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

Septic shock in obstetrics is a major cause of mortality. Postpartum endometritis is often the first step of bacterial colonization inside the uterus which becomes the nidus of infection. Rapid spread into general circulation is favoured by hemodynamics patterns of pregnancy. Bacteremia would result in cardiovascular collapse and a myocardial depressant factor has been proposed to explain the fall in cardiac output. Later, endotoxin activates the substances of malignant intravascular inflammation and multiple systems organ failure may be observed in uncontrolled sepsis. Eight cases are reported hospitalized at Morelia's General Hospital, SSA, with septic shock and MSOF. Presumably because of aggressive acute resuscitation nobody succumbed during acute cardiac failure and hypotensive episode but two patients died later with multiple system organ failure. The mortality was 25%. Fluid, resuscitation, and vasoactive drugs are the most effective way to reduce mortality. Antibiotics, specific treatment of MSOF and taking away the nidus of infection are critical components of therapy.
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PMID:[Septic shock in obstetrics]. 207 37

A patient with photosensitivity is described who presented with an overlap syndrome combining features of systemic lupus erythematosus with a mild polymyositis and scleroderma and with symptoms of the sicca syndrome. In addition, he was anti-SSA/Ro positive and had a constellation of antibodies directed to ENA including the anti-SL-Ki antibody. The condition was fatal and he died from heart failure and respiratory insufficiency.
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PMID:Anti-SL-Ki antibody in a patient with fatal connective tissue overlap disease. 278 73

Isolated congenital complete heart block is frequently found in offspring of mothers who have IgG anti-Ro/SSA autoantibodies. IgG deposition was reported in the heart of a baby who died from heart block and heart failure. The pattern of antibody deposition observed was the same as that reproduced in animal models for anti-Ro/SSA binding. The IgG deposition was present in, but not limited to, the conduction system. Scattered small infiltrates of mononuclear cells and a limited, patchy deposition of complement were also observed. These findings support the possibility that isolated congenital heart block may be causally related to autoantibodies.
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PMID:Cardiac immunoglobulin deposition in congenital heart block associated with maternal anti-Ro autoantibodies. 331 97

Complete congenital heart block (CCHB) is the most severe manifestation of neonatal lupus syndrome, associated with a mortality rate of up to 31%. It is caused by irreversible damage to the cardiac conduction system due to the transplacental passage of maternal antibodies to the fetus. Anti-Ro (SSA) and anti-La (SSB) antibodies are usually detected in sera of mothers of children with prenatally diagnosed CCHB and in cardiac tissues of affected newborns. Their pathogeneic role in the development of CCHB has been established in several studies. When CCHB is detected during pregnancy, careful monitoring and delivery are needed before heart failure is developed. Treatment strategies are debatable and may include prophylactic therapy for high-risk pregnant women and a combination of intrauterine plasmapheresis with plasma exchange or with corticosteroids. Pacemaker insertion is required in most infants during the first three months of life. Assays for anti-Ro (SSA) and anti-La (SSB) antibodies should be performed on sera of pregnant women with SLE and newborns with CCHB.
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PMID:Anti-Ro (SSA) and anti-La (SSB) antibodies and complete congenital heart block. 925 27

Persistent fetal bradycardia is infrequent in prenatal life and difficult to manage optimally. It is generally attributable to sinus bradycardia due to fetal distress, blocked atrial extrasystoles, and congenital complete heart block. We reported four cases of persistent fetal bradycardia from 1995 to 1999 in our hospital. The first, second, and third cases of sustained fetal bradycardia had congenital complete heart block with positive titers for anti-Ro/SSA antibodies in both mothers and fetuses. Because of progressive fetal hydrops in the second case, the pregnancy was terminated. The first and third cases were isolated congenital complete heart block without structural anomaly. After prenatal examination the babies were followed up closely until term and both had a good prognosis without any implantation of pacemaker. In the fourth case there was no clinically known etiology associated with sustained fetal bradycardia. The fetal heart rate returned to normal after 6 weeks of follow-up and the baby was delivered without any cardiac problems. Congenital complete heart block is the most common cause of persistent fetal bradycardia. Prenatal detailed monitoring until delivery is necessary before heart failure develops. Treatment strategies (corticosteroids, ritodrine, and plasmapheresis) are debatable and may include prophylactic therapy for high-risk pregnant women.
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PMID:Prenatal diagnosis of persistent fetal bradycardia: report of four cases. 1129 78

