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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung volume reduction (LVR) is a new surgical approach designed to relieve shortness of breath and to improve exercise tolerance in patients with severe lung emphysema. Selection of patients for LVR is based on history, clinical investigation, chest X-ray studies, CT scan, lung perfusion scan, lung function testing, and blood gas analysis. Selection criteria are severe emphysema (FEV1 20-35% pred., TLC > 120% pred., RV > 250% pred.), dyspnea despite optimized medical therapy, abstinence from smoking, acceptable nutritional status and rehabilitation potential. Patients with a uniform pattern of lung destruction benefit far less than those with a more localised pattern (> 30% on chest X-ray or CT scan) with the remaining lung being quite normal and a reduced perfusion of only the damaged areas. Prior to the final decision for LVR, all patients are enrolled in a supervised rehabilitation programme of 4 weeks duration. Some patients benefit so much that LVR can be postponed. The surgical approach of choice is a median sternotomy for bilateral LVR when the upper lobes are the target areas and a bilateral thoracotomy if the lower lobes are mainly affected. When a bilateral procedure is contraindicated, a unilateral approach may be an option. It is not yet clear whether an approach by thoracoscopy allows adequate surgical removal of all affected areas and whether the morbidity is lower. Laser ablation is a further therapeutic option but is much less effective than the surgical resection. Reinforcement of sutures using bovine pericardium strips reduces the chance of a prolonged air leak but is expensive. The results from our institution in 57 patients 1 month after LVR surgery showed the following improvement in dyspnea was a consistent finding in 88% of patients, the 6-min walking distance increased on average by 150 m, the FEV1 by 0.3 1 for unilateral LVR and 0.5 1 for bilateral LVR. The mean PaO2 in ambient air increased 6 mmHg after unilateral and 8 mmHg after bilateral LVR. There was also a significant improvement in respiratory muscle function and a reduction in respiratory drive. A significant improvement in quality of life was documented in 83% of the patients. Major hospital complications are prolonged air leak, pneumonia, and myocardial failure. Three cases of a delayed pneumothorax were observed. Early hospital mortality (< 30 days) was 1.7% and 90 days mortality 3.4%. Few follow-up data are available beyond 1 year, and the long-term benefit of LVR surgery therefore remains to be defined.
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PMID:[Principles of lung volume reduction]. 908 81

Among patients with heart failure who survive an admission to the hospital, those who are readmitted or die soon after discharge may warrant special attention. Therefore, we prospectively followed 257 patients admitted nonelectively to an urban university hospital, with a complaint of shortness of breath or fatigue and evidence of congestive heart failure on admission chest radiograph, who were discharged alive. Through survey of patients and families, review of the hospital computer system, and a search of the National Death Index, we recorded death and hospital readmission. Within 60 days of discharge, 13 patients (5%) died and 82 (32%) died or were readmitted to the hospital. Using Cox proportional-hazards modeling, the multivariable correlates of readmission or death were single marital status (adjusted hazard ratio [HR] 2.1, 95% confidence interval [CI] 1.3 to 3.3), Charlson Comorbidity Index score (HR 1.3 per point to maximum 4 points, 95% CI 1.1 to 1.6), admission systolic blood pressure of < or = 100 mm Hg (HR 2.8, 95% CI 1.6 to 5.0), and absence of new ST-T-wave changes on the initial electrocardiogram (HR 1.9, 95% CI 1.1 to 3.3). Self-reported patient compliance and clinical instability at discharge were not correlates. Almost all patients stratified by these factors had at least a 25% risk of readmission or death. Our independent correlates of readmission or death support the importance of both medical and social factors in the pathway to clinical decline. However, we could not reliably identify a truly low-risk group. Interventions to decrease early readmission or death among patients with heart failure should target both medical management and the adequacy of social support, and probably need to be applied to all admitted patients.
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PMID:Correlates of early hospital readmission or death in patients with congestive heart failure. 920 55

Short-term goals of heart failure management are directed toward relieving symptoms such as shortness of breath, decreased exercise tolerance, and lower-extremity edema and improving functional capacity and quality of life. Long-term goals include decreasing mortality and slowing or reversing the underlying cardiac structural abnormalities of heart failure. Improvement in symptomatic endpoints (e.g., exercise tolerance) does not necessarily correlate with endpoints for improved survival (e.g., left ventricular ejection fraction). It is therefore important to evaluate the effects of drugs on these distinct endpoints separately. Symptoms of heart failure are commonly managed with the use of diuretics, vasodilators, and positive inotropes or digoxin. Ideally, therapy should consist of a diuretic plus vasodilator (e.g., angiotensin-converting enzyme [ACE] inhibitor or isosorbide dinitrate plus hydralazine), with or without digoxin. Prevention of further left ventricular dysfunction can be accomplished by inhibiting neurohormonal processes and ventricular remodeling that occur in heart failure using ACE inhibitors, nitrates and hydralazine, or beta blockers. Significant therapeutic advances have been made with respect to symptom relief, hospitalizations, and mortality reduction in patients with congestive heart failure. Despite these advances, patient morbidity and mortality remain high and underscore the necessity for optimal use of existing therapies along with research directed at achieving further improvements in both quality of life and life expectancy.
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PMID:Overview of the treatment of heart failure. 941 37

