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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart failure is a clinical syndrome characterized by impaired structure and/or function of the heart, leading to dyspnea and fatigue at rest or with exertion. The pathophysiology of heart failure is complex, and there is no single lesion. Any form of heart disease can lead to heart failure. Most heart failure can be explained by well-recognized etiologic factors, though ostensibly healthy patients may harbor risk factors for the later development of heart failure. A fundamental response to myocardial injury or altered loading conditions includes "remodeling" of the heart, so that the size, shape, and function of the affected chamber is grossly distorted. This is accompanied by a constellation of biologic changes, best recognized in advanced cases of heart failure. These multiple alterations may be primary or secondary events but, nonetheless, add importantly to the morbidity and mortality of the patients. More emphasis should be placed on recognition and correction of risk factors related to the development of heart failure.
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PMID:Pathophysiology of congestive heart failure. 1277 9

Obesity is a progressive disease of unwanted fat accumulation which has multiple, organ-specific pathological consequences. The manifestations of obesity occur within virtually every subspecialty of medicine or surgery and they interact importantly to accelerate the ageing process in many organs. Many of the hazards of obesity have multiple causes (e.g., diabetes, heart disease, stroke, colonic and breast cancer, urinary incontinence, tiredness, back pain, breathlessness). All of these conditions become more prevalent with age and are also more prevalent among overweight persons, particularly those with a central fat distribution marked by a high waist circumference. Hypertension may be caused or aggravated by weight gain. It is mediated by the physical demands of an expanded circulating volume and increased metabolic rate by metabolic mechanisms related to central fat distribution and the "metabolic syndrome", and to increased sodium consumption by overweight people (because they need more food to maintain a higher metabolic rate). Since body mass index (BMI) and waist circumference increase significantly with age there is an escalation of the burden of ill health from obesity with age. The best simple indicator of disease risk with obesity is the waist circumference since this identifies people who have a high body fat content and also those who have an increased intraabdominal accumulation of fat. The quantitative burden of ill health from overweight and obesity varies within different specialties, but up to 80% of type 2 diabetes or polycystic ovarian syndrome can be attributed to obesity. Obesity is the cause of sleep apnea syndrome in around 50% of cases and heart disease in perhaps 10-20% of cases. In Scotland 80% of people with existing cardiovascular disease are overweight compared with 57% of the general population. The financial burden to health services from overweight and obesity has been incompletely assessed, although it is estimated that around 4% of total health care budgets are attributable to people having BMI > 25 kg/m(2). This is similar to the entire cost of diabetes, epilepsy or major cancers. Obesity is therefore an extremely expensive disease based on these conservative estimates from limited evaluations. More general assessments show how obesity increases the amount of time taken off work, the number of drugs prescribed and the expenditure from social services support. Thus, obesity represents a huge burden not only on the individual patient physically, psychologically, socially and financially but also on families and careers and is a huge drain on health care resources. Overweight affects well over half of all adults worldwide, progressing to BMI > 30 kg/m(2) in around 20% outside subsistence rural communities. Its rapidly increasing prevalence now described as an epidemic demands major preventive measures, as well as better medical treatment for individuals affected.
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PMID:Obesity: burdens of illness and strategies for prevention or management. 1284 36

Most patients with cancer experience fatigue, a severe activity-limiting symptom with a multifactorial origin. To avoid cancer-related fatigue, patients are frequently advised to seek periods of rest and to reduce their amount of physical activity. This advice is reminiscent of that formerly given to patients with heart disease. However, such recommendations can paradoxically compound symptoms of fatigue, since sedentary habits induce muscle catabolism and thus cause a further decrease in functional capacity. By contrast, there is scientific evidence that an exercise programme of low to moderate intensity can substantially reduce cancer-related fatigue and improve the quality of life of these patients. Current knowledge, combined with findings soon to be published, could launch new opportunities for patients with cancer. In this new century, exercise physiology could soon prove to be very useful for oncologists.
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PMID:Cancer-related fatigue: can exercise physiology assist oncologists? 1455 39

