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

In 15,645 consecutive ultrasound examinations of the abdomen (1986 to 1988), free fluid in the peritoneal cavity was found in 247 patients by internal trial during 397 sessions (= 2.5%). Most frequent basic diagnosis for the reason of this symptom were tumorous diseases (99 patients corresponding to 40.1%), cirrhosis of the liver (52 patients corresp. to 22.1%) and heart failure (31 patients corresp. to 12.6%, among these complex gayprooft myocardial insufficiency 24, right heart failure 7). Ovarian cysts or cystomas (7), acute/chronic-recurrent pancreatitis (6), Crohn's disease (3), infections (3), rheumatoid disorders (3), nephrotic syndrome (2), and extra-uterine pregnancy (2) were more rarely represented. In 23 patients (corresp. to 9.3%) the cause of an ascites remained obscure. Among these, a high prevalence of the female sex in the premenopausal age was remarkable with a score of 20:3 (statistically significant difference in terms of the other patients of our group). This observation suggests that an ovarian factor plays a role in the development of ascites in the absence of other evident causes. The literature implies that endometriosis is rather prominent, followed by oligosymptomatic infections or inflammatory diseases.
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PMID:[Cryptogenetic ascites. Attempts at original pathophysiologic explanation of a monomorphic sonographic image pattern]. 150 31

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

Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology. The purpose of this study is to assess qualitative and quantitative changes in biological factors involved in the evolution and the development of right ventricular hypertrophy (RVH) and right ventricular failure in response to pressure overload in rats with pulmonary hypertension induced by monocrotaline injection, and to clarify the process from compensation to deterioration in cardiac hypertrophy biochemically and morphologically. Significant RVH was produced in rats at 2 weeks after single subcutaneous injection of monocrotaline, and signs of right ventricular failure became obvious at 4 weeks as RVH became more severe. In the right ventricle of these rats, we found that: 1) myosin isoenzymes shifted from V1 to V3 both at 2 and 4 weeks; 2) total collagen content increased, and type III and type V collagens increased with a relative decrease in type I collagen at both 2 and 4 weeks; 3) intracellular Ca2+ transient recorded from isolated myocytes showed a lower peak and slower descent slope compared to those of control rats; 4) ultrastructural changes observed by scanning electron microscopy at 1 and 2 weeks disappeared gradually as heart failure developed, and degeneration or destruction of mitochondria or sarcoplasmic reticulum became remarkable at 3 and 4 weeks. These findings suggest that cardiac hypertrophy might be an ominous sign of cardiac failure rather than a benign adaptive process, at least in this model.
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PMID:Changes in contractile and non-contractile proteins, intracellular Ca2+ and ultrastructures during the development of right ventricular hypertrophy and failure in rats. 153 55

An experimental model for right ventricle free wall infarct associated with double ventriculotomy and tricuspid insufficiency was created to evaluate whether right ventricle failure can cause profound refractory heart failure or whether modifications in right ventricular afterload are more influential in this regard. In our model, the left ventricle, interventricular septum and right atrial wall were maintained intact and pulmonary banding made it possible to modify right ventricular afterload during the experiment. The results of our study showed that pure right ventricular failure does affect the hemodynamic state negatively, but it is not itself, a cause of death in dogs. A slight increase in the dysfunctional right ventricular afterload produced a profound deterioration in the hemodynamic state that required pulmonary artery debanding within no more than 10 minutes.
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PMID:Does a critical hemodynamic situation develop from right ventriculotomy and free wall infarct or from small changes in dysfunctional right ventricle afterload? 157 83

