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

Dyspnea is the medical term for the patient's or subject's complaint of shortness of breath. It encompasses the respiratory discomfort experienced in many different diease states as well as the shortness of breath felt by a normal subject during or after strenuous exercise. Several parameters which have been shown to correlate with the onset or severity of dyspnea are described, including reduced vital capacity, the ratio of minute ventilation to vital capacity, reduced breathing reserve, the work of breathing, and the oxygen cost of breathing. Attempts at quantitation of dyspnea have usually consisted of measuring physiological parameters associated with the sensation, such as the "dyspneic index". The direct measurement of respiratory sensations using modern psycho-physical methods is at an early stage of development. Since the observation that the existence of dyspnea is often unrelated to any disturbance of arterial blood gas composition, it has been generally held that the mechanism of dyspnea is primarily neurophysiological. The neural pathways may conceptually be divided into those which transmit the "dyspnea message" from the respiratory apparatus to integrating centers in the brain, and those concerned with subsequently bringing the sensation to the level of consciousness. It seems likely that there is no single sensing mechanism and neural pathway which will be able to explain dyspnea in the diverse populations of patients and subjects who experience unpleasant respiratory sensations. Three theories concerning mechanisms of dyspnea are briefly described: "length-tension inappropriateness", vagal afferent activity especially from the J-receptors, and the recent concept of diaphragmatic fatigue. Some specific characteristics of the shortness of breath experienced in certain disease states are described, including chronic bronchitis and emphysema, bronchial asthma, pulmonary fibrosis and congestive heart disease.
 ...
PMID:Dyspnea. 50 81

Chest radiographs of 39 patients with ankylosing spondylitis were studied. Three showed apical pulmonary fibrosis, two with cavitary lesions. Other known causes of lung disease were excluded. Symptoms and roentgenographic evidence of spondylitis were present for many years prior to the onset of pulmonary symptoms, which variably included shortness of breath, cough, hemoptysis, pleuritic chest pain, fever, and chills. Apical pulmonary lesions of unknown cause were absent in 53 age, sex, and racematched osteoarthritis control patients. The findings suggest that apical pulmonary fibrosis may be an extra-skeletal manifestation of ankylosing spondylitis, the frequency of which approaches that of spondylitic heart disease.
 ...
PMID:Pulmonary manifestations of ankylosing spondylitis. 120 76

Pulmonary function is known to be related inversely to incidence of coronary heart disease, congestive heart failure, chronic obstructive lung disease, lung cancer, and death from all causes. Reasons for some of these associations are poorly understood. Relationships between cardiovascular disease risk factors and pulmonary function were examined in 5,115 18- to 30-year-old black and white male and female participants in the study of Coronary Artery Risk Development in Young Adults (CARDIA). Forced expiratory volume in 1 s adjusted for height (FEV1/Ht2) was significantly lower in smokers than nonsmokers and in persons who reported shortness of breath; FEV1/Ht2 was correlated positively with a history of strenuous physical activity, duration of exercise on the treadmill, and high-density lipoprotein cholesterol. It was associated negatively with skinfold thicknesses, serum triglycerides, fasting serum insulin, and the Cook Medley scale of hostility. The association between pulmonary function and heart disease risk may reflect associations with physical fitness, vigor, fatness, and lipid profiles, as well as with cigarette smoking.
 ...
PMID:Pulmonary function and cardiovascular risk factor relationships in black and in white young men and women. The CARDIA Study. 198 78

The specific aim of this study is to compare and contrast the biophysical and psychosocial profile of men and women undergoing cardiac surgery (coronary artery bypass graft and valve replacement) during the perioperative and home recovery period. Coronary artery disease appears to be qualitatively worse in women than men although the prevalence in women does not approach that in men until the seventh decade. Valvular disorders also reveal a different profile by sex with the greater valvular problems in women related to the fact that women have more rheumatic heart disease. A prospective, longitudinal design with a convenience sample of 117 patients undergoing cardiac surgery and their spouses (234 subjects) from five Northern California hospitals was used to tap patient response at three critical perioperative data points. Female patients were observed during the perioperative period to have significantly more shortness of breath, poorer cardiac functional status (New York Heart Association), significantly longer intensive care unit stays, and proportionately more deaths. At 1 and 3 months after discharge, however, their recoveries did not differ significantly from men's when they were compared on sexuality, recreation, or return-to-work variables. Surprisingly, female patients had significantly less mood disturbances as measured by the Profile of Mood States than their male counterparts, and they scored higher on measures of family satisfaction than did male patients. Implications of the study involve early recognition of heart disease in women, preparation of families for longer intensive care unit stays, and appreciation of different psychosocial responses to surgery.
 ...
PMID:Differences in recovery from cardiac surgery: a profile of male and female patients. 221 Nov 55