Congenital atrioventricular block is a rare, but severe occurrence in the newborn can be related to various cardiac malformations or to maternal autoimmune diseases, particularly systemic lupus erythematosus. We report an extremely low-birth-weight infant affected by congenital heart block, due to positive anti-RO/SSA and anti-LA/SSB antibodies of the mother, with progressively increasing respiratory distress syndrome and heart failure. The infant was successfully treated with an external constant-current, single-chamber ventricular (VVI) temporary epicardial pacing, placed on the second day of life, at the weight of 810 g. After this treatment, cardiac failure resolved and respiratory assistance could be rapidly stopped. A single-chamber, rate-responsive, permanent pacemaker was placed at 3 months of life with steroid-eluting, epicardial-pacing leads. We emphasize that early extrathoracic temporary epicardial pacing is able to resolve heart failure in an extremely low-birth-weight infant.
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PMID:Temporary epicardial pacing in an extremely low-birth-weight infant with congenital atrioventricular block. 1837 66

Sjogren syndrome is associated with lymphoproliferative disease in 7% of cases; however, association with AL amyloidosis is uncommon. We present a patient who presented simultaneously with Sjogren syndrome (supported by dry mouth, positive Schirmer's test, anti-Ro/SSA antibodies, and a lower lip salivary gland biopsy) and AL amyloidosis revealed by heart failure without myeloma. Although is it know that amyloidosis can masquerade as Sjogren syndrome, the occurrence of simultaneous AL amyloidosis and primary Sjogren syndrome has been reported rarely.
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PMID:Systemic light chain amyloidosis and Sjogren syndrome: an uncommon association. 1963 91

The incidence of congenital atrioventricular (AV) block is between 1 in 15,000 and 1 in 20,000 births. It may occur in isolation or as a consequence of anomalous development of the conduction tissue in the context of a cardiac malformation. In this review, we use the term congenital AV bock to describe complete heart block when it is diagnosed in utero or at birth. The pathophysiological process is believed to be due to immune-mediated injury of the conduction system, which occurs as a result of transplacental passage of maternal anti-SSA/Ro-SSB/La antibodies. Many mothers are asymptomatic carriers, and less than one-third have a preexisting diagnosis of a rheumatological disorder. The AV block that develops months or years after birth probably occurs as a result of a different disease process that is poorly understood. The diagnosis of congenital AV block is usually confirmed by fetal echocardiography before birth and by electrocardiography after birth. The implantation of a pacemaker is recommended for symptomatic patients and for asymptomatic patients presenting with profound bradycardia, left ventricular dysfunction, a wide QRS interval, or a prolonged QT interval. It is now recognized that a subset of paced patients develop dilated cardiomyopathy and heart failure, and therefore regular follow-up is important. They are also at high risk of developing complications related to the presence of intracardiac material as a result of prolonged exposure to pacing materials. Future areas of research to minimize these risks include assessing the impact of alternative stimulation sites and the development of new cardiac stimulation techniques.
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PMID:Pathophysiology, clinical course, and management of congenital complete atrioventricular block. 2327 18

This case presents a patient with biopsy-proven, wild-type transthyretin (TTR) senile amyloidosis. The case was that of a man in his early 70s who presented with gradually progressive symptoms and signs of heart failure. The recent history included an episode of severe pancreatitis secondary to cholelithiasis and subsequently (and incidentally) noted hepatomegaly and marked ascites. Further evaluation of the aetiology of the heart failure, through echocardiography, coronary angiography and endomyocardial biopsy, led to an exact diagnosis of SSA. The patient is being treated with conventional heart failure medications while consideration is given to the use of diflusinal as an antiamyloidogenic small molecular stabiliser of TTR. Monitoring and further management advice are being coordinated by the National Amyloidosis Centre.
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PMID:Senile cardiac amyloidosis: an underappreciated cause of heart failure. 2339 47

Fetuses with anti-SSA-mediated complete atrioventricular block (CAVB) are at high risk for perinatal death if they present at <20 weeks of gestation and develop ventricular rates of <55 beats per minute (bpm), cardiac dysfunction, or hydrops [Izmirly et al.: Circulation 2011;124:1927-1935; Jaeggi et al.: J Am Coll Cardiol 2002;39:130-137; Eliasson et al.: Circulation 2011;124:1919-1926]. After our experience with two such fetuses who died with pulseless electrical activity despite being paced within 30 min of birth, we performed an ex utero intrapartum treatment procedure to ventricular pacing on a 36-week CAVB fetus with cardiac dysfunction, mild hydrops, and a ventricular rate of 46 bpm. While still on placental bypass, temporary epicardial ventricular pacing leads were successfully placed; the infant was delivered and made a successful transition to postnatal life. This approach can improve the 11-fold increase in mortality for the preterm fetus with long-standing CAVB, severe bradycardia, and heart failure.
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PMID:Ex utero Intrapartum Treatment to Ventricular Pacing: A Novel Delivery Strategy for Complete Atrioventricular Block with Severe Bradycardia. 2857 50


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