Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007222 (cardiovascular disease)
 65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adolescents and young adults meeting DSM-III criteria for anorexia nervosa (n = 13) and atypical eating disorders (n = 7) were compared with weight-recovered anorectics (n = 6) and normal weight controls (n = 11) using a type-A structured interview and a computerized stress procedure. Heart rate, blood pressure, and electrocardiographic changes were monitored. Anorexia nervosa subjects demonstrated significantly more type-A characteristics than controls. The emaciated and weight-recovered anorectics had elevated hostility scores on the type-A interview, which has been shown in recent studies of type-A behavior to be a risk factor for cardiovascular disease. This pilot study is the first to demonstrate a significant relationship between anorexia and the type-A behavioral pattern. Also the anorectic subjects showed significantly more cardiovascular reactivity than controls as measured by failure of stressed anorectic subjects to lower their systolic blood pressure to baseline levels as controls did. These results support the importance of monitoring stress reactions and personality traits as well as traditional biological measures.
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PMID:A controlled study of type A behavior and psychophysiologic responses to stress in anorexia nervosa. 261 89

Increasing recognition of the importance of calcium in the pathogenesis of cardiovascular disease has stimulated research into the use of calcium channel blocking agents for treatment of a variety of cardiovascular diseases. The favorable efficacy and tolerability profiles of these agents make them attractive therapeutic modalities. Clinical applications of calcium channel blockers parallel their tissue selectivity. In contrast to verapamil and diltiazem, which are roughly equipotent in their actions on the heart and vascular smooth muscle, the dihydropyridine calcium channel blockers are a group of potent peripheral vasodilator agents that exert minimal electrophysiologic effects on cardiac nodal or conduction tissue. As the first dihydropyridine available for use in the United States, nifedipine controls angina and hypertension with minimal depression of cardiac function. Additional members of this group of calcium channel blockers have been studied for a variety of indications for which they may offer advantages over current therapy. Once or twice daily dosage possible with nitrendipine and nisoldipine offers a convenient administration schedule, which encourages patient compliance in long-term therapy of hypertension. The coronary vasodilating properties of nisoldipine have led to the investigation of this agent for use in angina. Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke. In general, the dihydropyridine calcium channel blockers are usually well tolerated, with headache, facial flushing, palpitations, edema, nausea, anorexia, and dizziness being the more common adverse effects.
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PMID:Differential effects of 1,4-dihydropyridine calcium channel blockers: therapeutic implications. 332 59

Fifteen patients with the hypereosinophilic syndrome were studied during a period of 6.5 years. The mean age at onset was 36 years. Two were female. The commonest presenting symptoms were nocturnal sweating with or without severe coughing attacks, symptoms of cardiovascular disease, anorexia and weight loss, neurological and gastrointestinal symptoms and itching with or without skin lesions. The mean blood eosinophil counts at presentation were 20.1 X 10(9)/l. Eight patients had previous allergic or parasitic disease which could have predisposed them to the development of hypereosinophilia. Eight patients had raised serum immunoglobulin levels: IgM in five, IgE in four and IgG in one. Five of nine patients had raised serum eosinophil cationic protein levels. Episodes of clinical relapse occurred with increased white blood counts and were treated with prednisolone and cytotoxic drugs. Thrombotic and embolic complications developed in 10 patients, despite treatment with anticoagulants and inhibitors of platelet function, and were the cause of death in three. Two patients with severe endomyocardial fibrosis responded well to cardiac surgery, and a third required emergency mitral valve replacement. The 12 surviving patients have lived 0.8-11.5 years (mean 4.4), since the onset of their illness. It is concluded that the hypereosinophilic syndrome has distinctive features with an episodic course. The principal complications affect the cardiovascular system, especially endomyocardial fibrosis and thromboembolic occlusion of large and small blood vessels in many organs. Although treatment is usually effective in overcoming relapses, the underlying disease process appears to be unaffected. Despite this, patients can have prolonged periods of remission and may survive for many years.
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PMID:Clinical features of fifteen patients with the hypereosinophilic syndrome. 687 18

