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

Carnitine is an endogenous cofactor involved in the transport of long-chain fatty acids into the mitochondria where they undergo beta-oxidation. Through another reaction, carnitine produces free coenzyme A and reduces the ratio of acetyl-coenzyme A to coenzyme A, thereby enhancing oxidative use of glucose, augmenting adenosine triphosphate synthesis, and reducing lactate production and acidosis. Because of its regulatory action on the energy flow from the different oxidative sources, especially under ischemic conditions, carnitine has been used in cardiovascular diseases such as coronary heart disease, congestive heart failure, peripheral vascular disease, dyslipidemia, diabetes, and chronic renal diseases with satisfactory results. A flap is also a relatively ischemic tissue and may obtain benefit from carnitine. To investigate this, 30 rats were divided into three groups of 10 animals: a control group and two carnitine-treated groups. Random dorsal skin flaps were elevated on the rats. In the control group, no pharmacologic agents were used. Of the two treated groups, group 1 was treated with 50 mg/kg/day carnitine for 1 week and group 2 was treated with 100 mg/kg/day carnitine for 1 week. The areas of flap necrosis were measured in each group. The median areas of flap necrosis of the groups were 12.55, 9.23, and 4.9 cm2, respectively. There was a statistically significant improvement of flap necrosis in carnitine-treated groups compared with the control group (group 2, p = 0.001; group 3, p = 0.000). Furthermore, there was less necrosis in the high-dose carnitine-treated group than the low-dose carnitine-treated group. As a conclusion, carnitine may have a dose-dependent effect to increase flap survival in random skin flaps.
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PMID:The effect of carnitine on random-pattern flap survival in rats. 1154 53

Obesity has been shown to be an independent risk factor for coronary heart disease. The insulin resistance associated with obesity contributes to the development of other cardiovascular risk factors, including dyslipidemia, hypertension, and type 2 diabetes. The coexistence of hypertension and diabetes increases the risk for macrovascular and microvascular complications, thus predisposing patients to cardiac death, congestive heart failure, coronary heart disease, cerebral and peripheral vascular diseases, nephropathy, and retinopathy. Body weight reduction increases insulin sensitivity and improves both blood glucose and blood pressure control. Metformin therapy also improves insulin sensitivity and has been associated with decreases in cardiovascular events in obese diabetic patients. Antihypertensive treatment in diabetics decreases cardiovascular mortality and slows the decline in glomerular function. However, pharmacological treatment should take into account the effects of the antihypertensive agents on insulin sensitivity and lipid profile. Diuretics and beta-blockers are reported to reduce insulin sensitivity and increase triglyceride levels, whereas calcium channel blockers are metabolically neutral and ACE inhibitors increase insulin sensitivity. For the high-risk hypertensive diabetic patients, ACE inhibition has proven to confer additional renal and vascular protection. Because hypertension and glycemic control are very important determinants of cardiovascular outcome in obese diabetic hypertensive patients, weight reduction, physical exercise, and a combination of antihypertensive and insulin sensitizers agents are strongly recommended to achieve target blood pressure and glucose levels.
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PMID:Treatment of obesity hypertension and diabetes syndrome. 1156 61

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.
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PMID:Diabetic Cardiomyopathy. 1169 68

We identified predictors of prognosis among n = 2,677 health maintenance organization enrollees 30 to 79 years old who survived a first hospitalized myocardial infarction (MI) during 1986-1996 (mean follow-up 3.4 years). Independent risk factors for reinfarction/fatal coronary heart disease (CHD) (incidence = 49.0/1,000 person-years, 445 events) were age, diabetes, chronic congestive heart failure (CHF), angina, high body mass index (BMI), low diastolic blood pressure (DBP), high serum creatinine, and low/high-density lipoprotein (HDL) cholesterol. Independent risk factors for stroke (incidence = 13.0/1,000 person-years, 124 events) were age, diabetes, CHF, high DBP, and high creatinine. Independent predictors of death (incidence = 44.2/1,000 person-years, 431 events) were age, diabetes, CHF, continued smoking after MI, low DBP, high pulse rate, high creatinine, and low HDL cholesterol, while BMI had a significant U-shaped association with death (elevated risk at low and high BMI). The occurrence of study end points did not differ significantly between men and women after adjustment for other risk factors and use of preventive medical therapies, although men tended to have higher rates of reinfarction/CHD than women among older subjects. In summary, we demonstrated that the major cardiovascular risk factors age, diabetes, CHF, smoking, and dyslipidemia are important prognostic factors in the years after nonfatal MI. Elevated BMI was associated with increased risk of reinfarction/CHD and death and elevated DBP with increased risk of stroke, but we also observed high mortality among those with low BMI and high risk of recurrent coronary disease and death among those with low DBP. Finally, high creatinine was a strong, independent predictor of a variety of adverse outcomes after first MI.
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PMID:Predictors of subsequent coronary events, stroke, and death among survivors of first hospitalized myocardial infarction. 1216 Sep 13