The ratio of anaerobic threshold (AT) to maximal oxygen consumption (Max VO2), which is referred to as relative AT, was evaluated in six athletic students (S), 12 normal male subjects (N) and 39 patients with chronic heart disease (C). Group C was categorized in three subgroups according to the New York Heart Association functional class (CI: 10, CII: 16 and CIII: 13 patients). The symptomatic-maximal graded treadmill exercise test was performed and respiratory parameters were measured by R1500S Autoaerobics. AT was determined as the oxygen consumption (VO2) at which a linear relationship between pulmonary ventilation and VO2 was lost during progressive exercise. All subjects performed maximal exertion until they were limited by either shortness of breath or leg fatigue. AT (ml/min/kg) was 36.4 +/- 6.0, 25.9 +/- 5.7, 21.4 +/- 4.5, 16.3 +/- 4.0 and 11.1 +/- 2.6, and MaxVO2 (ml/min/kg) was 77.3 +/- 6.5, 47.6 +/- 10.2, 29.5 +/- 6.1, 22.5 +/- 5.8 and 15.5 +/- 3.1, respectively, in group S, N, CI, CII and CIII (p less than 0.01 between each group). Relative AT(%) was 46.8 +/- 4.4, 54.9 +/- 7.2, 72.1 +/- 6.4, 73.0 +/- 8.6 and 72.6 +/- 8.7, respectively, in groups S, N, CI, CII and CIII (p less than 0.01 between S and N, between N and CI-CIII, between S and CI-III). The anaerobic threshold appeared at mid-point in the graded symptomatic maximal exercise test. However, the appearance of AT relative to the maximal oxygen consumption varied from 47 to 73% in the study groups tested. AT appeared relatively early in normal subjects compared to cardiac subjects.
 ...
PMID:[Relation between anaerobic threshold and maximal oxygen consumption during graded treadmill exercise]. 281 44

A worker exposed to fluorocarbons in an automobile plant for seven years experienced shortness of breath (in 1977) and was referred to the hospital. The clinical examination revealed electrocardiographic abnormalities. He recovered quickly and returned to work. During the following year (1978) he suffered subarachnoid bleeding with hemiparesis, and four years later he had an operation for a thymoma. Hygienic measurements in 1980-1981 showed large variations in the fluorocarbon concentrations in the plant, the average 8-h concentrations being below the occupational exposure limit of 500 ppm but several short-time measurements reaching levels of over 750 ppm. It was suggested that, persons with heart disease do not necessarily have to be removed from work with fluorocarbons without careful review of the exposure but that the evaluation of the exposure should not only be based on time-weighted average concentrations, but also on values for brief periods, in that such concentrations can often be decreased by simple and cheap measures.
 ...
PMID:Exposure to fluorocarbons during the filling and repair of air-conditioning systems in cars--a case report. 343 54

Intravenous immune globulin (IVIg) is advocated as a safe treatment for immune-mediated neurologic disease. We reviewed the medical records of 88 patients who were given IVIg for a neurologic illness. Major complications in four patients (4.5%) included congestive heart failure in a patient with polymyositis, hypotension after a recent myocardial infarction, deep venous thrombosis in a bed-bound patient, and acute renal failure with diabetic nephropathy. Other adverse effects included vasomotor symptoms 26, headache 23, rash 5, leukopenia 4, fever 3, neutropenia 1, proteinuria (1.9 g/day) 1, viral syndrome 1, dyspnea 1, and pruritus 1. Fifty-two patients (59%) had some adverse effect of IVIg infusion, most commonly vasomotor symptoms, headaches, fever, or shortness of breath in 40 (45%), which improved with reduced infusion rate or symptomatic medications. Five (6%) had asymptomatic laboratory abnormalities and seven (8%) had other minor adverse effects. Adverse effects led to discontinuation of therapy in 16% and permanent termination of therapy in 10% of patients. There was no mortality or long-term morbidity. Although adverse effects were frequent, serious complications were rare except in patients with heart disease, renal insufficiency, and bed-bound state.
 ...
PMID:Complications of intravenous immune globulin treatment in neurologic disease. 930 72

The purposes of this study were to describe: clinical symptoms in a sample of consecutive patients with supraventricular tachycardia (SVT); incidence of sudden death, syncope, and other disabling symptoms; whether these symptoms differ by tachycardia mechanism; and to identify predictor variables of syncope in patients with SVT. Data were collected from chart reviews of 167 consecutive patients with SVT admitted for radiofrequency ablation. Three patients (2%) had nonlethal cardiac arrest, and a total of 16% (26 of 183) received at least 1 external direct-current shock for arrhythmia management. Twenty percent of subjects (33 of 167) reported at least 1 episode of syncope which was preceded by palpitations. The most frequent symptoms were: palpitations (96%), dizziness (75%), and shortness of breath (47%). We found atrioventricular nodal reentrant tachycardia (AVNRT) in 64 patients, atrioventricular-reciprocating tachycardia (AVRT) in 59, atrial tachycardia in 22, and atrial flutter in 22. The symptom profiles of patients with AVNRT, AVRT, and atrial tachycardia were very similar, but differed significantly (p <0.05) from those reported in the atrial flutter group. Multivariate analysis showed that heart rate > or = 170 beats/min was the only independent risk factor for syncope. Chi-square analysis demonstrated that SVT patients with heart rate > or = 170 beats/min had significantly more dizziness and syncope. Thus, despite a low incidence of associated heart disease, and good left ventricular function, there was a high frequency of disabling, potentially life-threatening symptoms associated with episodes of SVT in this sample. SVT can have potentially lethal consequences, and is more disruptive than previously thought.
 ...
PMID:Frequency of disabling symptoms in supraventricular tachycardia. 919 13