Malnutrition and hypoalbuminemia, which are prevalent in patients with end-stage renal disease (ESRD), are strong predictors of increased mortality. However, cardiovascular disease predominates among direct causes of death, whereas malnutrition appears to be of minor importance in this respect. Reports in the literature demonstrate that cardiac failure may cause malnutrition and that infection/inflammation may predispose to atherosclerosis as well as to catabolism and hypoalbuminemia. Proinflammatory cytokines, generated in response to cardiac failure, infection, and other inflammatory stimuli, appear to play a pivotal role by causing muscle wasting, hypoalbuminemia, and anorexia as well as reduced cardiac contractility and atherosclerotic vascular disease. We hypothesize that this scenario also applies to ESRD patients, in whom congestion, hypertension, cardiac failure, and ischemic cardiovascular disease are common. Malnutrition rarely may be the direct cause of death, except in elderly dialysis patients, but may contribute to a poor prognosis by aggravating pre-existing heart failure and increasing the susceptibility to infections.
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PMID:Malnutrition, cardiac disease, and mortality: an integrated point of view. 982 Apr 57

Malnutrition, inflammation and atherosclerotic cardiovascular disease occur at high prevalence, and often concomitantly, in conjunction with chronic renal failure. Several features of malnutrition (e.g., increased oxidative stress, increased plasma levels of fibrinogen, Lp(a), and inflammation) may all, alone or in concert, increase the risk of cardiovascular disease. Recent findings suggest malnutrition and hypoalbuminaemia in chronic renal failure to be largely the consequence of such factors as heart failure, chronic infection and inflammation, that simultaneously trigger the development of atherosclerotic cardiovascular disease. Central to this scenario is the involvement of proinflammatory cytokines which may cause muscle wasting, hypoalbuminaemia, anorexia, and accelerated atherosclerosis. It is unlikely that the high mortality due to atherosclerotic disease among patients with chronic renal failure can be substantially reduced unless new treatment strategies are developed which address the complex relationships that exist between malnutrition, inflammation and cardiovascular disease.
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PMID:[Strong connection between malnutrition, inflammation and arteriosclerosis. Improved treatment of renal failure if underlying factors are attacked]. 1057 60

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Anorectic drugs are widely used for the treatment of obesity. They are thought to decrease appetite through their effects on catecholamine or 5-hydroxytryptamine (5-HT) levels in the brain. Their use has been associated with epidemics of pulmonary hypertension and the development of valvular heart disease, hypertension, stroke and digital or mesenteric ischemia. Understanding the mechanism of the cardiovascular toxicity of anorectic drugs is important because of the modern epidemic of obesity and the resulting plethora of new anorexigens, many of which share similar mechanisms with those that have previously caused cardiovascular disease. In addition, the mechanism by which anorexigens cause vascular disease has relevance to the etiology and treatment of pulmonary and systemic hypertension. Recent discoveries have clarified how the anorexigens cause vasoconstriction and hypertension. Most anorexigens directly inhibit voltage-gated K+ (KV) channels in vascular smooth muscle cells (SMCs). This reduced K+ efflux leads to depolarization, the opening of voltage-sensitive Ca2+ channels, an increase in intracellular Ca2+ and vasoconstriction. Endothelial dysfunction appears to be a predisposing factor for the development of anorectic-induced vascular complications. Vasoconstriction is weak at clinically relevant doses of anorectic drugs. However, when nitric oxide synthase is inhibited, vasoconstriction is significantly enhanced. Anorexigens are the only drugs in widespread clinical use that have KV-channel-blocking properties and it is probable that much of their cardiovascular toxicity relates to this mechanism. Investigators need to examine new anorexigens and other therapeutic molecules for inhibitory effects on KV channels, as this effect may be a marker of drugs that will elicit vascular complications.
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PMID:Anorectic drugs and vascular disease: the role of voltage-gated K+ channels. 1237 23

