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

We present a case of the rare coincidence of three mechanisms leading to development of congenital heart disease in intrauterine life: intrinsic defect of the development of the cardiac loop (dextrocardia), failure of normal expansion of the subpulmonary infundibulum (Fallot syndrome) and endocardial cushion defect (common atrium and common atrioventricular valve ). It was associated with partial viscera inversion. A 31-year old man with congenital cyanotic heart disease, and Blalock-Taussig anastomosis was admitted to the hospital due to symptoms of severe cardiac failure. On physical examination: systolic murmur, hepatomegaly, ascites, leg's edema and cyanosis were found. In ECG--atrial fibrillation with 3-d degree a-v block. Standard echocardiography revealed: dextrocardia, a large single atrium with ostia of pulmonary and systemic veins, single atrio-ventricular valve , large ventricular, Fallot-like septal defect. The papillary muscles were not visible in the left ventricle. Aorta and pulmonary trunk arose from morphological right ventricle. The patient died on the 3-rd day of hospitalization in the course of cardiac and respiratory insufficiency. Postmorten examination confirmed the diagnosis.
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PMID:[Combined heart defects: tetralogy of Fallot, common atrium and a single atrioventricular valve diagnosed by echocardiography]. 164 Jun 69

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

The case is reported of a 49-year-old chronic alcoholic woman, who presented with severe pulmonary arterial hypertension (PAH) mimicking as an acute abdomen. She was admitted with right-sided hypochondrial abdominal pain and hepatomegaly, with a moderate jaundice. On admission to intensive care unit, she had an arterial blood pressure of 110/70 mmHg, a heart rate of 100 b.min-1, and a respiratory rate of 36 c.min-1. An electrocardiogram showed sinus rhythm and right-sided heart failure. Whilst breathing 6 l.min-1 oxygen, her arterial blood gases were: PaO2 47 mmHg PaCO2 29 mmHg. Severe PAH was confirmed by measuring her mean pulmonary arterial pressure, which was 46 mmHg, whilst her pulmonary wedge pressure was 7 mmHg. Hepatic function was also altered: total bilirubin 41 mumol.l-1, alkaline phosphatase 145 UI.l-1 and gamma glutamyl transferase 1 340 UI.l-1. She developed arterial hypotension, which did not respond to increasing doses of isoproterenol. She died on the third day. Necropsy confirmed the diagnosis of primary PAH, with acute "cardiac liver".
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PMID:[Pseudosurgical acute abdomen syndrome in primary pulmonary hypertension]. 175 58

The clinicopathological features of five fatal cases of diffuse haemangiomatosis presenting in neonatal life or early infancy are presented. The infants all had multiple skin haemangiomas as well as deep-seated lesions in many different tissues that caused protean clinical manifestations and management problems. Because the outlook may be improved by early diagnosis and application of new modes of treatment, any infant with multiple cutaneous haemangiomas should be closely assessed for possible visceral involvement. Development of hepatomegaly, high-output cardiac failure, unexplained anaemia or thrombocytopenia in these infants should immediately suggest disseminated disease. Early recognition with implementation of steroid and/or antiangiogenic therapy, embolization and/or surgery is essential to improve the chances of survival.
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PMID:Diffuse infantile haemangiomatosis: clinicopathological features and management problems in five fatal cases. 139

