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

Insomnia is highly prevalent in patients with chronic disease including chronic heart failure (CHF) and is a significant contributing factor to fatigue and poor quality of life. The pathophysiology of CHF often leads to fatigue, due to nocturnal symptoms causing sleep disruption, including cough, orthopnea, paroxysmal nocturnal dyspnea, and nocturia. Inadequate cardiac function may lead to hypoxemia or poor perfusion of the cerebrum, skeletal muscle, or visceral body organs, which result in organ dysfunction or failure and may contribute to fatigue. Sleep disturbances negatively affect all dimensions of quality of life and is related to increased risk of comorbidities, including depression. This article reviews insomnia in CHF, cardiac medication side-effects related to sleep disturbances, and treatment options.
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PMID:Insomnia and chronic heart failure. 1875 45

Peripartum cardiomyopathy (PPCM) is a potentially devastating cause of heart failure that affects women late in pregnancy or in early puerperium. Recent findings showed that a 16 kDa fragment of prolactin may induce myocardial damage, and this offered a new option of treating PPCM by blocking prolactin with bromocriptine. We report on a 35-year-old woman with a twin gravidity who gave birth to two healthy boys at day 36/6 and developed a potentially fatal PPCM. Within 3 days since delivery she suffered from severe symptoms of heart failure (orthopnoea, pleural and pericardial effusion, reduced systolic function LVEF 15%). Bromocriptine 2.5 mg bid was added to standard heart failure therapy at day 6 after delivery, and within a week the patient recovered to NYHA functional class II. 2 months later she presented in a good state, NYHA class I, and MRI confirmed an LVEF of 60%. Balancing the potential side effects of bromocriptine against the very poor prognosis in severe PPCM our case supports the use of bromocriptine as a specific novel therapy.
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PMID:Recovery from peripartum cardiomyopathy after treatment with bromocriptine. 1916 24

The objective of this study was to compare newly diagnosed heart failure (HF) patients (n = 64) with chronic HF patients (n = 148) who had been hospitalized on their presenting symptoms and treatment delay times, whom the 2 groups notified and when, the advice they were given by those notified, and the actions they initiated before their hospitalization. Participants in the 2 groups similarly reported shortness of breath on exertion, orthopnea, weakness, edema, and cough. A greater percent of participants in the group with an HF history reported having fatigue compared to the group with no HF history (chi2 = 4.32, P < .05). Both groups were similar in the time they spent with symptoms before hospital admission (median of 7 days), the time until they notified family members after symptom onset (6 hours to 1.5 days), and the time until they notified their physicians after symptom onset (1.5 to 3 days). The 2 groups varied significantly on the following findings: physicians advised participants with an HF history to call 911 significantly more often than they told the participants with no HF history to call 911 (chi2 = 4.33, P < .05), physicians told those with no HF history to come to the office (chi2 = 5.04, P < .05) or wait for an upcoming appointment (chi2 = 4.78, P < .05) more often than they made those recommendations to the group with an HF history, and participants with an HF history were significantly more likely to call 911 than the participants with no HF history do (chi2 = 4.18, P < .05). The clinical implication is that individuals with either new or worsening HF need to recognize a constellation of possible HF symptoms. Those with chronic HF need to also be aware that increasing fatigue may be an important symptom of worsening HF for them. Both groups of HF patients should report their symptoms promptly to their healthcare providers for early intervention.
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PMID:Heart failure patients' time, symptoms, and actions before a hospital admission. 1895 14

