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)

Amyloidoses are a heterogeneous group of multisystem disorders, which are characterized by an extracellular deposition of amyloid fibrils. Typically affected are the heart, liver, kidneys, and nervous system. More than half of the patients die due to cardiac involvement. Clinical signs of cardiac amyloidosis are edema of the lower limbs, hepatomegaly, ascites and elevated jugular vein pressure, frequently in combination with dyspnea. There can also be chest pain, probably due to microvessel disease. Dysfunction of the autonomous nervous system or arrhythmias may cause low blood pressure, dizziness, or recurrent syncope. The AL amyloidosis caused by the deposition of immunoglobulin light chains is the most common form. It can be performed by monoclonal gammopathy. The desirable treatment therapy consists of high-dose melphalan therapy twice followed by autologous stem cell transplantation. Due to the high peritransplantation mortality, selection of appropriate patients is mandatory. The ATTR amyloidosis is an autosomal dominant disorder caused by the amyloidogenic form of transthyretin, a plasmaprotein that is synthesized in the liver. Therefore, liver transplantation is the only curative therapy. The symptomatic treatment of cardiac amyloidosis is based on the current guidelines for chronic heart failure according to the patient's New York Heart Association (NYHA) state. Further types of amyloidosis with possible cardiac involvement comprise the senile systemic amyloidosis caused by the wild-type transthyretin, secondary amyloidosis after chronic systemic inflammation, and the beta(2)-microglobulin amyloidosis after long-term dialysis treatment.
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PMID:[Cardiac amyloidosis]. 1834 65

Propofol (2, 6-diisopropylphenol) is a potent intravenous hypnotic agent that is widely used in adults and children for sedation and the induction and maintenance of anaesthesia. Propofol has gained popularity for its rapid onset and rapid recovery even after prolonged use, and for the neuroprotection conferred. However, a review of the literature reveals multiple instances in which prolonged propofol administration (>48 hours) at high doses (>4 mg/kg/h) may cause a rare, but frequently fatal complication known as propofol infusion syndrome (PRIS). PRIS is characterized by metabolic acidosis, rhabdomyolysis of both skeletal and cardiac muscle, arrhythmias (bradycardia, atrial fibrillation, ventricular and supraventricular tachycardia, bundle branch block and asystole), myocardial failure, renal failure, hepatomegaly and death. PRIS has been described as an 'all or none' syndrome with sudden onset and probable death. The literature does not provide evidence of degrees of symptoms, nor of mildness or severity of signs in the clinical course of the syndrome. Recently, a fatal case of PRIS at a low infusion rate (1.9-2.6 mg/kg/h) has been reported. Common laboratory and instrumental findings in PRIS are myoglobinuria, downsloping ST-segment elevation, an increase in plasma creatine kinase, troponin I, potassium, creatinine, azotaemia, malonylcarnitine and C5-acylcarnitine, whereas in the mitochondrial respiratory electron transport chain, the activity of complex IV and cytochrome oxidase ratio is reduced. Propofol should be used with caution for sedation in critically ill children and adults, as well as for long-term anesthesia in otherwise healthy patients, and doses exceeding 4-5 mg/kg/h for long periods (>48 h) should be avoided. If PRIS is suspected, propofol must be stopped immediately and cardiocirculatory stabilization and correction of metabolic acidosis initiated. So, PRIS must be kept in mind as a rare, but highly lethal, complication of propofol use, not necessarily confined to its prolonged use. Furthermore, the safe dosage of propofol may need re-evaluation, and new studies are needed.
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PMID:Propofol infusion syndrome: an overview of a perplexing disease. 2002 84

The goal of the present study was to describe the ultrasonographic findings in 22 cattle with traumatic pericarditis. A 5.0 MHz linear transducer or a 5.0 MHz convex transducer was used to examine the thorax, reticulum and liver. There was severe pleural effusion in 17 heifers and severe pericardial effusion in 13 animals. Echogenic deposits and strands of fibrin were seen on the epicardium of 7 animals. Eighteen cattle had signs of traumatic reticuloperitonitis, and 11 had ascites. Because of cardiac insufficiency, 14 cattle had a markedly enlarged liver due to congestion and 15 had dilatation of the caudal vena cava. Ultrasonography is a useful diagnostic aid for visualisation and characterisation of thoracic and abdominal lesions in cattle with traumatic pericarditis.
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PMID:[Ultrasonographic findings in 22 cattle with pericarditis traumatica]. 1860 19

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA), or Bland-White-Garland syndrome, is a rare congenital malformation described in children and adults. In this condition, the left coronary artery, which normally originates from the left coronary sinus in the aorta, instead originates from the pulmonary trunk, which results in retrograde flow of blood away from the myocardium into the lower-pressure pulmonary artery. Myocardial hypoxic-ischemic injury results in cardiac dysfunction, failure, and eventually in patient death if not surgically repaired. This report describes gross and microscopic findings in 4 beef calves with ALCAPA. All the calves had a history of being found dead with few or no premonitory signs, 2 shortly after sudden strenuous exercise. Gross necropsy lesions suggestive of heart failure included cardiomegaly with atrial and ventricular dilation and/or ventricular hypertrophy, and hepatomegaly. Dissection of each heart revealed the origin of the left coronary artery arising in the pulmonary trunk above the anterior cusp of the pulmonic valve. No degeneration; mineralization; and fiber loss, with replacement by fibrous connective tissue, predominantly in the left ventricular papillary muscle and the interventricular septum. Changes observed in the liver and lungs, including hepatomegaly, sinusoidal congestion, centrilobular fibrosis, and pulmonary congestion, edema, and intra-alveolar pigment-laden macrophages were consistent with heart failure.
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PMID:Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) in four calves. 1872 66