Even though depressions and depressive symptoms are frequently observed in patients with medical diseases, their psychological problems are often neither diagnosed nor treated. Diagnosis of mood state might be easy in isolated cases yet it often is not since the precise nature of normal mood cannot be expressed in quantitative terms. Furthermore, depression can only be diagnosed based on the doctor's clinical appraisal and the patient's own description of his/her complaints. There is no gold standard on which depressive symptoms can be based on--and further on, depression is not a diagnosis. Instead, it is a syndrome that calls for differential diagnoses before treatment can be offered. Diagnosing depressive comorbidity in patients with medical complaints is even more difficult because of the overlap between symptoms of depression and accompanying symptoms of the somatic illness e.g. lack of energy. Although depressive states have been known to be a risk factor for the prognosis of patients with coronary heart disease for a long time, there is a paucity of research about the therapy these patients undergo due to the fact that tricyclic anti-depressants can have cardiotoxic effects on patients with heart disease. The treatment of depression in these patients has become a much lower risk since the introduction of serotonin reuptake inhibitors. There is widespread evidence that depressive comorbidity has a negative impact on the prognosis of medical disorders. Despite the complex nature of diagnosing depression, proper diagnosis and treatment is increasingly important in internal medicine and especially cardiology.
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PMID:[Diagnosis and therapy of depression in the heart disease patient]. 1466 9

Hypertension commonly leads to heart disease, in particular left ventricular hypertrophy, heart failure and coronary artery disease. Left ventricular hypertrophy and coronary artery disease are both often subclinical diseases in hypertensives. Symptomatic coronary artery disease in hypertension may be due to atherosclerosis in epicardial arteries, microvascular dysfunction, reduced fibrinolytic capacity, or left ventricular hypertrophy; the latter is present in 20-50% of patients with mild to moderate and in up to 90% of patients with severe hypertension. Left ventricular hypertrophy in hypertension is associated with a twofold increase in risk of myocardial infarction, sudden death and stroke, and a fourfold increase in risk of heart failure. While coronary artery disease is the most common cause of heart failure in men, hypertension and in particular untreated isolated systolic hypertension is the most common cause in women. Heart failure symptoms may be subtle in hypertension, like tiredness or reduced physical capacity. Echocardiography can reveal subclinical heart disease as well as serve as a guide to correct diagnosis and treatment.
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PMID:[Hypertension and heart disease]. 1503 15

A young asymptomatic male athlete came to our laboratory to be enrolled in a research protocol on physical fatigue. Routine clinical and cardiological evaluations including echocardiogram were in the normal range. Several consecutive cardiopulmonary tests showed a fairly good tolerance to exercise, with no symptoms even when the effort was abruptly arrested. On the other hand, Holter ECG recordings showed long nocturnal sinus pauses. As he was absolutely asymptomatic and free from any structural heart disease, he underwent a follow-up with repeated Holter monitorings for one year. During this period he decided on his own to stop practising sports; in spite of this sharp reduction in his overall physical activity, consecutive Holter monitorings showed that the sinus pauses were progressively increasing in duration (up to 9.2 seconds). With the hypothesis of a malignant vagotonia, he underwent a tilt test; however, we could not elicit any pauses or symptoms. The pauses grew longer over time; a endocavitary electrophysiologic test was performed, which showed no evidence of disease. To rule out the hypothesis of a sleep apnoea syndrome, he also underwent a polysomnography, including EEG, eye movement electromyography, arterial blood oxygen saturation and thoracic impedance: no alterations were detected with the exception of the sinus pauses, which appeared to be strictly linked to REM sleep, as suggested by the concurrent increase in rapid eye movements and desynchronized EEG. We hence made a diagnosis of sinus arrest during REM sleep (SAdRS), a very uncommon disease belonging to the parasomnias. Pauses were then quantified for one month by implanting a ECG loop recorder. As the patient became more and more upset and worried, and the pauses increased to nearly 12 seconds, we decided to implant a pacemaker, which is the only therapeutic option established in the literature for patients with SAdRS.
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PMID:Prolonged asystolia in a young athlete: a case of sinus arrest during REM sleep. 1534 35

