Recovery of Heart Function in Children With Acute Severe Heart Failure

2008 ◽  
Vol 85 (7) ◽  
pp. 975-979 ◽  
Author(s):  
John J. OʼSullivan ◽  
Susan L. Roche ◽  
David S. Crossland ◽  
Milind P. Chaudhari ◽  
Richard C. Kirk ◽  
...  
2020 ◽  
pp. 112972982096931
Author(s):  
Jan Malik ◽  
Carlo Lomonte ◽  
Joris Rotmans ◽  
Eva Chytilova ◽  
Ramon Roca-Tey ◽  
...  

Chronic kidney disease is associated with increased cardiovascular morbidity and mortality. A well-functioning vascular access is associated with improved survival and among the available types of vascular access the arterio-venous (AV) fistula is the one associated with the best outcomes. However, AV access may affect heart function and, in some patients, could worsen the clinical status. This review article focuses on the specific cardiovascular hemodynamics of dialysis patients and how it is affected by the AV access; the effects of an excessive increase in AV access flow, leading to high-output heart failure; congestive heart failure in CKD patients and the contraindications to AV access; pulmonary hypertension. In severe heart failure, peritoneal dialysis (PD) might be the better choice for cardiac health, but if contraindicated suggestions for vascular access selection are provided based on the individual clinical presentation. Management of the AV access after kidney transplantation is also addressed, considering the cardiovascular benefit of AV access ligation compared to the advantage of having a functioning AVF as backup in case of allograft failure. In PD patients, who need to switch to hemodialysis, vascular access should be created timely. The influence of AV access in patients undergoing cardiac surgery for valvular or ischemic heart disease is also addressed. Cardiovascular implantable electronic devices are increasingly implanted in dialysis patients, but when doing so, the type and location of vascular access should be considered.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Chad M Trent ◽  
Li Liu ◽  
Xiang Fang ◽  
Ni-Huiping Son ◽  
Hongfeng Jiang ◽  
...  

Diacylglycerol acyl transferase 1 (DGAT1) catalyzes the final step in triglyceride (TG) synthesis, the conversion of diacylglycerol (DAG) to TG. Dgat1-/- mice exhibit a number of beneficial metabolic effects including reduced obesity and improved insulin sensitivity and no known cardiac dysfunction. In contrast, failing human hearts have severely reduced DGAT1 expression associated with accumulation of DAGs and ceramides. To test whether DGAT1 loss alone affects heart function we created cardiomyocyte specific DGAT1 knockout (hDgat1-/-) mice. hDgat1-/- mice hearts had 95% increased DAG and 85% increased ceramides compared to floxed controls. 50% of these mice died by 9 months of age. The heart failure marker brain natriuretic peptide (Bnp) increased 5-fold in hDgat1-/- hearts and fractional shortening (FS) was reduced. This was associated with a 30% increase in PPARalpha and a 40% increase in Cd36. We crossed hDgat1-/- mice with previously described enterocyte-specific Dgat1 knockout mice (hiDgat1-/-). This corrected the early mortality, improved FS 40%, and reduced cardiac ceramide and DAG content. Treatment of hDgat1-/- mice with GLP-1 receptor agonist exenatide for 1 week reduced Bnp mRNA by 50%, improved FS, and reduced heart DAG and ceramide content by 30-40%. Increased fatty acid uptake into hDgat1-/- hearts was normalized by exenatide. Reduced activity of protein kinase Cα (PKCα), which is known to be increased by DAG and ceramides, paralleled the reductions in these lipids. Our mouse studies show that loss of DGAT1 reproduces the lipid abnormalities seen in severe human heart failure.


2020 ◽  
Author(s):  
Elizabeth H Ketchum ◽  
Robert M Brooks ◽  
Jeffrey R Greenwald

Abstract Neonatal myocarditis and heart failure secondary to maternal infection with a myocarditis-associated virus in the weeks preceding delivery is rare. To our knowledge, this is the first report of an infant with myocarditis and heart failure in the setting of a maternal diagnosis of influenza A. Influenza is, however, known to be a cause of myocarditis in children, and several studies have shown vertical transmission of antibodies to influenza. Here, we present a full-term infant who presented with central cyanosis and respiratory distress at 30 minutes of life. No prenatal concerns had been identified. The infant continued to have poor saturations and mixed respiratory and metabolic acidosis despite intubation and administration of 100% FiO2. He was found to have severe biventricular dysfunction on echocardiogram. In discussion with the parents, it was elucidated that the mother had tested positive for influenza A 3 weeks before delivery. The presumptive diagnosis for this infant is heart failure secondary to influenza myocarditis that he contracted in utero. He demonstrated full return of heart function and was discharged home from the Cardiac Intensive Care Unit by day of life 10. Neonates with central cyanosis must be evaluated and treated emergently as these infants are at risk for life-threatening disease and downstream morbidity secondary to tissue hypoxia. The purpose of this case report is to highlight a rare but devastating etiology of cyanosis in neonates and to discuss the recommended course of evaluation and treatment for health care providers.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
James D Fett ◽  
Herriot Sannon ◽  
Emmeline Thélisma ◽  
Therese L Sprunger ◽  
Venkita Suresh

Peripartum cardiomyopathy (PPCM) is a form of heart failure from dilated cardiomyopathy with one of the greatest potentials for eventual full systolic function recovery. Traditional concepts of PPCM have held that if recovery did not occur by the six-month post-diagnosis mark, it would be unlikely to happen. This report shows that improvement and eventual full recovery may occur long after that initial period. PPCM patients have been identified from the Hôpital Albert Schweitzer PPCM Registry, Deschapelles, Haiti, from 2000 to 2008. All patients fully met diagnostic criteria for PPCM, which include onset of heart failure during the last month of pregnancy up to 5 months postpartum, absence of previous heart disease or other cause of heart failure, and echocardiographic criteria for systolic dysfunction. Recovery was defined as left ventricular (LV) ejection fraction (EF) greater than 50 percent. Echocardiography was carried out at initial diagnosis and at 6-month intervals, with a minimum of 24 months follow-up required for inclusion. Standard treatment included diuretics (lasix) and ACE-inhibitors (captopril), as determined by economic factors, which also excluded the routine use of beta-blockade. Thirty-two out of 116 (27.6 %) PPCM patients fully recovered LV systolic function. Mean follow-up was 35 months. The shortest time to recovery was 3 months and the longest time to recovery was 48 months. The number and cumulative percentage of recovery is shown in the following table : Table: Length of time required for recovery of left ventricular function in 32 Haitian PPCM patients, 2000–2008: Likelihood of recovery did not correlate with age (17–47 years), parity (1–10) or LV EF at diagnosis (12 to 40 %). Complete recovery of LV systolic function in PPCM often occurs after the first 6 to 12 months following diagnosis. It is important to continue treatment and follow-up sufficiently long to assure and document maximum benefit


2003 ◽  
Vol 2 (1) ◽  
pp. 108
Author(s):  
G DAN ◽  
A DAN ◽  
I DAHA ◽  
C STANESCU ◽  
V ILIE ◽  
...  

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