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

Opiate receptor inhibition causes adrenergic receptor-mediated increases in aortic pressure, cardiac output, and left ventricular contractile function in right heart failure. To study whether the effects of opiate receptor inhibition are mediated by means of an action on the central opiate system, we administered equimolar doses of naloxone hydrochloride and naloxone methobromide (MeBr) and normal saline to heart failure dogs. Chronic stable right heart failure was produced by progressive pulmonary artery constriction and tricuspid valve avulsion. Naloxone hydrochloride caused an increase in mean aortic pressure, cardiac output, left ventricular dP/dt and dP/dt/P, plasma catecholamines, and regional blood flows to the myocardium, quadriceps muscle, kidneys, and splanchnic beds. Plasma beta-endorphin and adrenocorticotropin also increased. In contrast, neither normal saline nor naloxone MeBr (which does not cross the blood-brain barrier) affected the systemic or regional hemodynamics or neurohormones. Naloxone hydrochloride was also administered to anesthetized heart failure dogs. Pentobarbital anesthesia removed cortical perception of nociceptive stimulation, reduced the increase in plasma epinephrine, and abolished vasodilation in skeletal muscle that occurred in conscious dogs after naloxone hydrochloride administration but had no major effects on responses of plasma norepinephrine, systemic hemodynamics, or other regional blood flows to opiate receptor inhibition. Naloxone hydrochloride had no effect in sham-operated dogs. The results indicate that the hemodynamic effects of naloxone are mediated by an action within the central nervous system. Furthermore, since pentobarbital anesthesia did not markedly alter the hemodynamic responses to naloxone hydrochloride, the acute salutary effects of opiate receptor inhibition probably are not caused by removal of the antinociceptive effect of endogenous opioids in heart failure.
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PMID:Opiate receptor antagonism in right-sided congestive heart failure. Naloxone exerts salutary hemodynamic effects through its action on the central nervous system. 254 17

A rare case of a 77-year-old man with primary liver cancer and an isolated metastasis in the right atrial endocardium is presented. The metastasis was 30/40 mm large and occupied a considerable part of the atrial cavity. Clinically the disease was manifested by progressing chronic right ventricular failure, ending with a total heart failure. The diagnosis was made at the post mortem examination. The rarity of the case is pointed out. The possibility of a correct diagnosis while the patient was still alive is discussed.
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PMID:[Cardiac metastasis in primary cancer of the liver]. 255 50

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
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PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

Chylous ascites is a well-documented sequelae of traumatic rupture of the thoracic duct and mechanical obstruction of the lymphatic system due to neoplastic, inflammatory, or congenital anomalies. Less commonly, chylous ascites results from altered hemodynamics and lymphatic flow, as seen in cirrhosis and constrictive pericarditis. Rarely, severe right-sided heart failure from a variety of causes has also resulted in chylous ascites or a protein-losing enteropathy. We report a case of chylous ascites due to dilated cardiomyopathy with autopsy findings. The pathophysiology of chylous ascites formation in right heart failure will be discussed, with a review of the literature.
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PMID:Dilated cardiomyopathy associated with chylous ascites. 259 59

We report a case of successful biventricular assist for severe heart failure after open heart surgery. A 62-year-old man suffering from advanced valvular disease accompanied with hepatorenal dysfunction underwent mitral valve replacement and tricuspid annuloplasty on September 22, 1988. Because of inability of weaning from cardiopulmonary bypass, left heart assisted circulation using a roller pump with heparin-coated tubing system was inserted. Following the left heart assist, an right ventricular assist device (RVAD) was subsequently applied to intractable right ventricular failure. He was successfully weaned from an RVAD after 24 hours, and from left heart assisted circulation after 46 hours. At present, he is doing well without significant complications. Earlier application of biventricular assist might be effective for biventricular failure with hepatorenal dysfunction.
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PMID:[A successful biventricular assist for postoperative patient with severe heart failure and hepatorenal dysfunction after mitral and tricuspid valve surgery]. 261 28

In this study, observation of the effects of verapamil on pulmonary arterial pressure and on treating right heart failure were done in 15 patients with chronic cor pulmonale complicated with heart failure using monitoring of hemodynamic changes by right cardiac catheter. The results showed that verapamil had remarkable effect on pulmonary arterial pressure. With no significant effect on systemic blood pressure, verapamil decreases right ventricular systolic pressure by 1.3 kPa (9.6 mmHg), pulmonary arterial systolic pressure by 1.5 kPa (11 mmHg) and mean pulmonary arterial pressure by 1.1 kPa (8.5 mmHg). Verapamil is clinically useful by decreasing cardiac afterload, improving cardiac function, treating right heart failure and relieving bronchial spasm.
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PMID:[Effects of verapamil on pulmonary arterial pressure in patients with cor pulmonale complicated by heart failure]. 263 53