Primary hyperparathyroidism (pHPT), caused by solitary parathyroid adenomas in 85% of cases and diffuse hyperplasia in most of the remaining cases, overproduces parathyroid hormone (PTH), which mobilizes calcium to the blood stream. Renal stones, osteoporosis and diffuse symptoms of hypercalcaemia, such as constipation, fatigue and weakness are well-known complications. However, in Western Europe and North America, patients with pHPT are nowadays usually discovered during an early, asymptomatic phase of the disease. It has been reported that patients suffering from symptomatic pHPT have increased mortality, mainly due to an overrepresentation of cardiovascular death. pHPT is reported to be associated with hypertension, disturbances in the renin-angiotensin-aldosterone system, and structural and functional alterations in the vascular wall. Recently, studies have indicated an association between pHPT and heart disease, and studies in vitro have produced a number of theoretical approaches. An increased prevalence of cardiac structural abnormalities such as left ventricular hypertrophy (LVH) and valvular and myocardial calcification has been observed. Associations have been found between PTH and LVH, and between LVH and serum calcium. LV systolic function does not seem to be affected in patients with pHPT, whereas any influence on LV diastolic performance needs further evaluation. The aim of this review is to clarify the connection between pHPT and cardiac disease.
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PMID:Primary hyperparathyroidism and heart disease--a review. 1547 92

In the RAte Control versus Electrical cardioversion for persistent atrial fibrillation (RACE) study, 522 patients were randomized to either rate or rhythm control therapy. Lone atrial fibrillation (AF) was present in 89 patients. Demographics, cardiovascular mortality and morbidity, and quality of life were compared between patients with lone AF and those with underlying structural heart disease. Patients with lone AF were significantly younger (65 +/- 10 vs 69 +/- 8 years) and had fewer complaints of fatigue (p = 0.01) and dyspnea (p = 0.005). With lone AF, quality-of-life scores were higher on almost all 8 Medical Outcomes Study Short-Form health survey questionnaire subscales, and comparable to healthy, age- and gender-matched controls. Mean follow-up was 2.3 +/- 0.6 years. Cardiovascular end points occurred in 9 patients with lone AF (10%), consisting of death (all bleedings) 3%, thromboembolic complications in 3%, nonfatal bleeding in 2%, and pacemaker implantation in 2%, but no heart failure and severe adverse effects due to antiarrhythmic drugs occurred. End points occurred in 95 patients (22%) with underlying diseases. Heart failure and severe adverse effects from drugs did not occur in patients with lone AF in this study. Despite the absence of demonstrable cardiovascular and cerebrovascular disease, lone AF is associated with bleeding and thromboembolism.
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PMID:Clinical characteristics of persistent lone atrial fibrillation in the RACE study. 1558 1

Injury to the myocardium disrupts geometric integrity and results in changes to intracardiac pressure, wall stress and tension, and the pattern of blood flow through the heart. Significant disruption to pump function results in heart failure which is defined in terms of symptoms: breathlessness and fatigue, signs of salt and water retention, and neurohormonal activation. This syndrome most commonly occurs in the context of injury due to ischaemic heart disease and dilated cardiomyopathy but because patients with congenital heart disease (CHD) are born with sometimes gross distortions of cardiac anatomy they too are subject to the forces that drive heart failure. This paper explores the available data relating to the clinical and neurohormonal manifestations of heart failure in patients with congenital heart disease and describes how, by additionally exploring events at a cellular level, we may be able to arrive at a definition of heart failure relevant to this population.
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PMID:Towards defining heart failure in adults with congenital heart disease. 1559 75

We examined symptom experiences, symptom attributions, and causal attributions reported by patients hospitalized for a first-time myocardial infarction (MI). We also explored the roles of symptoms, negative affect, and risk factors in promoting stress and other causal attributions. Patients (N = 65) completed measures of symptom experiences and attributions, perceived causes of their MI, state and trait negative affect, and risk factors. Patients attributed most of their symptoms to the heart condition, although rates varied from 48% (headaches) to 97% (nausea). The most common causal attribution was stress, followed by high cholesterol, heredity, fat consumption, and hypertension. Stress attributions were positively associated with state anxiety and specific, stress-related symptoms (e.g., fatigue and breathlessness). Anxious mood and stress-related symptoms appear to enhance the plausibility of stress as a cause of MI. Risk factors were moderately correlated with associated causal attributions. For many patients, however, attributions to hypertension, cholesterol, and family history of heart disease were discordant with their clinical data. Causal attributions remained stable over the subsequent 6 months.
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PMID:Symptom experiences, symptom attributions, and causal attributions in patients following first-time myocardial infarction. 1574 34


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