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

In reviewing the present-day status of cor pulmonale, it is clear that considerable progress has been made in almost all instances of the disease. It is clearly a preventable form of heart disease in most cases and it is treatable and curable in its most common form, i. e., in COPD. One must agree with Petty, that today we have effective means of caring for the majority of respiratory cripples. Therapy for lung disease now appears even to have reduced the expected rate of pulmonary function deterioration in some patients. Surely with improved gas exchange and early detection of respiratory insufficiency the outlook for patients with respiratory diseases leading to cor pulmonale is better today than it was 30 years ago.
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PMID:Cor pulmonale (pulmonary heart disease): present-day status. 12 8

Though breathing pattern is frequently analyzed during clinical exercise testing, there is little information regarding its usefulness in the differential diagnosis of impaired exercise tolerance. This study tested the hypothesis that differences in peak tidal volume during exercise between patients with different cardiorespiratory diseases are related largely to differences in severity of respiratory mechanical impairment (vital capacity), not to differences in disease state. Patients with chronic obstructive pulmonary disease, restrictive lung disease, bronchial asthma, and heart disease (mitral valve disease or left ventricular dysfunction) were studied. Subjects selected had one and only one of the above diagnoses. All subjects performed maximal (symptom-limited) incremental exercise on a cycle ergometer. Multiple linear regression of all subjects (n = 30) in all four groups showed a significant correlation between VTmax and VC: VTmax = 0.55, VC -0.09 L (r = 0.827, p less than 0.0001). The VTmax/VC (x 100) was (mean +/- SD) 44 +/- 15, 54 +/- 11, 56 +/- 11, and 54 +/- 12 for the COPD, RLD, BA and HD patients respectively. There was no significant difference between any of the groups. We concluded that differences in VTmax between different patients are related largely to differences in VC (ie, differences in severity of respiratory mechanical impairment), not to differences in disease state. Measurement of VTmax or the VTmax/VC ratio has little value in the differential diagnosis of exertional dyspnea.
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PMID:Diagnostic value of maximal exercise tidal volume. 224 73

To examine the effects of theophylline toxicity on cardiac rhythm, patients underwent continuous ambulatory ECG recording during acute theophylline toxicity and recovery. The patients, who were recruited form inpatient wards, intensive care units, and emergency departments of a University Medical Center and a Veterans Administration Medical Center, had serum theophylline concentrations (STC) greater than 30 mg/L. There were 14 men and two women with a mean age of 66 years. Fourteen patients had COPD and developed toxicity following long-term theophylline overmedication. Two patients had asthma and ingested an intentional overdose. The STC at the onset of ECG recording ranged from 23 to 67 mg/L. The principal rhythm was sinus in 15 patients; one patient had atrial fibrillation. Sinus tachycardia (heart rate greater than 100/min) was common, and heart rate fell in proportion to STC as toxicity resolved. Supraventricular ectopic beats (SVEs) were noted in seven patients with multiple runs of SVE being present in four. One patient developed multifocal atrial tachycardia (MAT) during toxicity that resolved spontaneously. During the 11 +/- 8 hours of recording during toxicity (STC greater than 20 mg/L), 80 percent of patients had ventricular premature beats (VPBs), 44 percent had paired VPBs, and 25 percent had ventricular runs. One elderly patient with heart disease developed sustained ventricular tachycardia (VT) when STC = 66 mg/L. No other patient had ventricular ectopy that required intervention. During the 10 +/- 6 hours of recording during the "recovery phase" (STC less than 20 mg/L), all patients with VPBs continued to have ectopy; however, the number of VPBs declined significantly. A follow-up 24-hour ECG recording obtained one week after recovery from toxicity in the patient with sustained VT demonstrated marked reduction in the frequency and complexity of VPBs. Patients with frequent (greater than 10/h) or repetitive VPBs were older (p less than 0.05) than those without complex ectopy. There was a trend (p = 0.07) suggesting patients with underlying heart disease were at risk for having complex ventricular ectopy. We conclude that sinus tachycardia, SVE, and VPBs are common among patients with theophylline toxicity; however, sustained ventricular or supraventricular tachyarrhythmias that require antiarrhythmic therapy are uncommon.
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PMID:Cardiac arrhythmias during theophylline toxicity. A prospective continuous electrocardiographic study. 188 98

