title: Renal and cardiac function during alpha1-beta-blockade in congestive heart failure.
abstract: The kidney and the neurohormonal systems are essential in the pathogenesis of congestive heart failure (CHF) and the physiologic response. Routine treatment of moderate to severe CHF consists of diuretics, angiotensin-converting enzyme (ACE) inhibition and beta-blockade. The need for control of renal function during initiation of ACE-inhibition in patients with CHF is well known. The aim of this study was to investigate whether supplementation by a combined alpha1-beta-blockade to diuretics and ACE-inhibition might improve cardiac function without reducing renal function.
  
  
  METHODS
  Fourteen patients treated for moderate to severe CHF with diuretics and ACE inhibitors were investigated at baseline, after 4 months of maximum carvedilol treatment and after withdrawal of carvedilol.
  
  
  RESULTS
  Carvedilol lowered blood pressure and heart rate but increased left and right ventricular ejection fractions without changing cardiac output or pulmonary blood volume. At the same time, a minor fall was seen in glomerular filtration rate (GFR). but renal blood flow was unchanged and effective renal plasma flow slightly increased. Carvedilol also lowered the plasma levels of angiotensin II and aldosterone. All changes were reversed after withdrawal of carvedilol.
  
  
  CONCLUSIONS
  Carvedilol augments ACE-inhibitor-induced vasodilation by lowering blood pressure, and angiotensin II beside reducing heart rate. The heart adapts to the haemodynamic alterations without changes in cardiac output and pulmonary blood volume. GFR is slightly lowered despite no changes in renal blood flow and a slight increase in effective renal plasma flow. The study emphasizes the need for control of renal function during treatment with carvedilol in patients with CHF.
authors: Department of Internal Medicine, Roskilde Hospital, Denmark. m.heitmann@dadlnet.dk
authors: M
authors: M
authors: Heitmann
authors: U
authors: U
authors: Davidsen
authors: K H
authors: KH
authors: Stokholm
authors: K
authors: K
authors: Rasmussen
authors: H
authors: H
authors: Burchardt
authors: E B
authors: EB
authors: Petersen
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000368:Aged; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002227:Carbazoles / Q000627:therapeutic use*; D002302:Cardiac Output / Q000187:drug effects; D000077261:Carvedilol; D004232:Diuretics / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006321:Heart / Q000502:physiology*; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000502:physiology*; D008875:Middle Aged; D011412:Propanolamines / Q000627:therapeutic use*; D012079:Renal Circulation / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002227:Carbazoles; D004232:Diuretics; D011412:Propanolamines; D000077261:Carvedilol; D000804:Angiotensin II; D000450:Aldosterone