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)

A woman with a three month history of progressive right heart failure was found to have sarcoid pericarditis complicated by pericardial tamponade. The pericardial fluid was serosanguineous, and numerous nodules were noted on the parietal and visceral pericardium. Non-caseating granulomas were found in biopsy specimens of the pericardium, lung and skin. Right-sided heart failure in sarcoidosis is usually attributed to cor pulmonale or primary myocardial sarcoid. Pericardial tamponade should be considered in patients who present with sarcoidosis complicated by right heart failure.
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PMID:Pericardial tamponade in sarcoidosis. 382 90

The effect of three months of prazosin treatment on the hemodynamics, cardiac extracellular space; plasma, tissue and intra-cellular Na+, K+, and Ca++ were investigated in dogs with left ventricular failure due to chronic mitral insufficiency. Mitral insufficiency of 6 months duration significantly decreased the LV systolic pressure, LV dp/dt, LV (dp/dt)/IIP, LVWI, CI, and increased the LVEDP, mean right atrial pressure, heart rate and systemic vascular resistance. Associated with these hemodynamic changes were an increase in the extra-cellular space, tissue and intracellular K+; and a decrease in the tissue and intracellular Ca++. Prazosin treatment produced an improvement in the hemodynamics which was associated with a decreased in the extracellular space, and intracellular K+, and an increase in the intracellular Ca++. Plasma Na+ and Ca++ increased with 6 months of M.I. Prazosin treatment brought back the plasma Na+ and K+ to control level. However, plasma Ca+ decreased significantly with prazosin treatment. The changes in right ventricular hemodynamics and electrolytes were not consistent with the right ventricular failure. These results indicate that decrease in the myocardial contractility in chronic heart failure due to mitral insufficiency might be due to a decrease in the intracellular Ca++. Prazosin treatment was able to reverse the hemodynamic and electrolyte changes induced by failing heart due to mitral insufficiency.
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PMID:Effect of chronic prazosin treatment on the cardiac function and electrolytes in failing heart due to chronic mitral insufficiency. 385 Jul 66

Emergency pneumonectomy for penetrating and blunt trauma has an attendant high mortality. Patients with major lung injuries presenting with prolonged shock followed by control of bleeding, resuscitation with or without aortic cross-clamping and pneumonectomy have had uniformly unsatisfactory results. From 1972 to 1982, eight patients at the University of Louisville Hospital underwent emergency pneumonectomy. All patients underwent expeditious evaluation, resuscitation, and thoracotomy with pneumonectomy. Three patients died of exsanguination (2 patients had major associated intra-abdominal injuries). Three other patients died due to pulmonary edema and right ventricular failure 2 to 3 hours after hemorrhage had been controlled and intravascular volume restored. Aortic cross-clamping was employed in four patients due to persistent hypovolemia with 100 per cent mortality. Of the two surviving patients, one presented with stable blood pressure and had pneumonectomy for tracheobronchial disruption, while the other had pneumonectomy for tangential laceration of the lung at the hilum. Pulmonary edema and right ventricular failure were responsible for mortality following emergency pneumonectomy and control of hemorrhage and restoration of blood volume. The addition of aortic cross-clamping did not seem to alter survival and may, indeed, hinder therapy due to increased vascular afterload and increased heart failure and pulmonary edema.
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PMID:Emergency pneumonectomy for penetrating and blunt trauma. 397 87

Approximately 20% of patients who receive left ventricular assist devices (LVADs) for refractory cardiac failure after open heart surgery have had complications of right ventricular failure. To evaluate this problem in the diseased heart we simulated an LVAD in the operating room by bypassing and unloading the left ventricle with the heart-lung machine before routine open heart surgery. Right ventricular function was assessed in 12 patients with preoperative left ventricular ejection fractions of less than 0.55 (poor left ventricular function) (mean +/- SEM 0.40 +/- 0.03) and 10 patients with ejection fractions greater than 0.55 (normal left ventricular function) (0.63 +/- 0.02). Measurements before and during left ventricular bypass in the normal left ventricular function group revealed no change in cardiac output (from 5.7 +/- 0.6 to 5.8 +/- 0.4 liters/min), with a decrease in right ventricular end-diastolic pressure (from 8 +/- 2 to 6 +/- 1 mm Hg). However, in the poor left ventricular function group, cardiac output was increased significantly during left ventricular bypass from 4.5 +/- 0.2 to 5.3 +/- 0.4 liters/min and right ventricular end-diastolic pressure was decreased significantly from 13 +/- 2 to 8 +/- 2 mm Hg. During bypass there were significant reductions in mean pulmonary arterial pressure from 17 +/- 3 to 10 +/- 2 mm Hg in the normal left ventricular function group and from 27 +/- 3 to 12 +/- 2 mm Hg in the poor left ventricular function group. These measurements reflect passive changes in pulmonary pressures due to reductions in left ventricular filling pressure during left ventricular bypass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Right ventricular function in an operating room model of mechanical left ventricular assistance and its effects in patients with depressed left ventricular function. 406 72

