Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The utility of B-type natriuretic peptide (BNP) testing in patients with atrial fibrillation (AF) is poorly defined. We analyzed patients (n=452) included in the BNP for Acute Shortness of Breath Evaluation (BASEL) study. Patients were randomly assigned to a diagnostic strategy with or without the use of BNP. Ninety-nine patients presented with AF (n=48 BNP group; n=51 control group). Although comparable with respect to gender and cardiopulmonary comorbidity, patients with AF were older and more often had heart failure as the cause of dyspnea. In addition, patients with AF had higher in-hospital mortality (13% versus 6%, P=0.012). The use of BNP significantly reduced time to discharge (BNP group median 8 days [1-16] versus 12 days [IQR 4-21] control group; P=0.046) in patients with AF. Initial total treatment costs (median) were $4239 [769-7422] in the BNP group and $5940 [4024-10848] in the control group (P=0.041). These benefits were maintained after 90 days: patients in the BNP group had spent fewer days in hospital (10 days [2-21] versus 15 days [IQR 9-27]; P=0.022) and induced lower total treatment costs ($4790 [1260-9387] versus $7179 [4311-13173]; P=0.016). In conclusion, the use of BNP seems to improve the management of patients with AF presenting with dyspnea.
 ...
PMID:The use of B-type natriuretic peptide in the management of patients with atrial fibrillation and dyspnea. 1861 86

Acute decompensated heart failure (ADHF) is a common syndrome that precedes over 100,000 hospitalizations in Canada per year (with length of stay in excess of six to eight days), making this the most costly disorder for patients older than 65 years of age. Over 85% of ADHF patients present with shortness of breath and exhibit evidence of volume overload. These findings may be variable in elderly patients, which complicates diagnosis. In fact, even in experienced centres, diagnostic accuracy is less than 80%. Despite advances in the treatment of chronic heart failure, meaningful improvements in outcomes associated with ADHF are very few. The basic assessment and treatments have not changed (early parenteral diuretics, electrocardiographic and oxygen saturation monitoring, supplemental oxygen administration). The introduction of measurement of natriuretic peptides in those in whom the diagnosis is uncertain may reduced the error rate by over 50%. The use of vasodilator therapy in the absence of cardiogenic shock can lead to earlier amelioration of symptoms, especially in those who do not respond to initial diuretics. Repeated monitoring of vital signs, body weight, electrolytes and creatinine levels is essential to minimize the risk of side effects of treatments. Noninvasive ventilation may reduce the need for endotracheal intubation in patients with severe ADHF and hypoxia at rest. Once the initial phase of heart failure treatment is completed, then the clinician should begin to focus on maximization of chronic heart failure therapy and discharge planning.
 ...
PMID:Current treatment options for early management in acute decompensated heart failure. 1862 82

Newer cancer therapies have improved the survival of patients with cancer and, in some cases, turned cancer into a chronic disease. Patients are now surviving long enough for the adverse cardiovascular effects of some cancer therapies to become apparent. The anthracyclines are perhaps the most notorious offenders. Acute reactions include chest discomfort and shortness of breath consistent with a myopericarditis. Toxicity can also develop months after the last chemotherapy dose and typically presents as new onset heart failure with left ventricular systolic dysfunction. Late reactions are seen years after presentation as new-onset cardiomyopathy, often in patients who were treated for childhood neoplasms. 5-Fluorouracil, its prodrug capecitabine, and trastuzumab, a tumor-specific antibody, have also been associated with cardiotoxicity. Until adequate predictive models, prevention modalities, and treatments can be identified, the clinician's focus should be on aggressive monitoring for early signs of cardiac dysfunction in order to prevent severe systolic dysfunction and its concomitant morbidity and mortality.
 ...
PMID:Chemotherapy and cardiotoxicity. 1866 Jul 28

