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 authors present the clinical history of a 70-year-old male with arterial hypertension who sought medical advice because of dyspnea on exertion, orthopnea and episodes of paroxysmal nocturnal dyspnea. The electrocardiogram showed left arterial hemiblock and abnormalities of ventricular repolarization compatible with a left lateral endocardiac lesion. Echocardiography revealed a hypertrophied left ventricle with a small ventricular cavity, compatible with an infiltrative-restrictive myopathy. Blood chemistry showed creatinine 4.9 mg/dl, BUN 133 mg/dl and alkaline phosphatase 204 i.v. The patient expired because of intractable heart failure. The histopathological examination of a piece of myocardium (authorized by the family) stained with Congo red confirmed the presence of abundant, diffuse deposits of amyloid, as had been suspected because of the echocardiographic findings.
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PMID:[Cardiac amyloidosis secondary to multiple myeloma detected by echocardiography]. 774 97

The aim of this study was to bring to light new and simple criteria, obtained during cardiopulmonary exercise testing, in order to demonstrate in patients the cardiac or the pulmonary origin of a comparable exertional dyspnea. Forty male subjects were compared, who exercised with a 30-W/3-min protocol and were divided into three groups: the cardiac heart failure (CHF) group (n = 15), the chronic obstructive lung disease (COLD) group (n = 15), and the control group (n = 10). The two groups of patients differed totally from the control group concerning their spirometric values at rest and a clear inability during effort which was confirmed by all the studied cardiopulmonary parameters at maximal exercise. The CHF and COLD groups differed slightly concerning their maximum symptom-limited oxygen uptake, only when related to body mass (13.26 +/- 0.69 ml/kg/min in CHF group, 17.05 +/- 1.59 ml/kg/min in COLD group; p < 0.05), and concerning their maximum ventilatory equivalent for oxygen which tended to be higher in the CHF group in comparison with the COLD group (p = 0.082). Furthermore, and as foreseen, the two groups of patients clearly differed at maximum exercise concerning the ventilatory reserve respiratory parameter (49.73 +/- 3.18 percent in CHF group, 8.38 +/- 5.85 percent in COLD group; p < 0.01). On the other hand, they did not differ concerning cardiac parameters or those considered as such (maximum heart rate [HR], HR reserve, HR response, maximum O2 pulse measurement). While their maximum ventilation was similar in the CHF and COLD groups, a difference in adaptation during exercise was found by observing their breathing pattern. In the CHF group, this was demonstrated by a significantly lower breathing frequency at maximum exercise (31.24 +/- 1.53 beats/min vs 37.75 +/- 2.24 beats/min; p < 0.05) and a tidal volume that tended to be higher at maximum exercise (p = 0.077) and significantly higher at 60-W work load (p < 0.05). This work shows that the study of ventilatory reserve and breathing pattern during exercise testing allows one to discriminate if dyspnea on exertion in patients is due to cardiac or respiratory disease.
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PMID:Cardiopulmonary exercise testing. Determinants of dyspnea due to cardiac or pulmonary limitation. 777 2

Patients with heart failure are frequently limited by exertional dyspnea. The mechanisms underlying dyspnea in these patients remain unclear. In this review, the pathologic changes that occur in the lung as a consequence of chronic pulmonary venous hypertension, pulmonary function test abnormalities, and potential mechanisms for dyspnea including airflow obstruction and/or respiratory muscle dysfunction are discussed.
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PMID:Pulmonary factors limiting exercise capacity in patients with heart failure. 777 67

