title: Multiple neurohumoral modulating agents in systolic dysfunction heart failure: are we lowering blood pressure too much?
abstract: BACKGROUND
  Disease-modifying drug treatment in heart failure (HF) reduces blood pressure. Titration of these agents is guided by clinic blood pressure readings; however, the impact of such treatment on blood pressure is unknown because diurnal blood pressure patterns remain poorly described. The aim of this study was to examine the impact of additional neurohumoral modulating agents on ambulatory blood pressure monitoring (ABPM) control in patients with systolic HF and examine the relationship between the burden of hypotension and clinical outcomes.
  
  
  RESULTS
  In a prospective analysis on 45 patients undergoing initiation and optimization of additional medications (angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, or beta-blockers), mean daytime systolic (P = .035) and mean daytime and nocturnal diastolic hypotensive episodes (both P < .001) increased significantly posttitration. There was no change in clinic blood pressure before and after titration. In a cross-sectional analysis on 144 patients, those with the most diastolic hypotensive episodes had higher rates of HF readmissions (P = .01) and the composite end point of all-cause mortality and all-cause readmissions (P = .03).
  
  
  CONCLUSIONS
  Additional neurohumoral modulating agents could produce significant increases in 24-hour hypotension burden despite reassuring clinic blood pressure readings. The burden of diastolic hypotension is independently predictive of HF readmissions and the composite end point of all-cause mortality and emergency readmissions.
authors: Heart Failure Unit, St Vincent's University Hospital, Dublin 4, Ireland.
authors: George
authors: G
authors: Mak
authors: Niamh F
authors: NF
authors: Murphy
authors: Akbar
authors: A
authors: Ali
authors: Alison
authors: A
authors: Walsh
authors: Christina
authors: C
authors: O'Loughlin
authors: Carmel
authors: C
authors: Conlon
authors: Dermot
authors: D
authors: McCaffrey
authors: Mark
authors: M
authors: Ledwidge
authors: Kenneth
authors: K
authors: McDonald
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects*; D018660:Blood Pressure Monitoring, Ambulatory; D002940:Circadian Rhythm; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D005260:Female; D006333:Heart Failure / Q000188:drug therapy*; D006801:Humans; D007022:Hypotension / Q000139:chemically induced / Q000175:diagnosis; D007668:Kidney / Q000503:physiopathology; D008297:Male; D017202:Myocardial Ischemia / Q000188:drug therapy; D018377:Neurotransmitter Agents / Q000627:therapeutic use*; D010359:Patient Readmission; D011446:Prospective Studies; D013318:Stroke Volume / Q000502:physiology; D015996:Survival Rate; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D018377:Neurotransmitter Agents