Cardiovascular complications are frequently encountered in the HIV-infected population. Cardiac care providers should implement appropriate preventive, screening, and therapeutic strategies to maximize survival and quality of life in this increasingly treatable, chronic disease. All HIV-infected individuals should undergo periodic cardiac evaluation, including echocardiography, in order to identify subclinical cardiac dysfunction. Left ventricular (LV) dysfunction can result from, or be exacerbated by, a variety of treatable infectious, endocrine, nutritional, and immunologic disorders. Aggressive diagnosis and treatment of these conditions may lead to improvement or even normalization of myocardial function. Endomyocardial biopsy should be considered to direct etiology-specific therapy. Standard measures for the prevention and treatment of congestive heart failure are recommended for HIV-infected patients. Afterload reduction with angiotensin-converting enzyme inhibitors may be indicated for patients with elevated afterload and preclinical LV dysfunction diagnosed by echocardiogram. However, judicious drug selection and titration are necessary in this cohort of patients with frequent autonomic dysfunction, at risk for a number of potentially lethal drug interactions. Carnitine, selenium, and multivitamin supplementation should be considered, especially in those with wasting or diarrhea syndromes. Monthly intravenous immunoglobulin (IVIG) infusions have been demonstrated to preserve LV parameters in HIV-infected children; ventricular recovery has been documented in some children with recalcitrant HIV-related cardiomyopathy following IVIG infusion. We support the use of immunomodulatory therapy in the pediatric population, and look forward to further study into the efficacy and broader application of this approach. Highly active antiretroviral therapy (HAART) may be associated with dyslipidemia and the metabolic syndrome. This should be treated with dietary and possibly with pharmacologic interventions. Drug interactions need to be considered when instituting pharmacologic therapies. Pericardial effusions are often seen in patients with advanced HIV infection. Asymptomatic effusions are most often nonspecific in nature, related to the proinflammatory milieu found in advanced AIDS. Nonspecific effusions are a marker of advanced disease and do not require exhaustive etiologic evaluation. In contrast, large or symptomatic effusions are often associated with infection or malignancy, and warrant thorough investigation and etiology-specific treatment.
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PMID:Myocardial and Pericardial Disease in HIV. 1240 91

The prevalence of marked obesity is increasing rapidly among adults and has more than doubled in 10 years. Sixty-one percent of the adult population of the United States is overweight or obese. Americans are the fattest people on earth. Paradoxically these increases in the numbers of persons who are obese or overweight have occurred during recent years when Americans have been preoccupied with numerous dietary programs, diet products, weight control, health clubs, home exercise equipment, and physical fitness videos, each "guaranteed" to bring rapid results. Overweight and obesity are also world problems. The World Health Organization estimates that 1 billion people around the world are now overweight or obese. Westernization of diets has been part of the problem. Fruits, vegetables, and whole grains are being replaced by readily accessible foods high in saturated fat, sugar, and refined carbohydrates. Since class 3 obesity (morbid or extreme obesity) is associated with the most severe health complications, the incidence of hypertension, stroke, heart disease, diabetes, and peripheral vascular disease will increase substantially in the future. Recently, obesity alone has been implicated in the development of cardiac hypertrophy and CHF. The metabolic syndrome associated with abdominal obesity, which includes insulin resistance, dyslipidemia, and elevated CRP levels, identifies subjects who have an increase in cardiovascular morbidity and mortality. Twenty to 25% of the adult population in the United States have the metabolic syndrome, and in some older groups this prevalence approaches 50%. The prevalence of overweight children in the United States has also been increasing dramatically, especially among non-Hispanic blacks and Mexican-American adolescents. Overweight children usually become overweight adults. Atherosclerosis begins in childhood. The degree of atherosclerotic changes in children and young adults can be correlated with the presence of the same risk factors seen in adults. As health providers, our direction is obvious!
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PMID:Obesity and the metabolic syndrome. 1262 76