Risk factors for temporal changes in chronic respiratory disease mortality were evaluated from two studies conducted in Washington County, Maryland. The first examined the mortality of a private census population (greater than 35,000 whites) enumerated in 1963 over two subsequent time periods by age, sex, and initial smoking status. The second examined the 10-yr mortality of a subset of the 1963 census (884 men who had undergone spirometry). We observed a fall in age-adjusted mortality from all causes and from arteriosclerotic heart disease (ASHD), but an increase in COPD mortality. However, the increase in these chronic pulmonary deaths is essentially confined to persons who were smoking cigarettes at the beginning of the study period. Furthermore, while smokers showed an increased mortality risk for all causes, the excess mortality risk did not fall uniformly across cigarette smokers. It is a major observation of this study that all-cause and cardiovascular (as well as pulmonary) mortality are significantly more often found among subjects with ventilatory impairment (independent of smoking status). Reasons for the association of ASHD mortality with impaired forced expiration are discussed. Thus, men at increased risk for three (ASHD, lung cancer, COPD) of the five leading causes of death (three of eight for women) may be identified by spirometry. Perhaps it is time that this test was more generally applied.
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PMID:Respiratory risk factors and mortality: longitudinal studies in Washington County, Maryland. 278 61

Although beta-blockers have established efficacy in treating ventricular ectopy and PSVT, their applicability for acute antiarrhythmic interventions in patients with organic heart disease or COPD, is frequently limited by negative inotropic or bronchospastic side effects. The development of an ultrashort acting beta-blocker with rapid reversibility of its side effects would widen their applicability. Therefore, we tested the electrophysiologic properties of such a new short acting beta-blocker, esmolol, in 14 patients (10 with organic heart disease) with a mean EF of 47.6 +/- 17%, undergoing standard clinical electrophysiologic studies for various indications. Like most other beta-blockers, esmolol's major direct effects were on sinus node function and AV nodal conduction characteristics; significantly prolonging sinus cycle length, cycle length to Wenckebach and AH interval in sinus rhythm and at a paced cycle length of 600 ms. In contrast to most other beta-blockers, following termination of its infusion, esmolol shortened parameters of sinus node function and AV nodal refractoriness, with respect to the control values, suggesting a possible rebound phenomena. These effects occurred within 5 min of terminating the intravenous drug infusion. Esmolol had no significant effect on systolic blood pressure, electrocardiographic intervals and had rare adverse reactions. We conclude that esmolol is an ultra-short acting beta-blocker, with typical direct electrophysiologic effects on sinus node and AV nodal function, and a possible rebound phenomena following its discontinuation that may make it particularly suited to acute antiarrhythmic interventions in patients susceptible to adverse beta-blocker side effects.
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PMID:The electrophysiologic properties of esmolol, a short acting beta-blocker. 290 Feb 17

Making a diagnosis of asthma is often complicated, especially in the older patient. Problems that are specific to this population include a larger reduction in pulmonary function than is suggested by the patient evaluation, a higher rate of comorbid diagnosis of COPD and other chronic disease, as well as an increased risk of death associated with asthma. Older patients may also have reduced awareness of bronchial constriction or airway obstruction, which may delay their seeking of medical care. For this reason, measurements of air flow are critical to objectively assess the severity of acute asthma in the older patient. Special concerns in patients over age 50 include exacerbation of co-existing heart disease and potential interactions with medications used for other chronic conditions.
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PMID:Asthma: new insights in the management of older adults. 795 73