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

Dissection of the inferior wall of the right ventricle during the acute phase of myocardial infarction with right ventricular involvement is a mechanical complication which has been recently identified, the diagnosis being almost exclusively post-mortem. The authors report the clinical, echocardiographic and pathological features of myocardial dissection in four patients. Between 1985 and 1988, the diagnosis of myocardial dissection was made by echocardiography in 4 patients aged 77 to 80 years, admitted to hospital for an acute inferior wall myocardial infarction. All 4 patients had signs of acute right ventricular failure indicating right ventricular necrosis and a loud systolic murmur at the left sternal border; 2 patients were in shock. The ECG showed signs of inferior wall infarction with, in 2 patients, electrical changes suggestive of right ventricular involvement. Echocardiography showed dissection of the inferior wall of the right ventricle as a pulsatile, echo-free space in the diaphragmatic wall of the right ventricle which appeared to obstruct right ventricular ejection in end systole to a variable degree. The outcome was fatal in all cases with death resulting from refractory myocardial failure. Pathological analysis confirmed biventricular inferior wall infarction also involving the posterior part of the interventricular system, the site of a small tear on the left side which communicated with a neo-cavity dissecting the RV posterior wall. The right coronary artery was totally occluded in all cases. The anatomical lesions were fully concordant with the echocardiographic data: the dissection filled with blood from the left ventricle at each systole creating a pulsatile space in the diaphragmatic wall of the ventricle obstructing ejection.
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PMID:[Myocardial dissection in infarction of the right ventricle. Clinical echocardiographic and pathological aspects]. 164 2

To study myocardial beta-adrenoceptor internalization in heart failure, we measured beta-adrenoceptor density in the particulate, light vesicle and supernatant fractions of ventricular tissue of dogs with experimental right ventricular failure and sham-operated dogs. Tissue was fractionated by centrifugation, and beta-adrenoceptors were measured by [125I]iodocyanopindolol binding. Compared to sham-operated controls, beta-adrenoceptors were reduced in all fractions of right ventricular tissue from heart failure animals. Thus, the decreased surface (particulate fraction) receptors observed cannot be explained by internalization alone, and must be associated with altered receptor synthesis or degradation.
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PMID:Both cell surface and internalized beta-adrenoceptors are reduced in the failing myocardium. 166 86

Left ventricular and biventricular bypasses (LVBs, BVBs) were performed in 102 experiments in sheep, goats, and donkeys. Biventricular bypass was performed in the assisted circulation mode or in the paracorporeal artificial heart bridge (PCAHB) mode when the natural heart fibrillates. During implantation of artificial ventricles instead of a heart-lung bypass, counterpulsation was used. Several types of connective conduits were developed and tested in experiments. The conduits included bifurcational connective pipes that permit "intake" of blood into artificial ventricles from atria and ventricles of the natural heart simultaneously and consequently provide effective blood flow through shunts not depending on the state of the natural heart (acute cardiac weakness or asystole). Monitoring gas content (PO2, PCO2, and pH) in the myocardium of both ventricles suggested development of right ventricular failure under conditions of LVB before hemodynamic changes occurred and confirmed the preferability of BVB over other methods of assisted circulation, as it is most effective and capable of normalizing short-term cardiac disturbances in the course of the 1st 2 days. Survival time of experimental animals (2-3 days for dogs, 5-12 days for sheep, goats, and donkeys) is sufficient to overcome acute cardiac insufficiency. This suggests that BVB in the assisted circulation mode or PCAHB mode can serve as a bridge for cardiac transplantation for the time of search for the available organ.
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PMID:Biventricular bypass: alternative to univentricular bypass and total artificial heart-bridge. 174 77

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.
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PMID:[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension]. 174 69

An abdominal murmur was first heard in a now 46-year-old man four years after laminectomy at the age of 21. Signs of right heart failure and, ultimately, of global heart failure developed progressively and increasingly 20 years later. Echocardiography demonstrated enlargement of the right heart cavities, and atrial fibrillation was diagnosed. Cardiac catheterization revealed the typical picture of high output failure (cardiac output 13.9 l/min). Intra-arterial subtraction angiography demonstrated a fistula between the left iliac artery and vein. After operative closure of the fistula the signs of heart failure disappeared. Six months later a residual but insignificant fistula was still present, as well as persistent atrial fibrillation. Medical treatment having failed cardioversion successfully re-established sinus rhythm and the patient became symptom-free. Arteriovenous fistula after laminectomy is a rare cause of heart failure and often diagnosed very late. The prognosis is good once the fistula has been closed.
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PMID:[A iatrogenic arteriovenous fistula following laminectomy. A rare differential diagnosis of heart failure]. 185 45


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