Serum albumin, transferrin, and prealbumin levels decrease as glomerular filtration rate (GFR) declines, even prior to the start of dialysis. The levels of these serum proteins are also associated with creatinine levels and lean body mass. Lean body mass also decreases with advancing renal failure. While all of these measures are regarded as reflections of nutritional status, each are strongly associated with any of several indicators of inflammation: positive acute-phase proteins or the cytokines that regulate their synthesis rate, in both longitudinal and cross-sectional studies. Inflammation in turn is associated with comorbid conditions, cardiovascular disease, chronic infections, age, and vascular access type. Additionally, dialysis patients are subjected to oxidative stress and exposure of blood to foreign antigens in the dialysis process that also potentially contribute to inflammation. In otherwise healthy individuals reduced protein and calorie intake does not cause hypoalbuminemia since albumin fractional catabolic rate (FCR) and resting energy expenditure (REE) normally decrease in response. The simultaneous occurrence of decreased protein intake and inflammation prevent these homeostatic compensations to reduced nitrogen and energy intake from occurring, resulting in decreasing albumin, transferrin, and prealbumin levels and loss of muscle mass. Nutritional intake may also be challenged as a result of renal failure associated with anorexia, gastroparesis, and socioeconomic factors, which may all cause nutritional intake to be sufficiently marginal so that the combined effects of inflammation and decrease protein intake are expressed as decreased visceral and somatic protein stores.
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PMID:Serum albumin concentration in dialysis patients: why does it remain resistant to therapy? 1453 80

The process whereby a stimulus or stress at a critical or sensitive period of development has long-term effects is termed "programming." Studies in humans and animals convincingly demonstrate that environmental perturbations in utero may permanently change organ structure and metabolism and/or alter homeostatic regulatory mechanisms among the offspring. These programmed changes may be the origins of adult diseases, including cardiovascular disease, obesity, and diabetes. Throughout evolution and development, humans and animals have been exposed to two common environmental stresses, drought and famine. Notably, drought-induced water deprivation is associated with dehydration anorexia and thus a concomitant potential nutrient stress. Our laboratory has performed studies among pregnant rat and sheep in which we simulate drought conditions via maternal dehydration and famine conditions via nutrient restriction. Maternal dehydration results in low-birth-weight offspring, which demonstrate gender-specific plasma hypernatremia and hypertonicity and arterial hypertension. Gestational nutrient restriction also resulted in low-birth-weight offspring. If permitted rapid catch-up growth by nutrient availability, these offspring demonstrate evidence of increased body weight and body fat, and leptin resistance as adults. Conversely, if the catch-up growth is delayed by nutrition restriction, the offspring exhibit normal body weight, body fat, and plasma leptin levels as adults. These studies indicate that osmoregulatory and cardiovascular homeostasis and phenotypic predisposition to obesity may be programmed in utero. Importantly, these results suggest that programming effects may be either potentiated or prevented by interventions during the neonatal period.
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PMID:Gestational programming: population survival effects of drought and famine during pregnancy. 1559 Sep 94

Calcium (Ca) overload by Ca-containing phosphorus (P) binder has been suggested to be implicated in the pathogenesis of soft tissue and vascular calcification, which contribute to increased morbidity and mortality of cardiovascular disease in patients undergoing dialysis. Recently, a noncalcium P binder, sevelamer hydrochloride (sevelamer), has become available in Japan. However, Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment, and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients. We evaluated the effects of combination therapy with sevelamer and calcium carbonate (CC) on mineral metabolism in Japanese hemodialysis patients, as an alternative form of P management. A total of 210 hemodialysis patients were enrolled, and were given a small dose of sevelamer (0.75-1.5 g/day) on CC treatment. Sevelamer dose was gradually increased, while CC decreased during 24 weeks. Five patients discontinued sevelamer treatment because of severe constipation, anorexia, and parathyroidectomy for severe secondary hyperparathyroidism. After 24 weeks, the dose of sevelamer was significantly increased to 3.29 g/day (initial dose: 1.47 g/day), while CC was decreased by 54%. Adjusted serum Ca significantly decreased (9.63 +/- 0.57-9.45 +/- 0.67 mg/dL; P = 0.0012), although serum P increased (5.89 +/- 1.32-6.25 +/- 1.32 mg/dL; P = 0.017). Serum intact PTH (iPTH) significantly increased in patients with a low or normal iPTH level (< or =300 pg/mL), while it did not change in patients with secondary hyperparathyroidism (>300 pg/mL). The results suggest that the therapeutic regimen is more tolerant and reduces Ca load in Japanese hemodialysis patients while avoiding hypocalcemia. In addition, the mitigated Ca overload could improve PTH hyposecretion in patients with adynamic bone disease, which is associated with soft tissue calcification and higher mortality in uremia.
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PMID:Combination therapy with sevelamer hydrochloride and calcium carbonate in Japanese patients with long-term hemodialysis: alternative approach for optimal mineral management. 1582


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