Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin B12 deficiency damages nerve cells and aggravates nervous system disorders even in the absence of evidence of anaemia. Prevalence of B12 deficiency increases with age especially over 65 and is frequently associated with Alzheimer's disease. Recent American surveys record a higher prevalence of B12 deficiency and of undiagnosed and untreated pernicious anaemia in the elderly than reported earlier. B12 deficiency is also reported to be a risk factor for heart disease, stroke and accelerated ageing.
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PMID:The danger of B12 deficiency in the elderly. 983 1

Prior to 1972, the increased cardiovascular morbidity and mortality that diabetics endure had been attributed to vascular disease. In 1972, Rubler et al. proposed the existence of a diabetic cardiomyopathy based on their expereince with four adult diabetic patients who suffered from congestive heart failure (CHF) in the absence of discernable coronary artery disease, valvular or congenital heart disease, hypertension, or alcoholism. Alternative explanations for CHF, such as anemia and vascular and renal disease in these four patients, gave rise to criticisms, but a wave of subsequent studies in the 1970s and 1980s provided credence to this new disease entity. This review of the studies done since 1972 appears to support the concept of a diabetic cardiomyopathy independent of atherosclerotic cardiovascular disease. The exact mechanism is still questionable, and several mechanisms have been proposed including small and microvascular disease, autonomic dysfunction, metabolic derangements, and interstitial fibrosis. However, the weight of evidence leans toward the development of fibrosis, possibly caused by the accumulation of a peroxidase acid schiff (PAS)-positive glycoprotein, leading to myocardial hypertrophy and diastolic dysfunction.
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PMID:Diabetic cardiomyopathy. 985 79

The target organ failures associated with uremia are most often considered to be caused by processes other than uremia per se. Heart disease, for example, is considered the product of hypertension, lipid abnormalities, and so forth, rather then the uremic state. Erythropoietin deficiency, blood loss, and iron deficiency are believed to cause anemia, rather than the uremic state. Malnutrition is believed to be the product of poor nutrient intake and perhaps nutrient losses, rather than uremia per se. This article reviews evidence suggesting that anemia and malnutrition share a common cause; the acute-phase inflammatory process that is a normal host-defense mechanism. Given the high prevalence of heart disease among patients with end-stage renal disease (ESRD), data indicating activation of the acute-phase process in patients with kidney failure, and emerging evidence that the process has a significant role in the risk for cardiovascular disease among patients without kidney failure, there is a strong likelihood that heart disease will share with anemia and malnutrition the acute-phase state as a contributing cause. Thus, instead of disconnected target organ failures, each with different antecedent causes, we see emerging the likelihood of a unifying pathobiology for uremia. The antecedents of morbidity and mortality appear as a web of organ failures connected by a common pathobiology. Whereas each failure likely has contributing causes other than the acute-phase state, they probably share the state as a causative, contributing, or exacerbating factor.
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PMID:Acute-phase inflammatory process contributes to malnutrition, anemia, and possibly other abnormalities in dialysis patients. 989 76

