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

The patient was a 74-year-old woman who had been obese since age 18. Her obesity was refractory to dietary manipulation. She had been suffering from increasing dyspnea for several months and eventually could not even move. She was admitted to a hospital and diagnosed as having heart failure. Although her cardiac function recovered with medical treatment, her symptoms did not improve. The patient was then sent to our hospital. On admission, her height and weight were 149 cm and 81.9 kg, respectively, yielding a body mass index (BMI) of 36.6 kg/m2. Arterial blood gas analysis in room air revealed hypoxemia and an apnea index of 27 per hour. She was given a daily 500-1000 kcal diet. After four months of treatment, her weight decreased to 65 kg with a BMI of 29.3 kg/m2. Weight reduction together with the usage of progesterone-derivatives resulted in marked improvement of sleep apnea. The apnea index decreased to 3/h and arterial blood gas values normalized. This patient seemed to have suffered from both obesity hypoventilation syndrome and sleep apnea syndrome. Improvement of respiratory function was achieved through relief of airway obstruction and weight reduction, with activation of the respiratory center due to progesterone treatment.
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PMID:[Improvement of respiratory function with weight reduction in obese elderly]. 149 51

Physicians analyzed December 1982-November 1989 data on 48 2-60 month old children with empyema thoracis at the University of Calabar Teaching Hospital in southeastern Nigeria to determine the incidence and etiology of empyema thoracis in this region. The incidence rate stood at 2/1000 pediatric admissions. 3 children died (6.3%), all of heart failure. 47 children suffered from fever, cough, and breathlessness, the symptoms for pneumonia. Even though bronchopneumonia is a common complication of measles which occurs frequently in Calabar, only 3 children (6.25%) also had measles. The most frequent complication of this accumulation of pus in the thoracic cavity was congestive heart failure (16 cases). 47 patients suffered from anemia (hemoglobin levels 11 gm/dl). Hemoglobin levels of 54% of all patients decreased over time to 8 gm/dl. In fact, 2 children had hemoglobin levels of 4.4 gm/dl and they experienced cardiac failure. Laboratory personnel were only able to examine pleural aspirates from 37 patients. They did not detect any organisms in 27% of these aspirates. This may have been due to parent's widespread practice of giving medication to all the children before coming to the hospital. 45.9% of the aspirates only grew Staphylococcus aureus while another 8.1% grew it and other pathogens. About 90% of the pathogens were resistant to ampicillin and penicillin and almost 90% were sensitive to cloxacillin, gentamicin, and erythromycin. Cloxacillin was very expensive and parenteral erythromycin was unavailable. Nevertheless the pediatricians used parenteral gentamicin and cloxacillin. The parents were responsible for buying the antibiotics which tended to be costly. All the patients required emergency closed tube thoracostomy drainage within 24 hours of admission. 83.3% remained in the hospital for 2 weeks and 33.3% for 1 month. Despite the rarity of empyema, long hospitalization and expensive drugs make it an important disease in Calabar.
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PMID:Clinical and bacteriological study on childhood empyema in south eastern Nigeria. 150 92

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
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PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

The clinical features of congestive heart failure in the elderly were investigated in 104 patients (57 males, 47 females, mean age of 79.2). Patients were divided into two subgroups, the readmission group, 33 patients who were readmitted within 6 months after discharge, and the non-readmission group. Chief complaints were dyspnea, edema, chest pain, loss of appetite, chest compression, and palpitation. Heart failure was caused by infection, myocardial ischemia, arrhythmia, inappropriate drug usage including poor drug compliance, the use of beta-blockers, excessive intake of sodium, and anemia. Careful use of drug was essential especially in the readmission group. Major underlying heart disease were ischemic heart disease (39.4%), valvular disease (26.9%), hypertensive heart disease (9.6%), with cardiomyopathy, congenital heart disease seen in the minority. There was no statistically significant difference in underlying heart diseases between the two groups. Supraventricular arrhythmias such as atrial fibrillations, paroxysmal atrial fibrillations, paroxysmal supraventricular tachycardias, and premature atrial contractions were noted in 85.3% of the cases. Drugs for treatment were diuretics, digitalis, isosorbide dinitrate, calcium antagonists. ACE inhibitors and alpha-blockers were also used, showing that vasodilators were more extensively used than before. The major complications were hypertension (39.4%), renal dysfunction (27.9%), cerebrovascular disease (26.9%), diabetes mellitus (16.5%), arteriosclerosis obliterans (7.7%). Renal dysfunction, arteriosclerosis obliterans was seen significantly more frequently in the readmission group. The prognosis at one year after admission was significantly worse in the readmission group. In summary, the major underlying diseases were ischemic heart disease, valvular disease, and hypertensive heart disease. Ischemic heart disease was seen more frequently than in previous investigations at our hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congestive heart failure in elderly readmitted patients]. 152 7

To determine the reliability and validity of a patient outcome questionnaire for chronic heart failure, a randomized, double-blind, placebo-controlled, 3-month trial of pimobendan, an investigational medication with inotropic and vasodilator activities, was performed. Evaluated were 198 ambulatory patients with primarily New York Heart Association (NYHA) class III heart failure from 20 referral centers. Baseline therapy included digoxin, diuretics and, in 80%, a converting enzyme inhibitor. Oral pimobendan at 2.5 (n = 49), 5.0 (n = 51), or 10 (n = 49) mg daily or matching placebo (n = 49) was administered. The Minnesota Living with Heart Failure (LIhFE) questionnaire was a primary outcome measure, along with an exercise test. Interitem correlations identified subgroups of questions representing physical and emotional dimensions. Repeated baseline scores were highly correlated (r = 0.93), as were the physical (r = 0.89) and emotional (r = 0.88) dimension scores. Placebo did not have a significant effect with median (25th, 75th percentile) changes from baseline scores of 1 (-3, 5), 1 (-2, 3), and 0 (-1, 2), respectively (all p values greater than 0.10). The 5 mg dose significantly improved the total score, 7.5 (0, 18; p = 0.01) and the physical dimension, 4 (0, 8; p = 0.01), compared with placebo. Changes in the total (r = 0.33; p less than 0.01) and physical (r = 0.35; p less than 0.01) scores were weakly related to changes in exercise times, but corresponded well with changes in patients' ratings of dyspnea and fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of patient outcome with the Minnesota Living with Heart Failure questionnaire: reliability and validity during a randomized, double-blind, placebo-controlled trial of pimobendan. Pimobendan Multicenter Research Group. 152 75

