Heart failure in pediatric patients.
Paradigms in understanding heart failure have changed as the knowledge of pathophysiology and its molecular basis has deepened. In the chronic compensated state of heart failure recent research has focussed on the body's regulatory mechanisms. Today heart failure is understood as a complex interplay of hemodynamic and neurohormonal factors. In pediatrics a large variety of heterogeneous conditions cause heart failure. Some require special therapeutic approaches such as the infusion of prostaglandin for ductal patency, the careful maintenance of balance between systemic and pulmonary circulations or operative treatment. In newborns with critical congenital lesions and in patients in the postoperative period management of acute heart failure becomes important. Chronic heart failure as it is understood today is present in patients with cardiomyopathies and in an increasing number of pediatric patients after palliative surgery. In heart failure due to left-to-right shunts a similar activation of compensatory neurohormonal mechanisms as in adults with chronic heart failure was found. In small clinical trials treatment of these activated compensatory mechanisms with angiotensin-converting enzyme inhibitors and beta-blockers showed beneficial effects in pediatric patients. However large clinical multicenter trials as performed in the adult population should be conducted.
Hoch
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Department of Pediatric Cardiology and Intensive Care, Ludwig- Maximilians-University, Munich, Germany. martin.hoch@med.uni-muenchen.de
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D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000527:Alprostadil / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002118:Calcium / Q000502:physiology; D002316:Cardiotonic Agents / Q000627:therapeutic use; D002395:Catecholamines / Q000627:therapeutic use; D002675:Child, Preschool; D004071:Digitalis Glycosides / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D002149:Energy Intake; D006330:Heart Defects, Congenital / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D018377:Neurotransmitter Agents / Q000378:metabolism; D014665:Vasodilator Agents / Q000627:therapeutic use; D018754:Ventricular Dysfunction / Q000503:physiopathology
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002316:Cardiotonic Agents; D002395:Catecholamines; D004071:Digitalis Glycosides; D004232:Diuretics; D018377:Neurotransmitter Agents; D014665:Vasodilator Agents; D000527:Alprostadil; D002118:Calcium