Dyspnea is a frequent and devastating symptom among advanced cancer patients and is often difficult to control. However, there has been considerably less emphasis in the literature on the appropriate characterization and management of this symptom than of other cancer-related symptoms. The purpose of this paper is to review issues relating to the prevalence, causes, prognosis and treatment of dyspnea in patients with advanced cancer. A Medline search of the literature published from 1966 to February 1999 was conducted. Dyspnea occurs in 21-78.6% of advanced cancer patients and is reported to be from moderate to severe in 10-63% of the patients. The frequency and severity of dyspnea increase with the progression of the disease and/ or when death is approaching. Lung cancer patients with dyspnea have shorter survival than patients with other types of cancer. Dyspnea can be a direct effect of the cancer, an effect of therapy or not related to the cancer or therapy. In addition to cancer, patients may suffer from chronic obstructive pulmonary disease, congestive heart failure, nonmalignant pleural effusion, pneumonitis, air flow obstruction, or bronchospasm associated with asthma. In the absence of lung or heart disease, dyspnea may be a clinical expression of the syndrome of overwhelming cachexia and asthenia or of severe asthenia. Many different causes may co-exist in a patient. Whenever possible, an attempt should be made to treat underlying cancer. Radiotherapy and chemotherapy may relieve dyspnea also in patients who fail to achieve a major objective response. Symptomatic measures in addition to specific treatments for the underlying cancer and/or other pulmonary and cardiovascular diseases are indicated. Oxygen therapy has proved effective in hypoxemic and nonhypoxemic patients. The role of transfusion therapy to relieve anemia-related dyspnea in advanced and terminal cancer patients is still controversial. Oral, subcutaneous and intravenous opioids are effective but underused in these patients, whereas currently available evidence does not support the clinical use of nebulized opioids. While benzodiazepines are frequently used in patients with dyspnea, these drugs were ineffective in four out of five randomized controlled trials. Other components of the symptom expression are better managed by supportive counseling, occupational therapy or physiotherapy. While the mechanism of breathing and the consequences of different pathologic conditions for both respiratory function and gas exchange are well known, the genesis and pathophysiology of dyspnea as a symptom are much less well understood. Palliative care assessment should be focused on dyspnea as a symptom rather than on the functional and gas exchange abnormalities. Increased research on the appropriate management of dyspnea is needed.
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PMID:Management of dyspnea in advanced cancer patients. 1042 43

The target hematocrit to be achieved when treating anemia in hemodialysis patients with erythropoietin is controversial. Current evidence-based recommendations suggest a target hematocrit range of 33% to 36%. Small studies suggest that normalization of hematocrit with erythropoietin may benefit hemodialysis patients in terms of brain function, physical performance, quality of life, and prevention of progressive left ventricular dilatation. However a recent study of the effects of erythropoietin-induced normalization of hematocrit in hemodialysis patients with symptomatic heart disease has shown an increase in both mortality and the rate of vascular access thrombosis. Currently, normalization of hematocrit in patients with symptomatic heart disease is not recommended, nor is it possible to conclude that possible benefits of normalization of hematocrit will outweigh risks in hemodialysis patients without symptomatic heart disease.
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PMID:Erythropoietin therapy in chronic uremia: the impact of normalization of hematocrit. 1054 Dec 20

The long-term consequences of cardiac alterations in children with chronic renal failure (CRF) and after renal transplantation (TX) are largely unknown. Studies in adults with end-stage renal disease (ESRD) assume that the fate of many pediatric patients is determined by a high cardiovascular morbidity and mortality. This review describes clinical manifestations, pathophysiology, cardiac function and structure, and management of heart disease in children with CRF and post transplant. Echocardiography and Doppler ultrasonography allow differentiation of three functional disturbances: hypercirculation, systolic left ventricular (LV) dysfunction, and diastolic LV dysfunction, in addition to analysis of LV size and myocardial mass. From adult studies LV hypertrophy is recognized as an early prognostic marker of cardiovascular disease. It is present in about half of children with ESRD and after TX. It may regress, at least in part, by control of hypertension, hypervolemia, and anemia. Experimental studies have shown that, independent of these hemodynamic complications, uremia is associated with structural abnormalities of the heart, which were also described in adult patients with ESRD. These lesions consist mainly of hypertrophy of cardiomyocytes, interstitial fibrosis, and vascular changes (rarefied capillaries, thickened arteriolar walls). Cardiac complications in children with CRF and after TX deserve regular clinical and echocardiographic monitoring in order to minimize later cardiovascular morbidity by appropriate treatment.
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PMID:Cardiac function and structure in patients with chronic renal failure. 1060 58

