan was then performed and showed an increased fluorodeoxyglucose uptake in the entire pericardium with no sources of possible malignancy identified. Rapid acid fast bacilli culture and Genprobe examination of the pericardial fluid then demonstrated the growth of Mycobacterium tuberculosis. She was started on anti-TB medications and tolerated them well. Follow-up echocardiographic study showed no re-accumulation of pericardial fluid.
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PMID:Tuberculous pericarditis presenting as massive haemorrhagic pericardial effusion. 2274 46

BACKGROUND Drug induced lupus erythematosus is considered an autoimmune entity which is precipitated by medications. Hydrochlorothiazide has been recognized to cause subacute cutaneous lupus erythematosus, but very few cases of systemic drug induced lupus systemic erythematosus have been reported. CASE REPORT A 57-year-old Caucasian male with a past medical history of hypertension and hyperlipidemia presented with recurrent fevers, chest pain, and dyspnea. Initial evaluation revealed diffuse ST elevations, small pericardial effusion, anemia, and leukopenia. He was initially treated with nonsteroidal anti-inflammatory drugs and prednisone for pericarditis. Six months later, he reported fatigue, arthralgias, morning stiffness, weight loss, fevers, and night sweats. Laboratory tests revealed persistent anemia and leukopenia. Extensive workup, including bone marrow biopsy and infectious evaluations, was negative. Autoimmune workup, however, revealed positive antihistone and antichromatin antibodies despite negative antinuclear antibody. A diagnosis of drug induced lupus secondary to hydrochlorothiazide was made. The medication was stopped, and prednisone was initiated resulting in marked improvement in his symptoms and hematologic abnormalities. CONCLUSIONS This report is one of the few known cases of systemic lupus erythematosus most likely induced by hydrochlorothiazide. Based on our finding, hydrochlorothiazide should be considered a possible offending agent when a patient presents with symptoms suspicious of drug induced lupus.
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PMID:When Chest Pain Reveals More: A Case of Hydrochlorothiazide-Induced Systemic Lupus Erythematosus. 3061


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