We experienced 2 patients of valvular heart disease in Parkinson's patients taking cabergoline. Patient 1 was a 79-year-old woman who began taking 4 mg cabergoline daily after being diagnosed with Parkinson's disease (PD) in June 2003. She presented with dyspnea in November 2005. The patient had cardiomegaly, pulmonary congestion, and pleural effusion, and an echocardiogram showed valvular heart disease in the form of aortic regurgitation (AR) (grade I), tricuspid regurgitation (TR) (grade I), and mitral regurgitation (MR) (grade III). Cabergoline was thought to have caused these phenomena, so it was replaced with pramipexole, and after administration of diuretics and angiotensin-converting enzyme inhibitors (ACEIs) the patient's symptoms gradually disappeared. MR, AR and TR also disappeared 3 months later. Patient 2 was a 74-year-old woman who presented with sluggish movement in April 2001 and subsequently developed Parkinson's. While being administered 700 mg levodopa (Menesit) and 4 mg cabergoline, the patient presented with shortness of breath in April 2005. An echocardiogram showed valvular heart disease in the form of MR (grade I) and TR (grade I). Heart function improved with the administration of diuretics. However, heart function again worsened in November 2005, and the patient presented with edema of the lungs and lower limbs. An echocardiogram in January 2006 showed worsening MR (grade III) and TR (grade II), and the patient also had pulmonary hypertension. ACEIs were administered along with diuretics and cabergoline was replaced with pramipexole, but the patient also developed malignant syndrome and disseminated intravascular coagulation (DIC) and later died. Patient 2 is the first case in Japan of death due to heart failure caused by the side effects of cabergoline. Caution is usually needed when treating a Parkinson's patient for valvular heart disease due to a dopamine agonist, and periodic checks for heart murmurs and echocardiography are crucial. When signs of heart failure develop during treatment with an ergot preparation of dopamine agonist, it is essential to immediately either stop the administration of the ergot preparation or change to a non-ergot preparation of dopamine agonist.
 ...
PMID:[Two cases of patients with Parkinson's disease developing valvular heart disease while taking cabergoline]. 1871 82

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.
 ...
PMID:Heart failure patients' time, symptoms, and actions before a hospital admission. 1895 14

The purpose of this review is to enlighten the mechanisms of skeletal muscle dysfunction in heart failure. The muscle hypothesis suggests that chronic heart failure (CHF) symptoms, dyspnoea and fatigue are due to skeletal muscle alterations. Hyperventilation due to altered ergoreflex seems to be the cause of shortness of breath. Qualitative and quantitative changes occurring in the skeletal muscle, such as muscle wastage and shift from slow to fast fibers type, are likely to be responsible for fatigue. Mechanisms leading to muscle wastage in chronic heart failure, include cytokine-triggered skeletal muscle apoptosis, but also ubiquitin/proteasome and non-ubiquitin-dependent pathways. The regulation of fibre type involves the growth hormone/insulin-like growth factor 1/calcineurin/ transcriptional coactivator PGC1 cascade. The imbalance between protein synthesis and degradation plays an important role. Protein degradation can occur through ubiquitin-dependent and non-ubiquit-independent pathways. Systems controlling ubiquitin/ proteasome activation have been described. These are triggered by tumour necrosis factor and growth hormone/ insulin-like growth factor 1. However, an important role is played by apoptosis. In humans, and experimental models of heart failure, programmed cell death has been found in skeletal muscle and interstitial cells. Apoptosis is triggered by tumour necrosis factor and in vitro experiments have shown that it can be induced by its second messenger sphingosine. Apoptosis correlates with the severity of the heart failure syndrome. It involves activation of caspases 3 and 9 and mitochondrial cytochrome c release. Sarcomeric protein oxidation and its consequent contractile impairment can form another cause of skeletal muscle dysfunction in CHF.
 ...
PMID:Physiological basis for contractile dysfunction in heart failure. 1899 74