Although glucagon exerts positive inotropic effects in patients with no or mild impairment of cardiac function, similar effects are not consistently observed in patients with chronic heart failure. Accordingly, the inotropic effects of glucagon on papillary muscles from normal cats and cats in which right ventricular failure had been produced for 4-145 days by pulmonary artery banding were compared. At the peak of the concentration-response curve, glucagon increased peak isometric tension (T) in normal muscles from 4.4+/-0.4 to 6.6+/-0.5 g/mm(2) (P <0.001), and maximum rate of tension development (dT/dt) from 16.9+/-0.9 to 25.1+/-1.6 g/sec per mm(2) (P < 0.001). In contrast, glucagon produced no significant increases in T or dT/dt in failure muscles. The percentage increases in T and dT/dt caused by norepinephrine were the same in muscles from normal and failing hearts. Since the cardiac effects of glucagon and norepinephrine may be mediated by adenyl cyclase, responsiveness of adenyl cyclase was determined in particulate fractions of the right ventricle. Glucagon activated adenyl cyclase in normal, but had no effect in failure preparations. Norepinephrine-induced activation of adenyl cyclase, however, was unaltered by failure. Thus, in contrast to norepinephrine, glucagon loses the capacity to augment myocardial contractility and activate adenyl cyclase in hearts derived from cats in chronic failure.
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PMID:Effects of experimental heart failure on the capacity of glucagon to augment myocardial contractility and activate adenyl cyclase. 544 51

Parasympathetic neural regulation of the failing heart is impaired. In order to investigate parasympathetic mechanisms in experimental heart failure, measurements were made of choline acetyltransferase (CAT) activity and [3H]-quinuclidinyl benzilate (QNB) binding in hearts of 1) hamsters with skeletal and cardiac myopathy, 2) dogs with pulmonary artery constriction and tricuspid avulsion, and 3) guinea pigs with pulmonary artery constriction. Tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) activities and norepinephrine levels served as indices of sympathetic innervation. In myopathic hearts, total CAT activity decreased (P less than 0.05) compared to age-matched controls. In canine and guinea pig right heart failure, total CAT activity was normal in contractile and specialized tissues. Alterations in [3H]-QNB binding paralleled CAT activity being decreased (P less than 0.05) only in myopathic hearts. In all three models, indices of sympathetic innervation were altered in ways qualitatively different from parasympathetic indices; TH and DBH activities were increased (P less than 0.05) in myopathic ventricles, decreased (P less than 0.05) in hypertrophied canine and guinea pig ventricles and non-hypertrophied canine ventricles, and normal in non-hypertrophied guinea pig ventricles. These results indicate that alterations in cardiac parasympathetic indices vary depending on the etiology of heart diseases and differ qualitatively from alterations in sympathetic indices. Selective determinants are necessary to explain the varied changes.
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PMID:Neurochemical indices of autonomic innervation of heart in different experimental models of heart failure. 613 6

In a prospective study of 50 patients a good correlation was found between the central venous pressure and the sonographic appearance of the inferior caval vein (ICV) behind the liver in right paramedian scanning. Dependent on central venous pressure (CVP) there were typical variations in the configuration, width and respiratory movements. These changes allowed a reliable estimation of the CVP. Decrease of the width in anteroposterior diameter in connection with a reduction of respiration-dependent caval movement indicated a deficiency of circulating blood volume. These alterations were always positive in cases of dehydration. Elongation of the vessel together with a widening over 2 cm and the lack of the normal end-inspiratory collapse were signs of an increased CVP. This non-invasive method is without risks or inconvenience for the patient. It is easily and quickly applied and very reliable for analyzing ICV haemodynamics. ICV ultrasonography can be recommended as a diagnostic aid for dehydration and hyperhydration as well as right heart failure, especially unrecognized, that means cardiac insufficiency without peripheral edema, constrictive pericarditis, tricuspid valve disease and for the assessment of the course of right cardiac failure.
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PMID:[Relations of the ultrasonic image of the inferior vena cava and central venous pressure]. 614 Aug 70

