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

A 57-year-old man, who had received a transfusion five years before, was admitted to our hospital complaining of worsening dyspnea on exertion. Cardiac catheterization was performed, and pulmonary hypertension was diagnosed. Liver dysfunction was also documented. We administered diuretics and observed his clinical course. Gradually worsening hypoxemia and radioisotope accumulation in the kidney following a lung perfusion scintigram suggested the existence of an intrapulmonary shunt. The patient died seven years later due to exacerbation of heart failure secondary to pulmonary infection. Autopsy revealed remarkable hypertensive pulmonary arteriopathy as well as abnormal dilation of precapillary pulmonary arterioles. Esophageal varices suggested portal hypertension. Marked hypoxemia and intrapulmonary vascular dilation suggest the contribution of an hepatopulmonary syndrome.
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PMID:[An autopsied case of primary pulmonary hypertension complicated by hepatopulmonary syndrome]. 769 75

We want to present our experience performed at the Institute of Radiology of Turin: 98 TIPS in 97 patients (in 1 patient, twice). METHODS. From March 1992, 97 cirrhotic patients (18 Child A, 48 Child B, 31 Child C) underwent the TIPS procedure for portal hypertension. The indications were digestive hemorrhage in 81 patients (20 of which performed in emergency for acute bleeding), intractable ascites in 13 patients and bleeding prevention in 3 patients. RESULTS. Immediate technical success was obtained in 95/98 cases (96.9%). Patients were monitored by US-Doppler at 24 hours, 2 months and every 6 months and by esophagogastroscopy at 2 and 6 months. Major clinical complications included CID (2 cases), hepatic failure (3 cases), renal insufficiency (2 cases), heart failure (1 case), recurrent bleeding (6 cases) and encephalopathy (15 cases). We had 5 early occlusion and 17 late stenosis of the shunt; 21 patients in this group were successfully treated either by PTA or restenting; one patient underwent a surgical shunt. Mortality rate follow-up was 0/17 among Child A patients, 7/48 (14.5%) among Child B patients and 12/29 (41.3%) among Child C patients. CONCLUSIONS. TIPS is a safe and valuable method for the treatment of portal hypertension. Though shunt stenosis may occur with a certain frequency (22/95, 23.1% in our study), a second intervention is usually effective in reducing gastro-oesophageal varices and ascites.
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PMID:[Intrahepatic portosystemic shunts]. 770 May 58

Eighteen patients with an acute thrombosis of the splanchnic veins were reviewed. Most of apparently idiopathic cases of splanchnic vein thrombosis are related to an increased coagulation related to a congenital or acquired defect of haemostasis. The aim of this study was to assess the effects of a new and effective treatment. Nine male and 9 female patients (range of age: 19 to 81 years) experienced a mesenteric venous thrombosis. There were 14 mesenteric vein thromboses with infarction, two transient mesenteric venous ischaemias without bowel infarction and two acute thromboses of the splanchnic veins without bowel ischaemia. A coagulopathy was detected in seven patients: oral contraception, protein C (PC) or antithrombin III (AT III) congenital deficiencies, acquired deficiency of AT III, PC and protein S (PS), polycythaemia in the post-partum period and primary myeloproliferative disorder. No coagulopathy was associated with thrombosis in eight cases: mesenteric haematoma, splenomegaly, cirrhosis, appendicectomy, cholescytectomy, chronic heart failure, treatment with beta-adrenergic receptor antagonist and digitalis, stenosis of the portal anastomosis after liver transplantation. Twelve patients required surgery: eight intestinal bowel resections with immediate anastomosis, four resections without immediate anastomosis. Only one patient underwent a second look for a repeat bowel resection. No death occurred in the early postoperative period and 17 out of 18 patients were alive after 12 years. An oral anticoagulant therapy was undertaken from two months to seven years. However, three patients suffered a recurrent thrombosis. Two of them required a long-term anticoagulation. Six patients experienced a portal hypertension and oral anticoagulants were discontinued in three of them because of bleeding oesophageal varices. Six patients were treated only by unfractionated heparin (UFH) or low molecular weight heparin (LMWH) followed by oral anticoagulants. After laparotomy, two were only treated with UFH without any bowel resection, as mesenteric venous ischaemia was too extensive. These observations suggest that the choice between an appropriate medical or surgical treatment is important and must be discussed. Since 1989, the therapeutic choice has been modified by ultrasonography and contrast enhanced computed tomographic scan which confirms diagnosis, allows to follow up and check the effects of anticoagulation and to choose the time for surgery. When the diagnosis is established and the patient's risk is low, the IU . kg(-1) . d(-1) to obtain an antifactor Xa activity between 0.3 and 0.6 antiXa IU mL(-1). When the diagnosis is uncertain and the patient's risk if high a laparotomy is required.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Mesentric venous thrombosis. Risk factors, treatment and outcome. An analysis of 18 cases]. 781 2