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co
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PMID:Pulmonary and pleural complications of cardiac disease. 268 66

Three patients with biventricular failure were managed postoperatively with the aid of a right ventricular assist device (RVAD) and intraaortic balloon pumping (IABP) with favorable results. Among these three cases, two had multiple rheumatic valvular disease with cardiac cachexia and underwent combined valve replacement. Another who was suffered from heart failure with a large ventricular septal defect and tricuspid regurgitation had a VSD closure and tricuspid valve replacement. In all patients, the weaning from pump oxygenator was difficult even with large doses of catecholamine. Therefore, the pump oxygenator was switched to RVAD for right ventricular assistance and IABP for left ventricular assistance because these patients had had right ventricular failure dominant biventricular failure preoperatively. Though case 2 was lost 64 days after the surgery by retroperitoneal bleeding due to inadequate anticoagulant treatment, the other two cases recovered successfully from postoperative biventricular failure and were discharged from the hospital. The indications of this method and the criteria for RVAD weaning were discussed.
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PMID:[A case report of biventricular assistance by means of ventricular assist device and IABP in postoperative biventricular failure]. 280 1

In recent years, the number of cases in which a ventricular assist device is required for serious heart failure not responding to conventional mechanical circulatory assistance, has been increasing. It should be pointed out, however, that the majority of the new device is to assist the left ventricle, and that the effect of right ventricular assist device (RVAD) has not been fully clarified yet. The effect of RVAD and intra-aortic balloon pumping (IABP) on right ventricular failure due to right ventricular infarction was studied in swine. Right ventricular infarction was made by means of right coronary artery ligation. After preparation of right ventricular infarction, both mean aortic pressure and cardiac output were reduced and elevated central venous pressure, increased right ventricular end-diastolic pressure, dilatation of right ventricular free wall, were noted and diagnosed as a cardiogenic shock due to acute right ventricular infarction. Right ventricular infarcted area was evaluated by epicardial mapping ECG and myocardial regional blood flow. It was found that in the cases using IABP, the effect of reducing the infarcted area due to diastolic augmentation was noted, but the effect on the right ventricular support was not satisfactory, while in the cases using RVAD, the right ventricular preload was reduced and the right ventricular stroke work was decreased, and the effect of reducing the infarcted area was observed. But hemodynamic effect of these method were not satisfactory, enough to assist recovery from cardiogenic shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of RVAD for right heart failure involved with right ventricular infarction--especially studies of myocardial regional blood flow and epicardial mapping electrocardiography]. 280 14

The effects of congestive heart failure on the physiological and biochemical functions of the cardiac beta-adrenoceptor-coupled adenylate cyclase system were studied in dogs with right heart failure produced by progressive pulmonary artery constriction and tricuspid avulsion. The cardiac inotropic response to dobutamine was attenuated in congestive heart failure, as determined by the right and left ventricular dP/dt responses. Adrenergic beta-receptor density, measured by [3H]dihydroalprenolol binding, was reduced in membrane fractions of the failing right ventricle, but not in the left ventricle. The functional activity of the adenylate cyclase system was studied in vitro by measuring the net cyclic AMP production following additions of isoproterenol, 5'-guanylylimidodiphosphate (Gpp(NH)p), forskolin, or manganese chloride, which act either directly on the beta-adrenergic receptors or on one of the post-receptor components of the adenylate cyclase system. Congestive heart failure reduced the net production of cyclic AMP by isoproterenol, Gpp(NH)p, and forskolin in both the right and left ventricles, but did not alter the effect of manganese chloride. Thus, beta-receptor down-regulation is chamber-specific, occurring only in the hemodynamically stressed right ventricle. In contrast, the post-receptor defect of the adenylate cyclase system occurred in both ventricles of the heart failure dogs. This decreased activation of adenylate cyclase by beta-agonists may be responsible, at least in part, for the diminished cardiac inotropic response to catecholamines in congestive heart failure.
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PMID:Alterations in cardiac beta-adrenoceptor responsiveness and adenylate cyclase system by congestive heart failure in dogs. 282 36


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