Although exertional dyspnea is an important symptom limiting daily lives in patients with chronic heart failure, there is no objective assessment of this symptom. To characterize the exertional dyspnea, ventilatory responses to exercise were studied in relation to exertional dyspnea. Gas exchange data were obtained during a maximal bicycle exercise in 43 patients with chronic heart failure and 20 normal subjects. In addition to standard ventilatory variables, the ventilation mode was assessed from the tidal volume-ventilation rate (VT-f) relationship. The exercise was performed again after sublingual administration of 5 mg of isosorbide dinitrate. In normal subjects, the f and VT increased almost proportionally with exercise intensity. In 17 (85 percent) of 20 patients with exertional dyspnea, the VT-f relationship abruptly lost linearity at the onset of exertional dyspnea. This change resulted from an inadequate increase in VT and a further increase in f. In 8 of these 17 patients, isosorbide dinitrate improved exertional dyspnea with normalization of the VT-f relationship; however, in 9 patients whose dyspnea was not improved, the abnormal VT-f relationship was unaltered. Only 2 (9 percent) of 23 patients without exertional dyspnea showed the abnormal VT-f relationship. Other ventilatory variables were not different between patients with and without dyspnea. Thus, exertional dyspnea is characterized by simultaneous appearance of rapid and shallow ventilation. The VT-f relationship appears to be a simple and useful objective assessment of exertional dyspnea in patients with chronic heart failure.
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PMID:A characteristic change in ventilation mode during exertional dyspnea in patients with chronic heart failure. 792 67

Spirometry was performed by 5,201 elderly participants of the Cardiovascular Health Study during their baseline examination and a subset of the ATS/DLD-78 respiratory questionnaire was administered by trained interviewers. In never smokers (46 percent of the cohort), the overall prevalence of chronic cough was 9 percent, chronic phlegm was 13 percent, attacks of wheezing with dyspnea were 8 percent, and grade 3 dyspnea on exertion was 10 percent. The prevalence of lung disease in current smokers (12 percent of the cohort) was 8/7 percent (men/women) with chronic bronchitis and 14/5 percent with emphysema. Overall, 6 percent reported asthma (a physician-confirmed history) and 12 percent reported hay fever. Using a logistic regression model, attacks of wheezing with dyspnea were strongly associated with a lower FEV1, coronary heart disease, heart failure, and a large waist size (in participants without a diagnosis of asthma, chronic bronchitis, or emphysema). Undiagnosed airways obstruction was twice as likely in women and those with lower income, and was associated with current and former smoking, pack-years of smoking, and chronic cough. Dyspnea on exertion (DOE) was three times or more likely if a participant reported heart failure, coronary heart disease, or emphysema; and much more likely if their FEV1 or FVC was substantially reduced. Dyspnea on exertion was also positively associated with older age, chronic bronchitis or asthma, a larger waist or hip size, pack-years of smoking, and less education. We conclude that DOE and attacks of wheezing with dyspnea are commonly associated with cardiovascular disease and a low FEV1 in those over 65 years and that airways obstruction frequently remains undiagnosed in the elderly.
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PMID:Prevalence and correlates of respiratory symptoms and disease in the elderly. Cardiovascular Health Study. 808 66

A 64-year-old man who had received a Carpentier-Edward mitral valve replacement seven years earlier was seen with dyspnea on exertion. After re-replacement of the mitral valve with SJM prosthesis, the patient developed acute left-sided heart failure on the third postoperative day. Transesophageal echocardiography revealed abnormal lumen posterior to the left atrium with regurgitant flow from the left ventricle. Right and left atriotomy revealed dissection of the interatrial septum and after removal of the prosthesis, communication between the left ventricle and the dissected lumen was recognized. After closing the communicating orifice, SJM prosthesis was again sutured on the mitral annulus with sub-annular pledgets to reinforce the annular attachment. Excessive debridement of the annular tissue was thought to be a causative factor to develop the dissection of the interatrial septum after mitral valve replacement.
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PMID:[Acute dissection of the interatrial septum after re-replacement of the mitral valve--a case report]. 808 81