Understanding of the causes of dyspnea and anasarca, the cardinal features of heart failure, has changed dramatically since Greco-Roman times, when sputum and pleural effusions were thought to originate in the brain, and the heart was believed to heat and distribute the vital spirit. It was not until the seventeenth century, when Harvey demonstrated that the heart was a pump and autopsy descriptions revealed valve abnormalities that interfered with the circulation, that it became possible to identify the role of heart disease in causing shortness of breath and edema. Morgagni's recognition, toward the end of the eighteenth century, that overload caused the heart to enlarge was followed less than 50 years later by Corvisart's distinction between hypertrophy and dilation. Differences in the architecture of failing hearts focused attention of nineteenth-century clinical scientists on the myocardial response to overload, and by the end of this century overload-induced hypertrophy was recognized not only to have immediate adaptive effects, but also to cause progressive degeneration of the heart muscle. This focus on the failing myocardium ended in the early years of the twentieth century, when new discoveries in hemodynamic physiology shifted attention to pressure and flow abnormalities caused by the then prevalent rheumatic valvular heart disease. During the past decade, new emphasis on prognosis, along with realization that drugs intended to correct hemodynamic abnormalities often had adverse effects on survival, has led to a reexamination of the biology of the failing heart. As a result, the focus in heart failure research has returned to the myocardium. This article reviews some of the misconceptions and errors of early physicians, who, while often careful and intelligent observers, lacked the means to explain and treat heart failure. It is hoped an appreciation of the evolving concepts of heart failure will help the reader meet today's challenge of incorporating new information from molecular biology that holds the key to further progress in understanding the causes and therapy of this syndrome.
 ...
PMID:Evolving concepts of heart failure: cooling furnace, malfunctioning pump, enlarging muscle--Part I. 954 47

Whatever facts we gather and no matter how many we have, you and I must eventually put the journal down and pick up our stethoscope, pen, and prescription pad and go to work. Hopefully we can do better than, "Therapy is not uniform and specific antibiotic regimens are usually selected based on local tribal custom." We can discard an old paradigm, "The absence of data bears no relation to the strength of opinion." Personally, I have used these new scientific data before I reached my conclusion. I have developed 10 points to structure my new approach. I invite you to compare my conclusions to yours. 1. In acute bronchitis, in otherwise healthy adults, my preference is to not prescribe an antibiotic. If I do, it is not over the phone. You should want to see and examine the patient. If there are no helpful hints to etiology, I choose a newer macrolide for those under age 50 and use a short course, five-seven days. For patients over age 50, especially if they are "healthy smokers," consider a short course of cefuroxime. (You can see, even in these acute bronchitis patients, you want an antibiotic effective against today's pathogens.) 2. In all chronic bronchitis patients, prevention of further damage to the airways should be attempted by instituting a program of smoking cessation and appropriate immunizations against influenza and pneumococcus. 3. Treatment outcomes will also improve if we recognize that in some patients the progressing SOB, cough, and increasing sputum production are due to congestive heart failure and not due to infection. I try to think about congestive heart failure in all of my patients, but especially in those with known heart disease and cardiomegaly on their chest x-ray. 4. Routine pulmonary function testing is important in smoking patients. Physicians underestimate the degree of obstruction present when they rely on physical exam alone. Hopefully long before the patient's acute illness you have established whether or not obstruction is present. This information helps identify the high risk patient for not only recurrent bouts of infection but also those at increased risk for lung cancer. 5. We will have more success in treating AECB when we elect to use an antibiotic only for patients with at least two of the following three cardinal symptoms: increased dyspnea, increased sputum production, and increased purulent sputum. COPD patients have many days when they feel more SOB. To use this or any one sign as the sole indication for starting an antibiotic has been proven not to make a statistically significant difference in outcome in most patients. Also, the value of prophylactic antibiotic therapy has not been established. 6. When airflow obstruction is moderately severe or more pronounced, AECB should usually be treated with oral steroids. Other measures such as chronic bronchodilator therapy, supplemental and home oxygen use, and pulmonary rehabilitation have been extensively reviewed elsewhere.
 ...
PMID:Challenging questions in treating bronchitis. 979 74


1 2 3 4 5 6 7 Next >>