The majority of patients with acute decompensated heart failure are admitted with symptoms of congestion. The classic symptoms of "congestive" heart failure reflect fluid overload, that is, orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema; these symptoms can be so dramatic that it is not surprising that patients seek hospitalization. Activation of the renin angiotensin system coupled with sympathetic hyperactivity results in marked sodium retention and high filling pressures that ultimately bring about these congestive symptoms. The treatment goal of patients hospitalized with volume overload and high filling pressures is to improve symptoms by normalizing the filling pressure and volume status without worsening renal function. The current use of diuretics, vasodilators, and ultrafiltration, as well as potential future use of investigational agents such as oral vasopressin antagonists and adenosine A1-receptor antagonists, is surrounded by the important issues of when to stop intravenous therapy in hospitalized patients and the exact mechanism by which the filling pressures are normalized. New data from evidence-based clinical trials and optimal strategies for monitoring fluid overload will help define this issue and ultimately reduce mortality in these patients.
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PMID:Inpatient management of patients with volume overload and high filling pressures. 1908 92

Patients with chronic heart failure (CHF) exhibit orthopnoea and tidal expiratory flow limitation in the supine position. It is not known whether the flow-limiting segment occurs in the peripheral or central part of the tracheobronchial tree. The location of the flow-limiting segment can be inferred from the effects of heliox (80% helium/20% oxygen) administration. If maximal expiratory flow increases with this low-density mixture, the choke point should be located in the central airways, where the wave-speed mechanism dominates. If the choke point were located in the peripheral airways, where maximal flow is limited by a viscous mechanism, heliox should have no effect on flow limitation and dynamic hyperinflation. Tidal expiratory flow limitation, dynamic hyperinflation and breathing pattern were assessed in 14 stable CHF patients during air and heliox breathing at rest in the sitting and supine position. No patient was flow-limited in the sitting position. In the supine posture, eight patients exhibited tidal expiratory flow limitation on air. Heliox had no effect on flow limitation and dynamic hyperinflation and only minor effects on the breathing pattern. The lack of density dependence of maximal expiratory flow implies that, in CHF patients, the choke point is located in the peripheral airways.
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PMID:Effect of heliox breathing on flow limitation in chronic heart failure patients. 1916 49

The clinical diagnosis of pulmonary embolism (PE) is difficult in coronary care units (CCUs) because many findings of PE are similar to those of acute coronary syndromes and heart failure. Immobilization of only 1 or 2 days may predispose to PE. Heart failure and acute myocardial infarction add to the risk. Dyspnea may be absent or occur only with exertion. The onset of dyspnea may occur over seconds to days. Orthopnea occurs with PE as well as heart failure. When the clinical probability and results of objective testing are discordant, the posttest probability of PE may be neither sufficiently high nor sufficiently low to permit therapeutic decisions. Objective scoring systems for clinical assessment have not been developed for patients in a CCU. d-dimer is likely to be of little value for the exclusion of PE in CCUs, because elevations occur with heart failure, unstable angina, and myocardial infarction. Computed tomographic pulmonary angiography with venous phase imaging of the low pelvic and proximal leg veins (computed tomographic venography) is recommended for imaging. Scintigraphy in women aged <50 years with normal or nearly normal results on chest x-ray may be the preferred imaging test to reduce the risk for radiation. Echocardiography with leg ultrasonography is a rapidly obtainable combination of bedside tests that may be useful for young patients and patients in extremis. In conclusion, the choice of diagnostic test depends on the clinical probability of PE, the condition of the patient, the availability of diagnostic tests, the risks of iodinated contrast material, radiation exposure, and cost.
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PMID:Diagnosis of pulmonary embolism in the coronary care unit. 1926 50

A young woman who had a delivery history 3 months previously presented with dyspnea and orthopnea. Initial findings of physical examination, chest radiography, and echocardiogram showed typical congestive heart failure with severe left ventricular (LV) dysfunction. At first, we considered peripartum cardiomyopathy because she had given birth to a baby 3 months previously. However, even though we massively tried conventional drug therapy for 10 days, the patient still remained with refractory heart failure. We performed additional laboratory studies such as complement level and autoantibodies, of which the results supported systemic lupus erythematosus. We could make the diagnosis of acute lupus myocarditis and treated her with corticosteroid. The symptoms were dramatically disappeared and LV function also improved.
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PMID:Lupus myocarditis presenting as acute congestive heart failure: a case report. 1927 Aug 36