Target hematocrit/hemoglobin values in dialysis patients are still controversial. The Spanish Cooperative Renal Patients Quality of Life Study Group (including 34 hemodialysis units) conducted a prospective, 6-mo study of the effect on patient functional status and quality of life of using epoetin to achieve normal hematocrit in hemodialysis patients with anemia. The possible adverse effects of increased hematocrit, patient hospitalization, and epoetin requirements were also studied. The study included 156 patients (age range, 18 to 65 yr). Given the minimal experience in the safety of increasing hematocrit in dialysis patients to normal levels with epoetin, stable patients on hemodialysis who had received epoetin treatment for at least 3 mo and had a stable hemoglobin level of > or = 9 g/dl were included in the study. Patients with antecedents of congestive cardiac failure, ischemic cardiopathy, diabetes mellitus, uncontrolled hypertension, cerebrovascular accident or seizures, malfunction of the vascular access or severe comorbidity (defined by a comorbidity index), and those over 65 yr of age were excluded from the study. Quality of life was measured with the Sickness Impact Profile (SIP) and Karnofsky scale. Patients completed questionnaires at home at onset and conclusion of the 6-mo study. Mean hematocrit increased from 30.9 to 38.4% and hemoglobin from 10.2 to 12.5 g/dl during the study. Health indicator scores improved significantly: mean Physical Dimension (SIP) from 5.38 to 4.1 (P < 0.005); mean Psychosocial Dimension from 9.2 to 7 (P < 0.001); mean global SIP from 8.9 to 7.25 (P < 0.001); mean Karnofsky scale score from 75.6 to 78.4 (P < 0.01). (SIP is scaled so that lower scores represent better functional status, and vice versa for the Karnofsky scale). Therefore, functional status and quality of life improved with increased hematocrit. No deaths occurred. Three patients (2%) were censored for hypertension and nine (5.7%) for thrombosis of the vascular access. The cumulative probability of thrombosis of the vascular access was 0.067. The average epoetin dose rose from 93 +/- 62 U/kg per wk at onset to 141 +/- 80 U/kg per wk at conclusion, a 51% increase. The number of patients hospitalized decreased and hospital lengths of stay were shorter during the study period than in the same patients in the 6-mo period preceding the study (P < 0.05). Nine patients (5.7%) had thrombosis of the vascular access. There were no changes in the prevalence of arterial hypertension, but three patients (2%) showed hypertension that was difficult to control. It is concluded that normalization of hematocrit in selected hemodialysis patients, i.e., nondiabetic patients without severe cardiovascular or cerebrovascular comorbidities, improves quality of life and decreases morbidity without significant adverse effects.
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PMID:Increasing the hematocrit has a beneficial effect on quality of life and is safe in selected hemodialysis patients. Spanish Cooperative Renal Patients Quality of Life Study Group of the Spanish Society of Nephrology. 1066 41

Cardiovascular disease is a major cause of mortality and morbidity in patients with end-stage renal disease. Anemia, a result of erythropoietin deficiency, is associated with increased all-cause and cardiovascular mortality in this population, and predisposes patients to the development of symptomatic heart disease. Anemia is also associated with the development and progression of left ventricular echocardiographic disorders, which strongly predict cardiac failure and death. Left ventricular dilatation with compensatory hypertrophy, the major pattern of echocardiographic disease progression in hemodialysis patients, is a particularly strong predictor of late mortality. Partial correction of anemia with recombinant human erythropoietin likely reduces left ventricular mass and volume. Complete correction of anemia may prevent progressive left ventricular dilatation in patients with normal left ventricular volumes. A recent trial, however, reports excess mortality and vascular access loss in patients with preexisting symptomatic heart disease when anemia was completely corrected. Consequently, hematocrit target ranges above 32% to 36% cannot be recommended in this population. In patients without symptomatic heart disease, it is not possible to conclude that potential benefits derived from a normalized hematocrit will outweigh potential risks.
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PMID:The impact of anemia correction on cardiovascular disease in end-stage renal disease. 1092 37