The air pollution disasters in London in 1952, the Meuse valley in 1930, and in Donoroa, Pennsylvania, in 1948 made it clear that extremely high levels of particulate-based smog could produce large increases in the daily mortality rate. Recent studies of fluctuations in daily air pollution and daily mortality have reported associations at much lower concentrations in London during the 1960s and in Philadelphia, Steubenville, Santa Clara, St. Louis, Utah valley, Detroit, and eastern Tennessee in the 1970s and 1980s. Whether these associations are causal or not is a matter of considerable public health concern. If the detailed pattern of the deaths at these lower concentrations appeared similar to the pattern in London, this would strengthen the argument for causality. To examine this issue, the death certificates from Philadelphia were examined on the 5% of the days with the highest particulate air pollution and the 5% of the days with the lowest particulate air pollution during the years 1973-1980. There was little difference in weather between the high and low pollution days, but total suspended particulate matter concentrations averaged 141 micrograms/m3 on the high pollution days versus 47 micrograms/m3 on the low pollution days. The relative risk of dying on the high pollution days was 1.08 P < 0.0001. The relative increase was higher for COPD (1.25) and pneumonia (1.13). Deaths were also elevated for heart disease and stroke; however, there was a substantial increase in the reports of respiratory factors as contributing causes for those underlying causes of death. Dead-on-arrival deaths and deaths outside of hospitals and clinics were also disproportionately increased. This paralleled the pattern seen in London in 1952. The age pattern of the relative risk of death was also similar. This adds to the evidence that the association is causal.
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PMID:What are people dying of on high air pollution days? 828 40

Smoking tobacco contributes to and exacerbates many chronic diseases of aging, including hypertension, stroke, COPD, heart disease, and atherosclerosis. It is also associated with an increased risk of peptic ulcers and of cancers of the lungs and oral cavity. Older patients generally continue to smoke because of physiologic and psychological addiction to nicotine. Nicotine administration through gum or patch eases the symptoms of nicotine withdrawal for highly-tolerant patients. Detecting and treating alcohol abuse, depression, or life stress may then make it easier to motivate the patient to quit smoking. Physician advice combined with follow-up visits and phone calls has been shown to be one of most effective methods of getting patients to stop smoking.
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PMID:Smoking cessation: clinical steps to improve compliance. 838 53

Seventy one patients with active pulmonary tuberculosis who died during the past 5 years (1989 to 1993) were evaluated on their causes of death. Twenty two patients (31%) died directly of tuberculosis, and among them, 18 patients (81%) of 22 patients who died of tuberculosis) had very advanced tuberculosis. The majority of them (64%) were old age over 70 years and were bedridden due mostly to cerebrovascular injuries. The serum level of albumin was low in all 17 patients in whom it was measured. Establishment of diagnosis of tuberculosis was delayed over one month after the onset of symptoms in 59% of patients who died of severe disease. Sixty one percent (11/18) of patients died within the first month after the initiation of chemotherapy and about 90% (16/18) died within 3 months. Two patients died from massive hemoptysis and other patients died of either respiratory failure or tuberculosis meningitis. From these observations it was found that very advanced tuberculosis was the major cause of death in patients who died of tuberculosis and that the advanced disease was chiefly caused by the delay on the establishment of diagnosis, and it was most important to detect tuberculosis as early as possible, with regular check up of chest X-ray and frequent examination for AFB (acid-fast bacilli) for tuberculosis suspected patients. On the other hand, the majority of patients (49/71) died of complicating medical problem unrelated to tuberculosis. Seventeen patients died from malignancy (seven lung cancer, four lymphoma, two laryngeal cancer, etc). Ten deaths were the result of bacterial superinfection. Other patients died from respiratory failure due to COPD, arteiosclerotic heart disease, or cerebrovascular injuries, etc. Two patients of old age died of hepatic failure possibly caused by adverse reaction of TB chemotherapy. It was found that diseases unrelated to tuberculosis were the cause of death in approximately 70% of patients with active tuberculosis, and it should be emphasized to detect early and to treat these diseases, in particular malignancy. And it is also imperative that the chemotherapy for TB must be instituted very carefully with frequent monitoring of liver function in patients with old age.
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PMID:[Clinical evaluation on causes of death in patients with active pulmonary tuberculosis]. 868 6

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.
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PMID:Challenging questions in treating bronchitis. 979 74


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