Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Familial partial lipodystrophy (FPLD), Dunnigan variety, is an autosomal dominant disorder characterized by marked loss of subcutaneous adipose tissue from the extremities and trunk but by excess fat deposition in the head and neck. The disease is frequently associated with profound insulin resistance, dyslipidemia, and diabetes. We have localized a gene for FPLD to chromosome 1q21-q23, and it has recently been proposed that nuclear lamin A/C is altered in FPLD, on the basis of a novel missense mutation (R482Q) in five Canadian probands. This gene had previously been shown to be altered in autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD-AD) and in dilated cardiomyopathy and conduction-system disease. We examined 15 families with FPLD for mutations in lamin A/C. Five families harbored the R482Q alteration that segregated with the disease phenotype. Seven families harbored an R482W alteration, and one family harbored a G465D alteration. All these mutations lie within exon 8 of the lamin A/C gene-an exon that has also been shown to harbor different missense mutations that are responsible for EDMD-AD. Mutations could not be detected in lamin A/C in one FPLD family in which there was linkage to chromosome 1q21-q23. One family with atypical FPLD harbored an R582H alteration in exon 11 of lamin A. This exon does not comprise part of the lamin C coding region. All mutations in FPLD affect the globular C-terminal domain of the lamin A/C protein. In contrast, mutations responsible for dilated cardiomyopathy and conduction-system disease are observed in the rod domain of the protein. The FPLD mutations R482Q and R482W occurred on different haplotypes, indicating that they are likely to have arisen more than once.
 ...
PMID:Mutational and haplotype analyses of families with familial partial lipodystrophy (Dunnigan variety) reveal recurrent missense mutations in the globular C-terminal domain of lamin A/C. 1073 51

With the advent of more effective therapies for human immunodeficiency virus (HIV) infection, HIV-infected patients are living longer and cardiovascular disease is becoming more obvious in this population. Patients with HIV infection represent one of the most rapidly developing groups with cardiovascular disease globally. Cardiovascular disease complicating HIV infection is likely to contribute to burgeoning healthcare costs. Pericarditis, myocarditis, cardiomyopathy, atherosclerotic coronary vasculopathy, arterial aneurysms, pulmonary hypertension, and endocarditis occur with increased frequency in these patients. Pericardial tamponade, dilated cardiomyopathy, endocarditis, and vasculopathy can lead to fatal outcomes in this population. The advent of cardiomyopathy heralds a very poor prognosis in patients infected with HIV. Coronary vasculopathy without obvious risk factors can lead to myocardial ischemia in young patients infected with the virus. Moreover, the protease inhibitors used to treat HIV infection induce a syndrome of lipodystrophy and dyslipidemia that may be associated with accelerated atherosclerosis as well as insulin resistance. All these factors contribute to increased cardiovascular morbidity and mortality in the HIV-infected population. HIV infection, opportunistic infections, secreted viral proteins such as gp120 (envelope protein) or Tat (transactivator of viral transcription), and cytokines elaborated during the course of HIV infection of the immune system all contribute to pathogenesis of these disorders. Further basic and clinical studies are required to understand the pathogenesis of cardiovascular complications and develop appropriate management strategies for these patients.
 ...
PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4

Diabetes mellitus is a major risk factor for the development of congestive heart failure (CHF). Diabetic cardiomyopathy has been acknowledged as a distinct disease entity that is an additional risk for diabetic patients to develop CHF, especially when they are affected by hypertension or epicardial coronary artery disease. Moreover, diabetic cardiomyopathy has been documented to lead to CHF even in the absence of other risk factors. As the combination of hypertension and diabetes has shown to be particularly detrimental, aggressive blood pressure control with a goal of less than 130/85 mm Hg is of critical importance. The first choice for pharmacologic treatment is angiotensin-converting enzyme inhibitors. Double- or triple-drug therapy is frequently required for good control. The increased risk of epicardial coronary artery disease in patients with diabetes warrants stringent treatment of dyslipidemia. If dilated cardiomyopathy with low ejection fraction is present, therapy with angiotensin-converting enzyme inhibitors, digoxin, diuretics, beta-blockers, and spironolactone (for patients with New York Heart Association class III to IV functional status) is indicated. If cardiac dysfunction consists predominantly of impaired diastolic function, heart rate control with a beta-blocker or a calcium antagonist is of particular importance. Control of blood glucose should be achieved, with hemoglobin A(1c) levels of less than 7%. Hyperinsulinemia should be avoided when possible; therefore, insulin-sensitizing agents are preferred over insulin-secretion-enhancing agents. Symptoms of CHF and acutely decompensated CHF should be treated no differently than nondiabetic patients. Care for patients with diabetes always includes lifestyle changes consisting of smoking cessation, decreasing obesity, regular exercise, and a heart-healthy diabetic diet.
 ...
PMID:Diabetic Cardiomyopathy. 1169 68