In 61 patients with class IV (NYHA) of chronic congestive cardiac failure treated for 2 weeks with digoxin (0.290 +/- 0.108 mg/d) and furosemide (13.0 +/- 4.1 mg/d), for 2 weeks with digoxin, furosemide and isosorbide dinitrate (44.5 +/- 9.8 mg/d) or nifedipine (42.0 +/- 12.2 mg/d), for 4 weeks with digoxin, furosemide, isosorbide or nifedipine and captopril (angiotensin converting enzyme inhibitor) (75.1 +/- 24.4 mg/d), and for the last 2 weeks with digoxin, furosemide, isosorbide or nifedipine without captopril, after each stage the clinical state, exercise tolerance and haemodynamic parameters determined echocardiographically were assessed. Ten weeks of treatment by this method caused regression of pulmonary congestion in 80%, oedema in 63.3% and hepatomegaly in 33.3% of the patients. Moreover, 60.7% of the patients returned to class III, 13.1% to class II, and 26.2% remained in class IV (NYHA). In the group treated with digoxin, furosemide, nifedipine with captopril (n = 30) a significant rise was observed of the value of the ejection fraction and cardiac index in relation to the treatment with digoxin and furosemide and the treatment with digoxin, furosemide, nifedipine (p less than 0.05). No drug improved significantly the tolerance of submaximal exercise. During the treatment with captopril no clinical improvement was achieved in 4 cases, and worsening occurred in 3 cases of severe cardiac failure (7 of 61 patients, 11.5%). The obtained results showed that vasodilating drugs are safe in congestive cardiac failure and in many cases of severe failure captopril contributed to rapid clinical and haemodynamic improvement.
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PMID:[Results of treatment for severe congestive heart failure with digoxin, furosemide and vasodilating agents]. 227 87

The patient is a 71-year-old female who underwent splenectomy due to splenomegaly 32 months after diagnosed as having primary myelofibrosis. On examination she was found to have massive skin nodules, lymph nodes swelling and an enlarged liver with an abnormal hematologic profile as follows: RBC count 3.68 x 10(6)/microliters; WBC count 151 x 10(3)/microliters with 11% blasts; and platelet count 42 x 10(3)/microliters. The bone marrow aspirate showed a hypocellular marrow with 19.2% blasts. Histological examination of the skin nodules revealed that they were myeloblastomas, thus suggesting leukemic transformation of primary myelofibrosis. Her WBC count dropped to about 20 x 10(3)/microliters through treatment with vindesine, cyclophosphamide, 6-mercaptopurine and prednisolone, but it did not drop further. Treatment with dexamethasone remarkably regressed the myeloblastomas, but she died of heart failure 4 months after diagnosis of leukemic transformation of primary myelofibrosis. The autopsy findings showed the formation of numbers of myeloblastomas in both the systemic fatty tissue and dura mater as well as extramedullary hematopoiesis in liver and lymph nodes. A rapid development of splenomegaly in a patient with primary myelofibrosis seems to be associated with leukemic transformation.
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PMID:[Blastic crisis of primary myelofibrosis associated with multiple myeloblastomas ]. 231 11

Two patients with similar symptoms referred for diagnosis and treatment of hepatic failure subsequently proved to have cardiomyopathy as the cause of their hepatic decompensation. Except for fatigue and edema, symptoms of congestive heart failure were absent and no history of dyspnea, orthopnea, or paroxysmal nocturnal dyspnea could be elicited. Hepatomegaly was present in both patients, but neck venous distension and hypotension were not apparent, and both patients were able to lie flat. The diagnosis of cardiomyopathy was made by echocardiogram showing global hypokinesis and low ejection fractions; right atrial pressures were markedly increased. Liver biopsies demonstrated centrilobular necrosis and congestion. Treatment for heart failure led to a prompt response in both patients with rapid return of all hepatic parameters toward normal. Paradoxically, our patients had striking evidence of hepatic failure and a notable absence of symptoms and signs of congestive heart failure. An awareness of this unique presentation may avoid prolonged evaluations in such critically ill patients.
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PMID:Cardiomyopathy unrecognized as a cause of hepatic failure. 236