A 57-year-old man was admitted with dyspnea and bloody sputum. The chest X-ray showed unilateral alveolar infiltration, and alveolar cell carcinoma was suspected. Physical examination showed orthopnea and a loud systolic murmur, and the echocardiogram showed mitral valve prolapse. A chest X-ray 4 days later revealed bilateral infiltration. The cardiac catheterization showed pulmonary congestion and the capillary wedge pressure revealed a prominent V wave. Papanicolaou's test of sputum was negative. These findings suggested heart failure due to mitral regurgitation rather than lung carcinoma. The patient underwent mitral valve replacement because of his refractoriness to the medical treatment. During the operation, the chordae tendineae of the anterior mitral leaflet was found to be completely ruptured. The mechanisms of unilateral pulmonary edema could not be ascertained, but the effect of posture and gravity was thought to be a possible mechanism.
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PMID:[A case of unilateral pulmonary edema associated rupture of mitral chordae tendineae]. 155 65

The factors that contribute to the symptoms of breathlessness and fatigue, and that limit exercise capacity in patients with chronic heart failure are poorly understood. Recent evidence suggests that the major mechanism is not related to central hemodynamics but to a reduction of skeletal muscle mass and diminished blood flow to skeletal muscle on exercise.
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PMID:Blood flow and skeletal muscle in patients with heart failure. 157 60

Multiple compensatory mechanisms operate to preserve exercise tolerance in patients with left ventricular failure. Exercise capacity of most patients with chronic heart failure is limited by dyspnea or fatigue, or both. Maximal stress testing with direct assessment of peak O2 uptake is an essential measurement in planning exercise conditioning programs, which are now attracting patients with chronic heart failure. The biochemical and histologic patterns of skeletal muscle changes seen in chronic heart failure patients are consistent with the effects of long-term exercise deconditioning in normal subjects. Recent studies have suggested beneficial effects of training in subjects with moderate or even severe left ventricular dysfunction by showing increased exercise tolerance or peak O2 consumption, anaerobic threshold, peak leg blood flow, peak central arteriovenous oxygen difference and decreased lactate accumulation. However, a number of questions remain unanswered. Exercise training for the treatment of chronic heart failure should be determined on an individual basis and used with caution.
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PMID:Physical training in patients with congestive heart failure. 157 63

Mexiletine is thought to exert minimal negative inotropic actions, but its effects have not been evaluated in patients with severe congestive heart failure. The haemodynamic response to an oral loading dose of mexiletine (400 mg) was assessed in 20 patients with severe chronic heart failure. Mexiletine caused marked haemodynamic deterioration, with stroke work index decreasing in 18 of the patients. Two hours after mexiletine, mean cardiac and stroke work indexes decreased by 15% and 25%, respectively (both P less than 0.001), while heart rate and systemic vascular resistance increased by 10% and 20%, respectively (both P less than 0.05). Simultaneously, left ventricular filling pressure and right atrial pressure increased by 37% and 36%, respectively (both P less than 0.001), but mean arterial pressure did not change. Furthermore, clinical deterioration, with onset of dyspnoea at rest, developed in five patients at the time of peak haemodynamic effect. Plasma mexiletine concentrations were within the accepted therapeutic range of 0.5 to 2.0 micrograms.ml-1 in all but two of the patients. Nevertheless, the plasma concentration was an important determinant of haemodynamic effect. The stroke work index decreased by 38% in the patients with a mexiletine level above the median value of 1.3 micrograms.ml-1 (range 25 to 56%), but only 13% (range 15 to 43) in patients with lower plasma concentrations. In conclusion, although mexiletine may cause cardiodepressant effects in any patient with severe left ventricular dysfunction, dosing which results in a high (but still therapeutic) plasma level is more likely to cause haemodynamic deterioration.
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PMID:Cardiodepressant effects of mexiletine in patients with severe left ventricular dysfunction. 157 27

Four years after an HIV infection and without any preceding illness characteristic of AIDS, a 24-year-old woman developed dyspnoea on exertion and peripheral oedema. She had for several years been an intravenous drug addict and contracted hepatitis A and B. There were no symptoms of the HIV infection. Clinical, radiological and echocardiographic examination demonstrated right ventricular failure caused by pulmonary hypertension not due to pulmonary embolism or another known aetiology. The patient died suddenly 9 months after the diagnosis from heart failure. Autopsy established primary pulmonary hypertension with pathognomonic plexogenic pulmonary arterial disease which had led to cor pulmonale with overload myocarditis. Although there had been no clinical signs of renal failure, there was histological evidence of mesangioproliferative glomerulonephritis and non-destructive interstitial nephritis. This case demonstrates that, in addition to the typical AIDS-associated diseases, other rarer syndromes may, in uncertain ways but connected with the HIV infection, decide the prognosis of such patients.
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PMID:[Primary pulmonary hypertension and mesangioproliferative glomerulonephritis in HIV infection]. 158 15


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