Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27 year old woman was hospitalized for progressive dyspnea, fatigue and retrosternal chest pain. She had progressive cardiac enlargement with clinical and laboratory confirmation of a dilated cardiomyopathy. Transvenous percutaneous right ventricular endomyocardial biopsy yielded a specimen showing a noncaseating granuloma. The patient's dyspnea responded dramatically to steroid therapy with corresponding improvement in radiographic and echographic measures of ventricular performance. This case illustrates the problem of diagnosing cardiac sarcoidosis when there is no apparent evidence of other organ involvement.
 ...
PMID:Cardiac sarcoidosis. Diagnosis with endomyocardial biopsy and treatment with corticosteroids. 67 30

Anomalous origin of the left coronary artery (LCA) from the pulmonary trunk (PT) is an uncommon but frequently lethal congenital lesion of infancy. Clinically it may be difficult to distinguish from congestive cardiomyopathy, and the diagnosis is usually made by angiography. We describe the case of a 38 years old woman, in whom identification of this anomaly was achieved by 2D-Echo, pulsed Doppler and color flow mapping. She complained of fatigue, effort dyspnea and atypical chest pain. A II/VI systolic murmur at left sternal border was heard. There was cardiac enlargement on chest X-ray and ECG was suggestive of an old anterolateral myocardial infarction. The 2D-Echo study showed a dilated, poorly contracting left ventricle. A prominent right coronary ostium was recorded, but the LCA ostium could not be visualized. There was retrograde diastolic and systolic flow in proximal PT, where an anomalous vessel was seen in continuity with it by color flow mapping. Cardiac catheterization confirmed the diagnosis. The patient underwent successful reimplantation of the anomalous LCA, from the PT to the aorta. This case demonstrates usefulness of Echocardiography in the assessment of coronary artery anomalies.
 ...
PMID:[Anomalous origin of the left coronary from the pulmonary artery in adults: diagnosis with bidimensional, pulsed and color Doppler echocardiography]. 152 May

A case of right ventricular dilated cardiomyopathy associated with primary biliary cirrhosis is described. The patient was a middle aged woman, who initially complained of fatigue and itching. The diagnosis of primary biliary cirrhosis was made based on clinical, biochemical and histological evidence of the disease. Seven years later severe right-sided heart failure developed. The diagnosis of right ventricular dilated cardiomyopathy was made based on echocardiographic and angiographic evidence of a globally dilated and poorly contracting right ventricle. Left ventricular function was within normal limits. Autoimmune serology screening at this time revealed the presence of organ-specific cardiac antibody (titre 1/20) and of antinuclear antibody (titre 1/80) by indirect immunofluorescence. There were no findings of mitochondrial antibody or other non-organ specific or organ-specific antibodies. Overall, this assessment demonstrates autoimmunity in both hepatic and heart muscle disease in a patient with primary biliary cirrhosis and right ventricular dilated cardiomyopathy.
 ...
PMID:Right ventricular dilated cardiomyopathy associated with primary biliary cirrhosis. 178 56

A novel, simple, rapid and reproducible microassay is used for kinetic analysis of Ca-sequestration by homogenates of myocardium of turkeys with furazolidone-induced congestive cardiomyopathy. The assay monitors Ca in real-time using dual-emission ratiometric spectrofluorometry and the Ca-indicator dye indo-1. Using this assay and isolated SR studies we make several novel findings regarding the mechanism of SR failure in furazolidone cardiomyopathy. Qualitative differences in Ca-sequestration were not detected between groups. However, compared to controls the furazolidone treatment resulted in: 1) 50% depression in maximal activities (1.54 +/- 0.36 vs 0.73 +/- 0.12 microM/sec); 2) 2-fold increases in post-sequestration concentrations of ionized Ca (79 +/- 23 vs 141 +/- 13 nmol Ca/L homogenate); 3) 2-fold increases in Ca half-life (415 vs 790 msec); and 4) 25% increased passive Ca-binding capacity of homogenates. The Ca-ATPase specific activity of isolated sarcoplasmic reticulum was 60% increased in congestive cardiomyopathy (543 +/- 140 vs 873 +/- 108 nmol ATP hydrolyzed/min/mg membrane protein) although membrane yield was 20% decreased (0.79 +/- 0.09 vs 0.63 +/- 0.03 mg/g heart). The increased ATPase and decreased Ca-uptake activities in combination with the occurrence of 36% cardiac hypertrophy and 19% decreased body weights resulted in estimates of the relative energy cost to the animal for myocardial Ca transport being 5.5-fold increased with cardiomyopathy (20.5 vs 111 nmol ATP hydrolyzed per microM decrease of sarcoplasmic free Ca/kg body weight). These data indicate that congestive cardiomyopathy is associated with markedly increased permeability of sarcoplasmic reticulum to Ca and compensatorily increased Ca-ATPase activity. Accelerated energy consumption due to the increased energy cost of Ca transport and increased time of myocyte activation are predicted to predispose the myocardium to fatigue and irreversible failure.
 ...
PMID:Myocardial Ca-sequestration failure and compensatory increase in Ca-ATPase with congestive cardiomyopathy: kinetic characterization by a homogenate microassay using real-time ratiometric indo-1 spectrofluorometry. 182 61