An autopsy case of malignant lymphoma of the central nervous system which showed extracranial disseminations was presented. A 50-year-old man developed mental and physical slowness over one year prior to admission followed by dementia and consciousness disturbance without general physical symptoms. Physical examination on admission showed no lymph node enlargement, hepatomegaly, splenomegaly, or abdominal mass. Neurological examination revealed mild dementia, left positive Babinski and Chaddock reflexes, and bilateral positive frontal lobe signs. CT scan revealed low density areas with contrast enhancement in the white matter of the bilateral parietal lobes adjacent to the trigon of lateral ventricles. Without any therapy, the low density area in the left cerebral hemisphere on CT scan disappeared and the low density area in the right cerebral hemisphere became unenhanced. Any other lesions except brain were found despite of the extensive systemic examinations including scintigrams, echograms, gastrointestinal examinations, body CT scan, aspiration of bone marrow, and lymphography. Primary intracranial malignant lymphoma was suspected and treated with steroid without any response. Subsequent radiation therapy made a transient improvement. But a few months later, the brain lesions gradually worsened, followed by general physical deterioration with diarrhea, pleural fluids, and ascites. Cytologic study of cerebrospinal fluid revealed neoplastic lymphocytes with atypical nuclei containing conspicuous nucleoli and mitosis, which were identified as B cell type malignant lymphoma by analysis using monoclonal antibody. The patient died of cardiac failure about two years after the initial symptom.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of primary intracranial malignant lymphoma showing extracranial disseminations]. 239 Mar 65

The knowledge of factors determining the risk of postoperative myocardial failure (MF) should allow a more rational approach to the timing and the management of mitral valve replacement (MVR). Using multivariate logistic regression analysis the influence of 41 preoperative and perioperative variables on MF was assessed in a training group of 353 consecutive patients undergoing isolated primary MVR between 6/76 and 12/82. Early MF mortality was 4.2%. Strongest independent preoperative predictors of MF were advanced NYHA functional class (p less than 0.001), hepatomegaly (p = 0.001), and reduced body weight (p = 0.01). Amongst preoperative and perioperative variables independent determinants of MF were NYHA functional class (p less than 0.001), hepatomegaly (p = 0.002), hypotension during extracorporeal circulation (ECC) (p = 0.005), body weight (p = 0.007), ECC duration (p = 0.008), female sex (p = 0.061) and the absence of cardioplegia (p = 0.065). From the combination of these determinants estimates of the probability of MF were calculated and adjoined to low or high risk by means of an optimum cutoff point. The sensitivity of this test performed before and after operation was 0.80 and 0.93, the specificity 0.92 and 0.94, respectively. The reliability of this prognostic test was prospectively evaluated on data of 107 consecutive MVR patients between 1/83 and 12/84. The observed diagnostic characteristics of the test group were comparable to those predicted from the training group. Multivariate logistic regression analysis selects independent determinants, estimates the risk of MF or other modes of postoperative events and identifies patients with low or high risk with a definable validity as an objective aid for medical decision-making.
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PMID:Estimation of the operative risk of mitral valve replacement by multivariate logistic regression analysis. 243 42

102 patients with myocardial infarction (MI) were examined by three clinicians, who independently recorded the following symptoms and signs: dyspnoea, a displaced apex beat, S3-gallop, rales, neck vein distension, hepatomegaly, and dependent oedema. Chest X-ray, radionuclide ventriculography, and (in 40 patients) right heart catheterization were carried out immediately after the physical examination. The clinicians frequently disagreed as to the presence of physical signs of heart failure in individuals. Moreover, these signs were of limited value in identifying patients with pulmonary vascular congestion on chest X-ray, reduced left or right radionuclide ventricular ejection fractions, enlarged ventricular volumes or haemodynamic evidence of ventricular dysfunction. We conclude that clinicians frequently disagree in the recognition of physical signs of heart failure, and that these signs have an unpredictable relationship to radiographic, radionuclide and haemodynamic measures of ventricular performance in patients with MI. Nevertheless, physical signs are useful in identifying patients with high risk of cardiac death.
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PMID:Symptoms and signs of heart failure in patients with myocardial infarction: reproducibility and relationship to chest X-ray, radionuclide ventriculography and right heart catheterization. 259 93


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