From 1972 to 1981, 40 valved extracardiac conduits have been implanted to bridge the right ventricular outflow tract (RVOT) in 37 patients for different complex congenital cardiac anomalies. The patients ranged in age from 2 to 23 years (mean 8.5 years). Two Dacron prostheses with incorporated Lillehei-Kaster valves, 1 valveless Dacron conduit, 27 Hancock conduits, and 9 lonescu-Shiley conduits were chosen according to availability and the progress in conduit technology. Thirty-three patients had had up to 4 previous palliative procedure before conduit repair. Although the complication rate appears considerable, the mortality rate seemed to be unaffected by the high percentage of prior surgery. Exchange of the conduit became necessary in 2 children, because of conduit stenosis with calcification of the Hancock valve 5 and 7 years respectively after implantation, and in another patient an outgrown Lillehei-Kaster valve Dacron conduit had to be replaced 9 years after repair. Five children died in the early postoperative course: one in pulmonary failure and kinking of the conduit; one with right heart failure and pulmonary hypertension stage IV; 2 in myocardial failure, and one due to severe bleeding from myocardial failure, and one due to severe bleeding from the prosthesis. Three patients died in the late postoperative course 11 weeks, 4 years and 4 years respectively after conduit repair. Conduit surgery offers new possibilities for repair of complex cyanotic cardiac malformations. At present, however, none of the commercially available conduits is an ideal substitute. Our limited experience with the hemodynamic results of lonescu Shiley conduits is promising although longer observation periods are needed for a definitive judgement. At present, the largest possible conduit should be used whenever possible; problems of compression or kinking can be avoided with proper positioning of the conduit.
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PMID:Conduit repair for complex congenital heart disease with pulmonary atresia or right ventricular outflow tract obstruction. part I: surgical results. 617 13

Although rare, cardiac amyloidosis is the commonest cause of infiltrative myocardiopathy. The diagnosis may be suspected clinically in patients with mainly right ventricular failure of sudden onset. The aim of this study was to assess the diagnostic value of M-Mode and 2D echocardiography in this condition. Seven cases of cardiac amyloidosis were studied. Biventricular hypertrophy, usually more severe on the left side with reduction in size of the left ventricular chamber, was observed in all cases. Parameters of systolic and diastolic function were abnormal. A significant pericardial effusion was demonstrated in 3 patients. 2D echocardiography also allows evaluation of the myocardial structure: in 3 cases the whole of the left ventricular myocardium seemed granular, sparkling and abnormally echogenic. In patients with cardiac failure these appearances are very suggestive of amyloidosis, especially when the ECG shows low voltage complexes and pathological Q waves. In 3 other patients, this abnormal echogenic myocardial appearance was observed only in the interventricular septum, which is much less suggestive of cardiac amyloidosis. In conclusion, in patients with cardiac failure with cardiomegaly and a low voltage ECG, echocardiographic findings of hypertrophic cardiomyopathy (only rarely with dilatation) and hypokinetic wall motion are suggestive of cardiac amyloidosis, especially when the myocardium has a granular, sparkling appearance.
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PMID:[M-mode and two-dimensional echocardiography of 7 cases of cardiac amyloidosis]. 624 Feb 37

A case, unique in the literature, is reported in which a primary carcinoma of the liver presented a right-sided heart failure and pulmonary hypertension. The diagnosis of hepatocarcinoma was established by needle biopsy of the liver. Later, postmortem examination demonstrated that the pulmonary arterial tree was severely compromised by multiple tumor microemboli, despite the persistent lack of characteristic roentgenographic abnormality in our patient. In reviewing the literature, we found rare cases of occult renal cell carcinoma, choriocarcinoma and one of occult hepatocarcinoma, which presented as pulmonary embolism. These were diagnosed by pulmonary embolectomy, human chorionic gonadotrophin levels or autopsy, respectively. In another small group of reported cases of known carcinoma (gastric, breast, colonic) the patients had a clinical picture of "idiopathic" pulmonary hypertension or of pulmonary hypertension with pulmonary metastases. Pulmonary hypertension in these cases resulted from carcinomatous lymphangitis and/or tumor microembolization, as in our case. We report this case to emphasize the necessity of including occult carcinoma in the differential diagnosis of pulmonary hypertension and right ventricular failure.
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PMID:Pulmonary hypertension as a presentation of hepatocarcinoma. Report of a case and brief review of the literature. 624 34


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