Despite of dramatic improvement in diagnostic procedures and treatment of diabetic patients, cardio-vascular complications are still the most frequent causes of death in these patients. Diabetes influences myocardial and coronary vessels function by coexisting macroangiopathy, microangiopathy, metabolic disturbances and autonomic nervous system neuropathy. All these factors result in diastolic and systolic dysfunction of the heart. Cardiomyopathy, congestive heart failure and serious arrhythmias are the end stage of diabetic complications. Macroangiopathy demonstrates accelerated atherosclerosis (involving coronary arteries), which consequences can be observed in 1 type diabetes patients at around the age of 30. Causes of increased risk of macroangiopathy in type 1 diabetic patients are not clear. There are not many clinical, prospective trials which can allow for etiology determination of the increased incidence of atherosclerosis and mortality due to coronary artery disease in this population. Adding to traditional risk factors of atherosclerosis like genetic factors, hypertension, dyslipidemia, obesity, smoking and improper diet, other important risk factors are observed in diabetic patients. Only few clinical trials suggest that hyperglycemia, glycation, glycoxidation of proteins, lipoproteins, changes in their composition, microalbuminuria, coagulation, fibrinolytic disturbances are additional risk factors of endothelium dysfunction and atherosclerosis. Prevention and treatment of accelerated coronary artery disease and it's consequences are more complicated in the diabetic population than in others. Some of the clinical trials suggest that even improved glycemic control does not eliminate the elevated risk of coronary artery disease in type 1 diabetic patients.
 ...
PMID:[Myocardial and coronary vessel dysfunction in diabetes I patients]. 1251 40

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.
 ...
PMID:HIV-related cardiovascular disease and drug interactions. 1544 73

This article describes the relationship between CVD and CKD, the current state of knowledge regarding medical interventions, and underscores the importance of attending to both CVD and kidney disease aspects in each individual. The burden of cardiac disease in CKD patients is high with severe LVH, dilated cardiomyopathy and coronary artery disease occurring frequently. This predisposes to congestive heart failure, angina, myocardial infarction, and death. Multiple risk factors for cardiac disease exist and include hypertension, diabetes, smoking, anemia, abnormal calcium and phosphate metabolism, inflammation, and LVH. The efficacy of risk factor intervention has not been established in these populations, although there is good evidence for good blood pressure control, partial correction of anemia, treatment of dyslipidemia, cessation of tobacco use, correction of divalent abnormalities, and aspirin us. Appropriate use of ACE inhibitors, beta-blockers, and statins should be encouraged.
 ...
PMID:Multiple risk factor intervention in chronic kidney disease: management of cardiac disease in chronic kidney disease patients. 1575 65

Cardiovascular disease has been well documented in patients with Human Immunodeficiency Virus infection, especially after the introduction of highly active antiretroviral therapy. At present, HIV infection is one of the leading causes of acquired cardiovascular disease including heart failure. Some of the changes observed in these patients include left ventricular systolic dysfunction, dilated cardiomyopathy, congestive heart failure, myocarditis, lipodystrophy, dyslipidemia, insulin resistance, accelerated atherosclerosis including myocardial infarction, prothrombotic state, pericardial effusion, pulmonary hypertension, autonomic dysfunction, and malignancy. This article summarizes the main findings in the principal HIV-associated cardiovascular manifestations in order to stimulate its early recognition so helping in early intervention and therapy.
 ...
PMID:Cardiovascular disease in HIV infection. 1720 95