1. Fifty patients with symptoms due to chronic heart failure despite diuretic therapy were randomised to receive additional treatment with either hydralazine or captopril. The dose was titrated; 24 received hydralazine and 26 captopril up to a maximum daily dosage of 225 mg and 75 mg respectively. Forty-three patients had coronary heart disease and seven dilated cardiomyopathy. 2. Dyspnoea and tiredness were assessed using a visual analogue scale (0-100) before and during 12 weeks' treatment. Captopril produced a significantly greater reduction in breathlessness (F = 31.6, P less than 0.001) and tiredness (F = 65.8, P less than 0.001) compared with hydralazine. 3. There was an increase in treadmill exercise time during treatment with both hydralazine (from 5.5 (3.47-7.53) min to 6.9 (4.87-8.93) min), and captopril (from 5.0 (3.05-6.95) min to 7.8 (5.85-9.75) min), but the degree of improvement was significantly greater in the patients treated with captopril (F = 7.4, P less than 0.001). 4. There was no significant change in right ventricular ejection fraction (from 27.9 (19.3-36.5)% to 28.7 (20.1-37.3)%) or left ventricular ejection fraction (from 22.2 (14.2-30.2)% to 23.9 (15.9-31.9)%) during treatment with hydralazine. However, both right and left ventricular ejection fraction increased significantly during treatment with captopril (from 27.1 (18.9-35.3)% to 32.0 (23.8-40.2)%, P less than 0.05; and from 25.0 (17.2-32.8)% to 29.6 (21.8-37.4)%, P less than 0.05 respectively). 5. These results suggest that in patients with symptoms due to chronic heart failure despite diuretic therapy, treatment with captopril produces a greater symptomatic and haemodynamic improvement than treatment with hydralazine.
 ...
PMID:Which vasodilator drug in patients with chronic heart failure? A randomised comparison of captopril and hydralazine. 201 67

A case of right ventricular dilated cardiomyopathy which also involved the left ventricle was reported. On health screening, a 16-year old woman was pointed out to have multifocal PVC and cardiomegaly. Subsequently, she was admitted to our hospital because of general fatigue. CTR was enlarged to 54.9% on chest X-ray. ECG showed LBBB-type PVC, right axis deviation, low voltage and T wave changes. On UCG, RVdD was dilated to 40 mm and LVdD was 37 mm. There was no finding of abnormality of the tricuspid valve. On cardiac catheterization, there was no shunt disease. Intracardiac pressure was normal. The end-diastolic volume index (ml/m2) of RV and LV was 196.7 and 67.4, respectively. And ejection fraction (%) was 20 and 40. Ventriculography revealed diffuse dilatation of the right ventricle. And lowered contractility existed not only in the right ventricle but also in the anterior and apical segment of the left ventricle. T(1)201 myocardial perfusion imaging showed irregular perfusion defect of the left ventricle. Endomyocardial biopsy revealed marked hypertrophy, partial atrophy, disarrangement of myocyte and interstitial fibrosis of the right ventricle. This case was considered to be right ventricular dilated cardiomyopathy. It seemed to be an intermediate form of dilated cardiomyopathy since it also involved the left ventricle. It was an interesting case to illustrate the spectrum of expression of cardiomyopathy.
 ...
PMID:[A case of right ventricular dilated cardiomyopathy, which involved left ventricle]. 228 24

Dynamic cardiomyoplasty aims at restoring ventricular contractility by means of a skeletal muscle sutured around the heart. It consists of transferring a latissimus dorsi muscle flap onto the heart through a window created in the thoracic wall by partial resection of the second rib. The skeletal muscle may be used to reinforce the ventricular systole in ischemic or dilated cardiomyopathy, or to replace the myocardium after resection of a large aneurysm or an extensive tumour. The electronic pacing material includes an implantable cardiomyostimulator, muscle stimulating electrodes and R wave detecting electrodes. Muscular pacing begins 2 weeks after the operation, this being the time required for adhesions to be formed between the heart and the muscle. A progressive and sequential electrostimulation procedure results in the transformation of glycolytic muscle fibres that are fatigue-sensitive into fatigue-resistant oxidative fibres. The purpose of this biomechanical cardiac assistance system, where cardiac surgery is combined with plastic surgery and biomedical engineering, is to prolong life and improve its quality in patients with severe heart failure.
 ...
PMID:[Cardiomyoplasty. Experimental bases, operative technic, indications]. 250 64