A 68-year-old man presented to another hospital with progressive shortness of breath, dry cough, and systemic edema. A chest X-ray, echocardiogram, and chest CT showed a mediastinal mass and massive pericardial effusion. His symptoms improved after the treatment for heart failure. The pericardial effusion was bloody. In that, malignant cell wasn't proved. Thoracotomy was performed to diagnose the mediastinal tumor and to extirpate it. Pathological diagnosis after operation was thymoma with direct invasion to pericardium and tunica externa of aorta. Thymomas are routinely asymptomatic for prolonged periods of time. Symptomatic pericardial tamponade as initial manifestation due to a thymoma with a massive pericardial effusion is uncommon.
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PMID:[Invasive thymoma with pericardial tamponade as initial manifestation]. 945 8

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.
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PMID:Evolving concepts of heart failure: cooling furnace, malfunctioning pump, enlarging muscle--Part I. 954 47

The majority of persons sustaining acute myocardial infarction are older, and in these older persons morbidity and mortality are high. Clinical presentations and characteristics are significantly different between older and younger infarction patients. Older infarction patients are more likely to be female and to have a history of heart failure, but they are less likely to have a family history of myocardial infarction, elevated cholesterol, or to smoke. Older patients will frequently have unrecognized or silent myocardial infarctions or, when present, symptoms will be atypical. Instead of chest pain, older patients may have shortness of breath or neurological symptoms, such as confusion. Also, older infarction patients will delay longer in seeking medical assistance after onset of symptoms, and often will not demonstrate ST elevation or Q waves on their electrocardiograms. Not infrequently, older infarction patients will demonstrate major complications such as heart failure or right ventricular infarction on hospital admission, and their presenting complaints will reflect these complications. Because of these atypical presentations and the wide variability of symptoms, physicians must be highly suspicious of the presence of an acute myocardial infarction in older patients who have an unexplained acute change in their physical condition.
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PMID:Management of the older patient with acute myocardial infarction: difference in clinical presentations between older and younger patients. 973 13

A case is reported in which an undiagnosed bronchogenic carcinoma presented clinically with sudden onset shortness of breath and cardiac failure due to the development of an acute bronchopericardial fistula.
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PMID:Bronchogenic carcinoma presenting as a bronchopericardial fistula. 1034 53

A 50-year-old man received an orthotopic heart transplant because of severe coronary heart disease and congestive heart failure. Two years after the transplantation, a continuous murmur occurred at the left sternal edge after repeated endomyocardial biopsies. Echocardiography and coronary angiography revealed a dilated left anterior descending artery with a fistula to the right ventricle. The circumflex was large with an equally postero-lateral branch, and the right coronary artery was rather small with collaterals to the distal part of the left anterior descending branch. The patient had refused any intervention to close the fistula. The left ventricular levogram was normal. Two years later, in a follow-up angiogram, the left ventricular ejection fraction had decreased as a result of hypo- and akinesis of the apex and posterior wall. We suggest that this local wall motion disturbance derives from a steal phenomenon rather than being a sequela of rejection. The decrease in left ventricular ejection fraction was associated with shortness of breath upon moderate exercise. Standard heart failure medication relieved the patient's symptoms. The observation of local wall motion disturbances in this case, as well as conflicting views in the literature, raises the question whether postbiopsy coronary fistulas in transplant patients should be closed.
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PMID:Segmental degradation of left ventricular wall motion after persistent coronary fistula in a posttransplantation patient: a case report and short review of literature. 1085 6

Because the transplanted heart is denervated, classic angina as a symptom of allograft coronary vasculopathy rarely is perceived. Any cardiac transplant patients who presents with decreased exercise capacity, shortness of breath, or syncope should be assessed thoroughly. Unfortunately, the initial presenting symptom of transplant vasculopathy may be acute myocardial infarction, heart failure, or even sudden death. Patients should be evaluated on an annual basis for the presence of transplant coronary vasculopathy in addition to when clinical suspicion warrants. Coronary angiography has been the main modality of invasive assessment, although it is insensitive. Recently, intracoronary ultrasound has been used in conjunction with angiography to detect the first evidence of transplant vasculopathy, manifested as thickening of the intimal layer of the vessel wall due to smooth muscle cell proliferation, which ultimately leads to luminal narrowing. Patients with evidence of vasculopathy should undergo functional evaluation with dobutamine echocardiography to document ischemic burden. Preventive measures include traditional coronary risk factor modification. Patients are started on statins early in the post-transplantation period and hypertension is treated aggressively using calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors. Because of their deleterious metabolic effects, steroids may be withdrawn under close surveillance for rejection. After transplant vasculopathy has developed, it is difficult to treat and options are limited. Patients with discrete luminal obstructions may undergo angioplasty, stenting, or coronary artery bypass. However, these procedures are palliative, and the only definitive therapy is retransplantation.
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PMID:Transplant Coronary Vasculopathy. 1113 90

A patient with a history of tachycardiac atrial fibrillation and pulmonary embolism was admitted to the emergency unit with acute shortness of breath. The patient was on coumarin medication. Pulmonary embolism, heart failure, or pulmonary edema could be ruled out. Laryngoscopy revealed a huge hematoma of both valleculae extending to the lateral pharyngeal wall and the epiglottis. The epiglottic cartilage was displaced to the posterior pharyngeal wall. The INR was > 6. Prothrombin complex, vitamin K1, corticoids, and fresh frozen plasma were administered immediately. The patient was monitored--without tracheotomy--in the intensive care unit and received oxygen. In a patient with dyspnea, impaired ventilation has to be considered besides impaired perfusion or diffusion.
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PMID:[Dyspnea caused by spontaneous hematoma of the oropharynx and larynx during marcumar therapy]. 1132 Jun 26


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