A 66 year old man with mild hypertension developed congestive cardiac failure of rapid onset associated with a continuous epigastric murmur suggesting an arteriovenous fistula. Doppler ultrasonography, computed tomography, magnetic resonance imaging and abdominal arteriography showed the fistula to arise from a large thrombosed aneurysm of the hepatic artery which had ruptured into the portal vein. Echocardiography and radionuclide angiography showed normal left ventricular systolic function. The patient underwent aneurysmorrhaphy and suture of the portal vein without any complications and the murmur and signs of cardiac failure disappeared. Histological examination showed the arterial lesion to be due to atherosclerosis. The authors underline the rarity of aneurysms of the hepatic artery and, above all, of their rupture into the portal system as there have only been 7 previously reported cases. Fistulae of the portal system are usually well tolerated, the commonest complication being portal hypertension. Cardiac failure is an exceptionally rare occurrence: it may be observed when the fistula develops suddenly and has a high flow rate, and in patients with abnormal myocardial function.
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PMID:[Congestive cardiac failure secondary to hepatico-portal arteriovenous fistula. Apropos of a case and review of the literature]. 821 73

Intrahepatic arterioportal fistulas (APF) are uncommon complications following hepatic trauma. Large fistulas can result in portal hypertension and cardiovascular compromise. A 46-year-old patient is described who presented with portal hypertension, variceal bleeding, and high output cardiac failure due to a large intrahepatic APF. Surgical closure of the APF by hepatic resection successfully resolved the portal hypertension, prevented further variceal hemorrhage, and restored normal cardiovascular function.
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PMID:Portal hypertension, variceal bleeding, and high output cardiac failure secondary to an intrahepatic arterioportal fistula. 826 Apr 35

A case of multiple focal nodular hyperplasia (FNH) of the liver associated with noncirrhotic portal hypertension and later complicated by pulmonary arterial hypertension leading to death from right heart failure is reported. In retrospect, the portal hypertension diagnosed in early life was most likely due to a congenital hypoplasia of portal vein branches and multiple FNH, a hyperplastic response of the liver parenchyma in association with anomalies of hepatic arterial branches as found within the lesions. This case may represent a form of multiple FNH syndrome restricted to the liver, because neither extrahepatic vascular malformation nor brain tumor was identified at autopsy. The FNH lesions had considerably expanded over the years, and the severe sinusoidal congestion due to chronic right-sided heart failure with subsequent prolonged parenchymal exposure to blood-borne hepatotrophic factors is a likely explanation for both the massive enlargement of FNH lesions and the nodular regenerative hyperplasia observed in the intervening parenchyma.
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PMID:Nodular transformation of the liver associated with portal and pulmonary arterial hypertension. 822 77

The transjugular intrahepatic portosystemic shunt (TIPS) is an exciting new addition to the therapeutic armamentarium against portal hypertension. It is currently indicated for salvage of patients with active variceal hemorrhage despite sclerotherapy or where sclerotherapy is not feasible. Its use for recurrent episodes of bleeding despite chronic sclerotherapy and for ascites and hepatorenal syndrome remains experimental. It is contraindicated in patients with right-heart failure and portal vein thrombosis. TIPS is not indicated for primary prophylaxis of variceal hemorrhage or portal decompression prior to liver transplantation. TIPS is associated with its unique spectrum of complications which can occasionally be life-threatening. Although initial experience with this procedure is encouraging, a great amount of work remains to be done to fully define its role in clinical practice.
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PMID:Transjugular intrahepatic portosystemic shunt: a medical perspective. 854 79