Pulmonary congestion is a hallmark feature of heart failure and is a major reason for hospital admissions in this patient population. Heart failure patients often demonstrate restrictive and obstructive pulmonary function abnormalities; however, the mechanisms of these changes remain controversial. It has been suggested that the bronchial circulation may play an important role in the development of these pulmonary abnormalities and in the symptoms associated with pulmonary congestion. Congestion may occur in the bronchial circulation from either a marked increase in flow or an increase in blood volume but with a reduction in flow due to high cardiac filling pressures and high pulmonary vascular pressures (a stasis like condition). Either may lead to thickened bronchial mucosal and submucosal tissues and reduced airway compliance resulting in airway obstruction and restriction and a lack of airway distensibility. These structural changes may contribute to "cardiac asthma" and dyspnea, characteristic features common in HF patients. Thus the bronchial circulation may be a potential target for therapeutic interventions. The aim of this paper is to review factors governing the control of the bronchial circulation, how bronchial vascular conductance may change with HF and to pose arguments, both supporting and in opposition to the bronchial circulation contributing to congestion and altered pulmonary function in HF. We ultimately hypothesize that the engorgement of the bronchial circulatory bed may play a role in pulmonary function abnormalities that occur in HF patients and contribute to symptoms such as orthopnea and exertional dyspnea.
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PMID:Does the bronchial circulation contribute to congestion in heart failure? 1946 10

Prospective population studies of incident heart failure (HF) are often limited by difficulties in assembling HF-free cohorts. In this study, public-use copies of the Cardiovascular Health Study (CHS) data sets were used to determine the sensitivity, specificity, and positive and negative predictive values of orthopnea and paroxysmal nocturnal dyspnea (PND), with and without the use of medications used in CHS HF criteria (diuretics plus digoxin or vasodilators), in the diagnosis of prevalent HF and in the assembly of a relatively HF-free population. Of the 5,771 community-dwelling older adults aged > or =65 years, 803 had orthopnea, 660 had PND, 1,075 had either symptom, 388 had both symptoms, 547 were using HF medications, and 4,315 had neither symptom and were not using HF medications. Definite HF was centrally adjudicated in 272 participants. The sensitivity, specificity, and positive and negative predictive values for either orthopnea or PND were 52% (95% confidence interval [CI] 46% to 58%), 83% (95% CI 82% to 84%), 13% (95% CI 11% to 15%), and 97% (95% CI 97% to 98%), respectively, and those for either orthopnea or PND or the use of HF medications were 77% (95% CI 72% to 82%), 77% (95% CI 76% to 79%), 14% (95% CI 13% to 16%), and 99% (95% CI 98% to 99%), respectively. In conclusion, only <20% of those with either orthopnea or PND had definite HF, which limits their usefulness in the diagnosis of prevalent HF in the community. However, nearly 99% (negative predictive value) of those with neither symptom nor using HF medications also did not have HF, which may be useful as a simple and inexpensive tool in assembling relatively HF-free cohorts for prospective population studies of incident HF.
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PMID:Value of orthopnea, paroxysmal nocturnal dyspnea, and medications in prospective population studies of incident heart failure. 1957 57

It seems that the causes of the insomnia are dyspnea and an orthopnea in the heart failure patient. But, only such a fit is not the cause of the insomnia because it complains about the insomnia even if heart failure is slight. An obstructive sleep apnea (OSA) is the risk of the heart failure. A heart failure patient often complicates a central sleep apnea (CSA) and a Cheyne-Stokes respiration (CSR), and has much sleep fragmentation and difficulty maintaining sleep. And sleep disorders are sometimes started by the medications such as the cardiovascular system agent thing; beta blocker and the statins. Sleep disorders represent a major challenge in terms of differential diagnosis in heart failure patients. This is particularly relevant to insomnia and sleep disordered breathing (SDB) such as OSA, CSA and CSR. Thus, expending the knowledge on both insomnia and SDB may contribute to improve medical quality among physician.
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PMID:[Heart failure]. 1976 33


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