This multicenter study evaluated the efficacy and tolerability of coenzyme Q10 in 1715 outpatients with chronic heart failure (New York Heart Association classes II and III), stabilized with standard therapy for 3 months. The patients were treated with coenzyme Q10 at a daily dose of 50 mg for 4 weeks, in addition to receiving conventional therapy. The efficacy of coenzyme Q10 was assessed by an open study that evaluated the improvement in clinical signs and symptoms of heart failure. After the baseline evaluation the subjects were seen on days 15 and 30. The intensity of signs and symptoms was assessed by a semiquantitative 4-point scale. Our results demonstrate that the administration of coenzyme Q10 in association with standard therapy improves dyspnea at rest, exertional dyspnea, palpitations, cyanosis, hepatomegaly, pulmonary rales, ankle edema, heart rate, and systolic and diastolic blood pressure in patients with stabilized heart failure. The rate of improvement and the low number of side effects in this large group of patients demonstrate that despite some methodological limitations in the study design and the short period of treatment (4 weeks) coenzyme Q10 given at a daily dose of 50 mg led to an improvement in the signs and symptoms of heart failure and in the quality of life.
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PMID:Italian multicenter study on the efficacy and safety of coenzyme Q10 as adjuvant therapy in heart failure. 824 96

Infundibular pulmonic stenosis with intact ventricular septum of primary origin is an uncommon condition. We report 15 such patients (nine males and six females, aged 7-36 years) who had undergone surgical correction for the anomaly during the period between 1975 and 1992. The occurrence of this clinical setting represents 0.19% (15/7826) of all cardiac operations and 0.46% (15/3222) of congenital heart diseases undergoing surgical correction during that period of time. The lesion was of discrete fibromuscular hypertrophy of the infundibulum in all 15 patients. The presenting symptoms of most patients were exertional dyspnea and syncope; however, five patients with severe obstruction were asymptomatic. The peak systolic pressure gradient across the infundibulum ranged from 71 to 230 mmHg. There was only one operative death; the remainder had remained well following the surgery over a mean follow-up period of 35 months. Surgical correction for infundibular pulmonic stenosis is rewarding in the absence of heart failure.
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PMID:Infundibular pulmonic stenosis with intact ventricular septum: a report of 15 surgically corrected patients. 828 34

A 39-year-old male was admitted with persistent cough, palpitations and dyspnea on exertion. Chest X-ray showed cardiomegaly, left pleural effusion and left hilar mass shadow. Echocardiogram revealed dilatation and hypertrophy of the right atrium and ventricle. Perfusion lung scintigram disclosed a complete defect of the left lung and a partial defect of the right upper lobe. CT scan showed an intravascular tumor mass in the bilateral main pulmonary arteries. Digital subtraction angiography of the pulmonary artery revealed complete obstruction of the left pulmonary artery and stenosis of the right pulmonary artery. MR image showed intravascular tumor infiltrating the mediastinum and surrounding tissue. Sarcoma was highly suspected, but a histopathological diagnosis could not be made. The patient died of heart failure two months after admission to our hospital. Postmortem examination showed that the pulmonary trunk and left main pulmonary artery were markedly dilated and completely occluded by the tumor. Tumor infiltrated into the left upper lobe and mediastinal lymph nodes. The tumor was histologically diagnosed as undifferentiated sarcoma.
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PMID:[A case of primary pulmonary artery sarcoma]. 834 15

Exertional intolerance is a major clinical problem in ambulatory patients with chronic heart failure and is associated with both muscle fatigue and dyspnea. The increased muscle fatigability is most likely caused by a combination of muscle underperfusion and muscle deconditioning; patients frequently exhibit skeletal muscle atrophy, altered muscle metabolism and reduced mitochondrial-based enzyme levels, consistent with deconditioning. The muscle underperfusion is largely due to impaired arteriolar vasodilation within exercising muscle. Exertional dyspnea appears to be due to increased respiratory muscle work mediated by excessive ventilation and decreased lung compliance. Both excessive carbon dioxide production, secondary to increased muscle lactate release, and increased lung dead space contribute to the excessive ventilation. Decreased lung compliance is caused by chronic pulmonary congestion and fibrosis. Optimal management of exercise intolerance in patients with heart failure requires an understanding of the role of these multiple potential contributors to exertional fatigue and dyspnea.
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PMID:Factors contributing to the exercise limitation of heart failure. 837 1


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