Sympathetic nervous system activation has been documented in several cardiovascular disorders. In some, characterized by cardiac failure and portal hypertension accompanying hepatic cirrhosis, the sympathetic nervous stimulation is reflex and, to some extent, compensatory but has adverse consequences. For example, in cardiac failure, the sympathetic nerves of the heart are preferentially stimulated, providing adrenergic support to the failing myocardium but at the probable cost of arrhythmogenesis and progressive myocardial deterioration. The sympathetic activation present in patients with essential hypertension, which involves the sympathetic outflows to skeletal muscle, heart, and kidneys and is seen particularly in younger patients, differs from these examples in that the sympathetic nervous stimulation is apparently not reflex and the primary cause is unknown. There is, however, evidence that activation of forebrain pressor noradrenergic nuclei may be of importance as an underlying central nervous system mechanism. This sympathetic nervous stimulation in patients with essential hypertension, in addition to initiating the blood pressure elevation, may also contribute to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidemia, with neural vasoconstriction having metabolic consequences, impairing glucose delivery and causing insulin resistance in muscle, and retarding postprandial clearing of lipids in liver. Trophic effects of sympathetic activation on cardiovascular growth are claimed but have yet to be demonstrated conclusively in humans.
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PMID:Sympathetic nervous system: contribution to human hypertension and related cardiovascular diseases. 864 1

Gall-bladder wall thickening is commonly seen in patients with cirrhosis, but its exact causes have not been well established. We evaluated clinical, biochemical and haemodynamic data of patients with cirrhosis with respect to the presence of thickening of the gall-bladder wall. After excluding patients who presented with gallstones, acute or chronic cholecystitis, heart failure, a serum creatinine level greater than 2 mg/dL and/or a serum alanine aminotransferase level greater than 400 U/L, 77 patients with cirrhosis (75 male, two female; mean age 58 +/- 8 years) were enrolled in the study. Clinical, biochemical, ultrasound and haemodynamic data were obtained in every patient. Forty-one (53%) of 77 patients with cirrhosis had gall-bladder wall thickening (> 4 mm). Compared with patients with a normal gall-bladder wall, patients with gall-bladder wall thickening had significantly lower serum albumin levels (3.6 +/- 0.6 vs 2.9 +/- 0.7 gm/dL, respectively; P < 0.05), a longer prothrombin time (13 +/- 6 vs 16 +/- 6 s, respectively; P < 0.05), more patients with Child-Pugh class C (6 vs 37%, respectively; P < 0.05) and more patients with ascites (8 vs 50%, respectively; P < 0.05). In addition, compared with patients with a normal gall-bladder wall, those patients with gall-bladder wall thickening had a higher hepatic venous pressure gradient (13.9 +/- 4.5 vs 17.1 +/- 4.1 mmHg, respectively; P < 0.01) and a lower systemic vascular resistance (SVR; 1144 +/- 332 vs 1010 +/- 318 dyn.s/cm5, respectively; P < 0.05). Using a multivariate analysis, the presence of ascites and SVR lower than 900 dyn.s/cm5 were independently correlated with the presence of gall-bladder wall thickening, while a hepatic vein pressure gradient greater than 10 mmHg had only a marginally significant association. The presence of ascites, decreased SVR and portal hypertension are related to the occurrence of gall-bladder wall thickening in patients with cirrhosis, indicating that the development of gall-bladder wall thickening may be multifactorial.
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PMID:Gall-bladder wall thickening in patients with liver cirrhosis. 919 2

The differential diagnosis of ascites often leads to confusion and an inability to exclude its multitude of causes in many patients. In this review, we outline the clinical features and laboratory investigations that usually elucidate the cause of ascites for the clinician in a simple and logical manner. Roughly 80-85% of cases of ascites are related to underlying chronic liver disease, but cardiac failure, tuberculosis, malignancy-related ascites and other less common causes should always be considered. Careful evaluation of the patient, including a clinical history, physical examination and diagnostic paracentesis should routinely be performed to determine the cause of ascites. Fluid should be sent for cell count and albumin along with simultaneous determination of serum albumin to determine the serum: ascites albumin gradient. This gradient allows classification of the cause of ascites into portal hypertension-related and nonrelated with a diagnostic accuracy of > or = 97%. The causes of ascites are individually discussed in relationship to their clinical features and to the laboratory investigations that are relevant in each situation.
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PMID:Differential diagnosis of ascites. 930 24


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