Four patients with chronically well-compensated, non-ischemic dilated cardiomyopathy (NIDC) presented with occlusive atherosclerotic coronary artery disease as the cause of subacute decompensation (FC III-IV heart failure) 8-13 years following the diagnosis of NIDC. In addition to the atherogenic condition of heart failure, 3 of the patients acquired major atherosclerotic risk factors (dyslipidemia, diabetes mellitus) during the interval between the diagnoses of NIDC and problematic atherosclerotic coronary disease. For each patient, dyspnea on exertion was the primary symptom during the subacute decompensation. Only 1 patient noted precordial chest pain in the form of atypical angina during some of the dyspneic events. The diagnosis of occlusive coronary artery disease was made by coronary angiography, followed by angioplasty-stent deployment in 3 patients and coronary artery bypass surgery in 1; all improved to their baseline FC I-II status following these coronary interventions. As survival of patients with NIDC increases, occlusive coronary artery disease may enter an otherwise stable clinical course to provoke unanticipated decompensation (principally dyspnea), and can do so without causing angina pectoris as a heralding symptom.
 ...
PMID:Latent development of occlusive coronary atherosclerosis as a cause of decompensation of non-ischemic dilated cardiomyopathy. 1858 63

Human immunodeficiency virus (HIV) is now a pandemic. It afflicts multiple organs, including the cardiovascular system. This occurs by direct invasion as well as opportunistic infections complicating acquired immunodeficiency syndrome. The presence of newer highly active antiretroviral therapy has led to longer survival of patients infected with HIV, but the cardiac abnormalities related to HIV have remained less well characterized. It is now evident that cardiac involvement in patients with acquired immunodeficiency syndrome is relatively common. This includes coronary artery disease, dilated cardiomyopathy, pericardial effusion, pulmonary hypertension, and ill effects of highly active antiretroviral therapy in the form of lipodystrophy, lipoatrophy, and dyslipidemia. In fact, HIV can now be viewed as a potential risk factor for coronary artery disease, and the dilemma facing clinicians is how to quantify this risk. Awareness of accelerated coronary artery disease and dilated cardiomyopathy is critical to implement preventive measures early in the course of HIV. However, better guidelines are still needed on the basis of prospective randomized controlled studies involving large populations. In conclusion, this review describes cardiac abnormalities associated with HIV, including possible molecular mechanisms. The co-morbid sequelae, their presentation, and pharmacologic management are also discussed.
 ...
PMID:Cardiovascular manifestations in human immunodeficiency virus-infected patients. 1912 56

Lipodystrophy is a rare disorder characterized by loss of adipose tissue and low leptin levels. This condition is characterized by severe dyslipidemia, insulin resistance, diabetes mellitus, and steatohepatitis. Another phenotypic feature that occurs with considerable frequency in generalized lipodystrophy is cardiomyopathy. We report here the cardiac findings in a cohort of patients with generalized congenital and acquired lipodystrophy, and present a literature review of the cardiac findings in patients with generalized lipodystrophy. We studied 44 patients with generalized congenital and acquired lipodystrophy, most of them enrolled in a clinical trial of leptin therapy. Patients underwent electrocardiograms and transthoracic echocardiograms to evaluate their cardiac status. We followed these patients for an extended time period, some of them up to 8 years. Evaluation of our cohort of patients with generalized lipodystrophy shows that cardiomyopathy is a frequent finding in this population. Most of our patients had hypertrophic cardiomyopathy, and only a small number had features of dilated cardiomyopathy. Hypertrophic cardiomyopathy was more frequent in patients with seipin mutation, a finding consistent with the literature. The underlying mechanism for cardiomyopathy in lipodystrophy is not clear. Extreme insulin resistance and the possibility of a "lipotoxic cardiomyopathy" should be entertained as possible explanations.
 ...
PMID:Cardiomyopathy in congenital and acquired generalized lipodystrophy: a clinical assessment. 2061 64


1 2 Next >>