Sustained hemodynamic efficacy of therapy tailored to reduce filling pressures in survivors with advanced heart failure.
BACKGROUND
During therapy to relieve congestion in advanced heart failure, cardiac filling pressures can frequently be reduced to near-normal levels with improved cardiac output. It is not known whether the early hemodynamic improvement and drug response can be maintained long term.


RESULTS
After referral for cardiac transplantation with initially severe hemodynamic decompensation, 25 patients survived without transplantation to undergo hemodynamic reassessment after 8+/-6 months of treatment tailored to early hemodynamic response. Initial changes included net diuresis, increased ACE inhibitor doses, and frequent addition of nitrates. After 8 months of therapy, early reductions were sustained for pulmonary wedge pressure (24+/-9 to 15+/-5 mm Hg early; 12+/-6 mm Hg late) and systemic vascular resistance (1651+/-369 to 1207+/-281 dynes x s(-1) x cm(-5) early; 1003+/-193 dynes x s(-1) x cm(-5) late). Acute response to doses persisted at reevaluation. Sustained reduction in filling pressures was accompanied by a progressive increase in stroke volume (42+/-10 to 56+/-13 mL early; 79+/-20 mL late), improved functional class, and freedom from resting symptoms. Study design did not control for amiodarone, which was initiated for arrhythmias in 12 patients and associated with greater improvement in cardiac index (1.8 to 3.2 L min(-1) x m(-2) late on amiodarone versus 2.0 to 2.6 L x min(-1) x m(-2), P<.05).


CONCLUSIONS
During chronic therapy tailored to early hemodynamic response in advanced heart failure, acute vasodilator response persists, and near-normal filling pressures can be maintained in patients who survive without transplantation. Stroke volumes at low filling pressures increase further over time. Chronic hemodynamic improvement was accompanied by symptomatic improvement, but the contributions of the monitored hemodynamic approach, increased vasodilator doses, and comprehensive outpatient management have not yet been established.
Steimle
A E
AE
Ahmanson-UCLA Cardiomyopathy Center, UCLA School of Medicine, Los Angeles, Calif, USA.
Stevenson
L W
LW
Chelimsky-Fallick
C
C
Fonarow
G C
GC
Hamilton
M A
MA
Moriguchi
J D
JD
Kartashov
A
A
Tillisch
J H
JH
D000638:Amiodarone / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D002302:Cardiac Output; D004232:Diuretics / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006830:Hydralazine / Q000494:pharmacology / Q000627:therapeutic use; D007548:Isosorbide Dinitrate / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D014665:Vasodilator Agents / Q000494:pharmacology / Q000627:therapeutic use*; D017725:Ventricular Pressure / Q000187:drug effects
D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D004232:Diuretics; D014665:Vasodilator Agents; D006830:Hydralazine; D002216:Captopril; D007548:Isosorbide Dinitrate; D000638:Amiodarone