The amount of oxygen delivered to an organ depends on three factors: blood flow and its distribution; the oxygen-carrying capacity of the blood, i.e. haemoglobin concentration; and oxygen extraction. Non-haemodynamic and haemodynamic mechanisms operate to compensate for anaemia. Non-haemodynamic mechanisms include increased erythropoietin production to stimulate erythropoiesis, and increased oxygen extraction (displacement of the haemoglobin oxygen dissociation curve). This decreased affinity of oxygen for haemoglobin is mediated by increased 2,3-diphosphoglycerate concentrations. Increased cardiac output is the main haemodynamic factor, mediated by lower afterload, increased preload, and positive inotropic and chronotropic effects. Decreased afterload is due to vasodilatation and reduced vascular resistance as a consequence of lower blood viscosity, hypoxia-induced vasodilatation, and enhanced nitric oxide activity. Vasodilatation also involves recruitment of microvessels and, in the case of chronic anaemia, stimulation of angiogenesis. With decreased afterload, the venous return (preload) and left ventricular (LV) filling increase, leading to increased LV end-diastolic volume and maintenance of a high stroke volume and high stroke work. High stroke work is also due to enhanced LV contractility attributed to increased concentrations of catecholamines and non-catecholamine inotropic factors. In addition, heart rate is increased in anaemia, due to hypoxia-stimulated chemoreceptors and increased sympathetic activity. In the long term, these haemodynamic alterations lead to gradual development of cardiac enlargement and LV hypertrophy (LVH). The LVH is eccentric, characterized by increased LV internal dimensions and a normal ratio of wall thickness to cavity diameter, as occurs in other forms of volume overload. When anaemia-related LVH develops in an otherwise 'healthy' humoral environment, the lesions are reversible and the type of LVH is primarily physiological and is not associated with impaired diastolic function. In the absence of underlying cardiovascular disorders, severe anaemia (Haemoglobin concentration < 4-5 g/dl) leads to congestive heart failure. In the presence of heart disease, especially coronary artery disease, anaemia intensifies angina and contributes to a high incidence of cardiovascular complications. In end-stage renal disease (ESRD), LVH is influenced by many other factors, leading to intense interstitial fibrosis, to alterations in diastolic function, and usually to poor reversibility. The chronic increase in cardiac output contributes to arterial remodelling of central elastic arteries such as the aorta and common carotid artery. This remodelling consists principally of arterial enlargement and compensatory arterial intima--media thickening. In ESRD, these geometric changes are accompanied by arterial stiffening. The principal consequences of arterial alterations are increased systolic pressure and high inertia due to higher blood mass in the dilated arterial system. These alterations contribute to the development of LVH and abnormal coronary perfusion.
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PMID:Pathophysiology of anaemia: focus on the heart and blood vessels. 1103 52

Blue rubber bleb nevus syndrome is characterized by gastrointestinal and cutaneous hemangiomas and gastrointestinal bleeding causing anemia. We report a unique case of this syndrome in an adult woman. It was associated with congenital heart disease, for which the patient underwent surgery at 12 months of age, and cutaneous hemangiomas, for which surgery was performed later in childhood. Gastrointestinal bleeding was diagnosed and treated when she was 21 years of age after a workup for iron deficiency anemia. Successful total resection of all gastrointestinal hemangiomas was performed by minimally invasive surgery with gastric, small intestinal, and colonic fiberscopy and laparoscopy. The postoperative course was uneventful. The patient could walk the day after surgery, and she was discharged from the hospital 14 days after surgery. Our experience and findings given in other reports suggest that total resection of hemangiomas should be the final goal and that minimal skin incision is preferable for this benign disease, with multiendoscope-assisted treatment to ensure that any hemangiomas remaining in the gastrointestinal tract are not overlooked.
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PMID:Multiendoscope-assisted treatment for blue rubber bleb nevus syndrome. 1126 70


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