Dynamic cardiomyoplasty is a new surgical procedure proposed for treatment of the failing heart. Clinically, the latissimus dorsi muscle is raised as a pedicled flap and wrapped around the heart. The skeletal muscle is transformed to produce a myocardium-like fatigue-resistant muscle. It is stimulated to contract in synchrony with the heart in hope of assisting the myocardial contraction. An R-wave synchronous pacemaker provides a pulse-train form of stimulation to simulate, for the skeletal muscle, the contractile characteristics of the myocardial syncytium. We have undertaken a critical review of the clinical results of dynamic cardiomyoplasty reported to date. Objective evidence of clinical improvement after dynamic cardiomyoplasty resulting from the contractile assistance of the myoplasty has been modest. Many of the beneficial results reported could be explained by concomitant procedures done, such as aneurysmectomy or coronary artery bypass grafting. Hemodynamic studies have failed to demonstrate consistent and convincing improvement as a result of the cardiomyoplasty stimulation. We have, however, identified an interesting subgroup of patients, in whom a striking hemodynamic response to cardiomyoplasty stimulation has been reported. These patients all possess large resting heart volumes characteristic of dilated cardiomyopathy. Thus, case selection may ultimately be one of the most important factors in determining the success of dynamic cardiomyoplasty for the treatment of heart failure.
 ...
PMID:Dynamic cardiomyoplasty for treatment of heart failure. 269 90

Dilated cardiomyopathy, owing to any cause, usually culminates in the clinical syndrome of congestive heart failure. Heart failure is characterized by exertional dyspnea and fatigue, but the precise mechanisms that produce these symptoms are still not clear. Sodium retention occurs early in heart failure, but this disturbance is dynamic in nature and is not always present in the patient. The mechanism of early salt and water retention in heart failure is not defined. Gross edema and ascites occur much later, undoubtedly owing to the convergence of a number of factors. The peripheral adaptations to heart failure include activation of the renin-angiotensin system and the sympathetic nervous system, and the release of AVP. The result is an increase in preload with a resultant increase in stroke volume for some patients, but the price is paid in the form of heightened impedance to ejection and circulatory congestion. The sympathetic nervous system disturbances in heart failure are striking, as disturbances in both circulating and myocardial NE levels are consistently found. Vasorelaxant and natriuretic hormones, as well as certain prostaglandins, may be released in an attempt to offset excessive "compensatory" pressor-sodium retentive mechanisms, but the net result seems to be excessive peripheral vasoconstriction and a downward spiral of deterioration in many patients. One would hope that an unraveling of the complex pathophysiology of heart failure would lead to therapy that would change the natural history of the disease. The results of the first V-HeFT trial give room for cautious optimism in this regard.
 ...
PMID:Pathophysiology of congestive heart failure secondary to congestive and ischemic cardiomyopathy. 304 87

In our approach to dynamic cardiomyoplasty, which consists of wrapping a skeletal muscle around the heart and stimulating the former in synchrony with heart contractions to augment ventricular contractility, we have transferred a latissimus dorsi muscle flap to the heart by way of a partial resection of the second rib and subsequently suturing the muscle flap around the ventricles. The muscle flap is stimulated by a Cardio-Myostimulator burst-pulse generator (Medtronic SP 1005) connected to intramuscular electrodes. In preclinical animal research, the latissimus dorsi muscle flap was shown to maintain adequate contractile force and to increase its fatigue resistance by gradual conversion of glycolytic-fatigue-sensitive-to-oxidative-fatigue-resistant muscular fibers (100%). Histochemical and biochemical studies of chronically stimulated muscles showed a total transformation of muscle fast myosin to slow myosin with characteristics similar to those of myocardium. Electron microscopy showed preserved myofibrillar cytoarchitecture and increased mitochondrial density in the cell. At 9 months, cardiac output and ultrasonic Doppler studies showed a significant increase in ventricular function (cardiac output, +21%; peak blood velocity, +40% -80%; and stroke volume, +98% -102%) during muscle stimulation. In the clinical situation, long-term (range of follow-up interval, 4-42 months) beneficial cardiac effects of cardiomyoplasty have been documented in eight patients with various pathologies (ventricular tumor, left ventricular aneurysm, ischemic disease, and dilated cardiomyopathy). Our current understanding of this process is that dynamic cardiomyoplasty acts in two ways: 1) it promotes more vigorous systolic contraction, and 2) it appears to limit heart dilatation.
 ...
PMID:Effect of latissimus dorsi dynamic cardiomyoplasty on ventricular function. 318 Apr


1 2 3 4 5 6 Next >>