Clinical heart failure has been defined for a long time as a clinical syndrome with symptoms and signs including shortness of breath, cyanosis, ascites, and edema. However, in recent years, with the thought of promoting early diagnosis and heart-failure prevention, the concept of heart failure has often been defined simply as a subject with severe LV dysfunction and a dilated left ventricle, or by some, defined by evidence of increased circulating levels of molecular markers of cardiac dysfunction, such as ANP and BNP. Heart failure has been considered an irreversible clinical end point. Current medical management for heart failure only relieves symptoms, slows deterioration, and prolongs life modestly. However, in the recent years, rejuvenation of the failing myocardium began to seem possible as the accumulating preclinical studies demonstrated that rejuvenating the myocardium at the molecular and cellular level can be achieved by gene therapy or stem cell transplantation. Here, we review selected novel modalities that have been shown in preclinical studies to exert beneficial effects in animal models of severe LV dysfunction and seem to have the potential to make an impact in the clinical practice of heart-failure management.
 ...
PMID:Heart failure management: the present and the future. 1920 20

St. Vincent's Homecare implemented a remote monitoring project in which researchers studied whether the telehome health patients exhibit enhanced clinical outcomes and patient perceptions of telehome healthcare. Fifty congestive heart failure patients (n = 50) participated in this program. Data collection included pre and post Outcome and Assessment Information Set items, 12-Item Short-Form Health Survey and Minnesota Living with Heart Failure Questionnaire, and data from patient charts were used to capture demographic information. In addition, interviews were conducted in order to assess overall perceptions and attitudes. Results indicate significant changes occurring among respondents in three important aspects that impact their quality of life, namely, physical, behavioral, and emotional improvements. Specifically, statistical significance was documented at the 0.05 level regarding improvement for home telehealth patients in shortness of breath, management of oral medications, ability to engage in moderate activities, amount of energy, swelling in legs/ankles, need to sit/lie down during day, fatigue, need for hospitalization, side effects from treatment, and worry. Additionally, patients found the service easy to use and perceived the care they received via telehealth to be as good as regular in-person care.
 ...
PMID:St. Vincent's Home telehealth for congestive heart failure patients. 1929 23

Coronary artery disease either presents with acute chest pain or with exercise induced chest symptoms or shortness of breath. The differentiation between stable and unstable Angina pectoris is prognostically important, unstable angina is managed as an acute coronary syndrome including hospital admission, patients with stable symptoms can be further evaluated in an outpatient setting. A broad differential diagnosis of other cardiac and non-cardiac causes must be considered. Important initial diagnostic steps are cardiovascular risk stratification and prove of ischemia (or scar, necrosis) either at rest or usually exercise-induced, if necessary by additional imaging. Exercise capacity is assessed by physiological parameters (watt, VO2max., MET and distance) during exercise tests like ergometry, spiroergometry or 6-minute walking test (e.g. heart failure patients). Additional factors must be considered for the assessment of working capacity.
 ...
PMID:[Outpatient diagnosis of coronary artery disease]. 1935 34

Heart failure (HF) is prevalent in the aging population. Both pharmacological and non-pharmacological therapies are employed in HF and have yielded significant improvements in survival and quality of life. Body fluid must be maintained at a level sufficient to ensure hemodynamic stability and adequate tissue perfusion, which may decrease neurohormonal activation caused by low cardiac output in patients with HF. However, shortness of breath and peripheral edema caused by fluid overload remain the most common clinical symptoms of HF, causing patient distress. In addition to routine pharmacologic approaches, fluid restriction is frequently suggested in HF management strategies. The purpose of this review of published studies that examined use of fluid/water restriction as an intervention was to determine the optimal fluid intake for HF patients in clinical practice. Four articles describing three clinical trials were identified via PubMed and CINAHL. Their findings suggest that patients with clinically stable HF receiving optimal pharmacological treatment may not benefit from fluid restriction. Patients in these studies had preserved renal function, however, and the trials had no long-term follow-up period. Clinicians choosing to restrict fluid intake for patients with HF should consider an individualized fluid prescription, potentially based on patient body weight, sodium intake, and likelihood of adherence. Further clinical trials are warranted to improve clinical practice in caring for patients with HF.
 ...
PMID:[Evidence-based practice of fluid restriction in patients with heart failure]. 1976 May 74


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>