In this review paper, the classical and more recently described mechanisms responsible for the structural and functional characteristics of large artery rigidity are described. Mostly important, these characteristics appear to be non-specific to the primary disease process involved in arterial hypertension, diabetes mellitus, dyslipidemia, congestive heart failure, chronic uremia, and perhaps senescence, including vascular dementia. Nonspecific in terms of aetiology, the vasculopathy encountered in these diseases exhibits common structural and functional abnormalities. The identification of such abnormalities could well become the target of potent nonpharmacological and (or) pharmacological interventions capable of preventing or retarding morbidity and mortality. The structural characteristics responsible for large artery rigidity include smooth muscle cell hypertrophy, matrix collagen deposition, and recently described, dysfunction in proteoglycan metabolism. Functional abnormalities, such as bradykinin-dependent hyper-reactivity of smooth muscle cells and vasa vasorum microcirculation network disturbances, also appear to alter aortic wall rigidity. The physiopathology of target organ damage is then revisited, based on endothelial dysfunction, documented in large and resistance arteries, as well as in microcirculation networks, where altered permeability to macromolecules leads to interstitial matrix disorganization and cell damage. The clinical evaluation of large artery rigidity is described, and one of the noninvasive methods, evaluation of pulse-wave velocity, is validated in normal conditions and in disease processes. Finally, non-pharmacological and pharmacological therapeutic measures are presented, and includes physical exercise to reduce insulin resistance, and renin-angiotensin-II-aldosterone modulators.
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PMID:Mechanisms and consequences of large artery rigidity. 1273 19

Obstructive sleep apnea (OSA) is a common disorder associated with an increased risk of cardiovascular disease and stroke. As it is strongly associated with known cardiovascular risk factors, including obesity, insulin resistance, and dyslipidemia, OSA is an independent risk factor for hypertension and has also been implicated in the pathogenesis of congestive cardiac failure, pulmonary hypertension, arrhythmias, and atherosclerosis. Obesity is strongly linked to an increased risk of OSA, and weight loss can reduce the severity of OSA. The current standard treatment for OSA-nasal continuous positive airway pressure (CPAP)-eliminates apnea and the ensuing acute hemodynamic changes during sleep. Long-term CPAP treatment studies have shown a reduction in nocturnal cardiac ischemic episodes and improvements in daytime blood pressure levels and left ventricular function. Despite the availability of effective therapy, OSA remains an underdiagnosed and undertreated condition. A lack of physician awareness is one of the primary reasons for this deficit in diagnosis and treatment.
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PMID:Obstructive sleep apnea and cardiovascular disease. 1274 77

Both type 1 and type 2 diabetic patients have an increased incidence of ischemic heart disease and congestive heart failure. Cardiovascular disease accounts for up to 80% of the excess mortality in patients with type 2 diabetes. The burden of cardiovascular disease is especially pronounced in diabetic women. Factors that underlie diabetic heart disease include multiple vessel coronary artery disease, long-standing hypertension, metabolic derangements such as hyperglycemia and dyslipidemia, microvascular disease, and autonomic neuropathy. There is also increased sudden death associated with diabetes, which is due, in part, to the underlying autonomic neuropathy. This article reviews diabetic cardiac disease, with an emphasis on type 2 diabetes.
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PMID:Heart disease in diabetic patients. 1276 70

Diabetes mellitus is a risk factor for congestive heart failure. Diabetics with congestive heart failure should have good glycemic control, treatment of hypertension and dyslipidemia, and treatment with diuretics, angiotensin-converting enzyme inhibitors, and beta blockers as well as digoxin, if the left ventricular ejection fraction is abnormal. Patients with chronic obstructive pulmonary disease may have left ventricular failure because of a coexistent cardiac disorder or right ventricular failure from pulmonary hypertension. An acute respiratory tract infection may precipitate right ventricular failure and should be treated. Alveolar hypoxia should be corrected by improving alveolar ventilation through relieving airflow obstruction with bronchodilators and by increasing inspired oxygen concentration. Loop diuretics should be used cautiously. Beta blockers may be given to patients with chronic obstructive pulmonary disease and left ventricular failure if bronchospasm is not present. Angiotensin-converting enzyme inhibitors should be used to treat left ventricular failure. Digitalis should not be used in patients with right ventricular failure due to chronic obstructive pulmonary disease. Nonsteroidal anti-inflammatory drugs are contraindicated in patients with congestive heart failure. There are controversial data about the negative interaction between aspirin and angiotensin-converting enzyme inhibitors in patients with congestive heart failure. Patients with arthritis and congestive heart failure needing large doses of aspirin for pain relief may be treated instead with acetaminophen, tramadol, or Percocet if necessary for chronic severe pain.
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PMID:Treatment of heart failure in older persons. Dilemmas with coexisting conditions: diabetes mellitus, chronic obstructive pulmonary disease, and arthritis. 1282 72


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