Echocardiographically documented tricuspid valve regurgitation appeared immediately after surgical treatment of cor triatriatum dexter in a two-month-old rottweiler. Medical treatment was instituted with benazepril, spironolactone and furosemide. Pimobendan was added after five months, and all treatment was discontinued two months later when clinical signs of ascites and hepatomegaly had resolved and tricuspid valve regurgitation was markedly reduced on echocardiography. To the authors' knowledge, this is the first report describing the development and spontaneous improvement of haemodynamically significant tricuspid valve regurgitation following surgical treatment of cor triatriatum dexter in a dog. It is hypothesised that the increase in right atrial volume and pressure following cor triatriatum dexter repair and transient ischaemia of papillary muscles led to dilatation of the right atrioventricular annulus and subsequent severe tricuspid valve regurgitation in the face of an anatomically normal valve. Time and pharmacological preload reduction as well as normalisation of right atrial inflow and subsequent cardiac remodelling substantially reduced tricuspid valve regurgitation and eliminated clinical signs of heart failure. It is also possible that heart recovery has been spontaneous.
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PMID:Transient tricuspid valve regurgitation following surgical treatment of cor triatriatum dexter in a dog. 1942 72

We report the rapid and dramatic efficacy of propranolol in 8 infants with infantile hepatic hemangiomas. The degree of response varied from a significant improvement to a complete resolution of hepatic lesions. Heart failure and hypothyroidism resolved, and hepatomegaly decreased. No side-effects of the drug were noted.
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PMID:Efficacy of propranolol in hepatic infantile hemangiomas with diffuse neonatal hemangiomatosis. 2048 55

Premature infants with intrauterine growth restriction (IUGR) are at greater risk for an adverse perinatal outcome. IUGR affects hepatocyte function, but the histopathological changes in the postnatal liver are not well known. We report a male infant with severe IUGR. His mother was transferred to our hospital at 26 weeks of gestation because of preterm labor and severe IUGR. An emergency cesarean section was carried out because of a non-reassuring fetal status. The birth weight of the infant was 332 g. He showed congestive heart failure and marked hepatomegaly from birth. After 1 week, blood examinations showed hyperbilirubinemia with high direct bilirubin. Because of liver dysfunction, he received the minimal total parenteral nutrition for 7 days. After 1 month, he progressively developed ascites and coagulopathy, and died 3 months after birth. Liver autopsy showed diffuse perisinusoidal fibrosis. Fibrosis was also prominent around the central vein. Immunohistochemical study revealed many alpha-smooth muscle actin-positive cells, which represent activated hepatic stellate cells, and a few transforming growth factor-beta1-positive cells in the perisinusoidal fibrotic area. These results indicate that the infant developed chronic (end stage) liver failure by 3 months of age. We excluded congenital infection, metabolic syndrome and citrin deficiency. It is therefore conceivable that intrauterine cardiac failure may be responsible for liver fibrosis. Early detection of liver dysfunction soon after birth is a key to predict the prognosis of severe IUGR in preterm infants.
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PMID:Liver fibrosis in an extremely small infant for gestational age. 2051 75

A 57-year-old male had suffered from back pain for years. Three years before the presenting symptoms he had had a lumbar disc operation during which he had bled markedly. Current symptoms of tiredness and dyspnea were new to this otherwise healthy and active man. Initial examinations revealed an enlarged liver, some ascites and signs of heart failure. A liver biopsy showed well-preserved structures with minor signs of inflammation. Cardiac cathetrization revealed increased pulmonary pressures and thus portopulmonary hypertension was suspected. A clinical examination, however, revealed a thrill and a strong systodiastolic murmur in the lower abdomen. CT-angiography confirmed the suspicion of an arteriovenous fistula. The fistula was successfully treated with a covered stent placed in the common iliac artery.
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PMID:[Chronic back pain, hepatomegaly and dyspnea]. 2082 71

A two-day-old, full-term male infant was admitted to the neonatal intensive care unit with heart failure. He was found to be non-dysmorphic, with no clinical evidence of sepsis. Physical examination was significant for hepatomegaly, active precordium, pansystolic murmur and hypotension requiring ionotropic support. A cranial bruit was detected on auscultation. Chest radiography revealed cardiomegaly and pulmonary oedema due to heart failure. Electrocardiogram and two-dimensional echocardiography were normal. Magnetic resonance imaging of the brain showed a large vein of Galen malformation, extensive cerebral ischaemia and multiple cerebral infarcts. This case illustrates the importance of auscultation of the cranium to rule out vein of Galen malformation, a potential cause of high-output cardiac failure in neonates in the absence of other common causes of heart failure.
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PMID:Clinics in diagnostic imaging (132). Vein of Galen malformation. 2114 Jan 18

Myeloid sarcoma (MS) is a neoplasm of immature granulocytes, monocytes, or both involving extramedullary sites. MS with no evidence of leukemia (nonleukemic MS) is very rare and the initial diagnosis can be difficult. This report describes an unusual case of nonleukemic MS of the liver in a 16-year-old patient presenting as debilitating hepatomegaly. A liver biopsy revealed diffuse infiltration by neoplastic cells of myeloid lineage (CD68, myeloperoxidase). A bone marrow biopsy showed no evidence of medullary involvement. The patient subsequently developed heart failure. Autopsy revealed infiltration of most organs by neoplastic cells but failed to identify abnormal myeloid cells in bone marrow.
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PMID:Nonleukemic myeloid sarcoma of the liver: a case report and review of literature. 2148 46


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