The Pilot Randomized Study of Nesiritide Versus Dobutamine in Heart Failure (PRESERVD-HF).
Acute heart failure syndromes (AHFS) are related to several diseases affecting not only the heart but also the kidneys and blood vessels. Emerging evidence indicates that myocardial injury may also play a role in the pathophysiology of AHFS, as suggested by increased levels of markers of injury, such as cardiac troponin (cTn). Although cTn is a known prognostic marker, the release of cTn during hospitalization has not been evaluated prospectively with serial measures. We prospectively evaluated patterns of cTn release by conducting serial measures of cTnI and cTnT in patients hospitalized for AHFS. This study enrolled 51 patients with AHFS who were admitted with worsening heart failure (HF) and a history of coronary artery disease (CAD) in whom an acute coronary event was not suspected. Levels of cTnI and cTnT were measured at 8, 32, 56, and 80 hours after study entry. At baseline, 73.9% of patients had detectable cTnI, and 43.5% had detectable cTnT levels. The median concentrations of cTnI and cTnT were unchanged from 0 to 32 hours, increased from 32 to 56 hours, then either plateaued (cTnT) or decreased to baseline (cTnI). Of the 26 patients who had no detectable cTn levels at baseline, 2 (7.7%) developed detectable cTnT and 5 (41.7%) developed detectable cTnI release during hospitalization. Detectable levels of cTn at baseline were related to short-term clinical events. In this study of patients with CAD in whom an acute coronary event was not suspected, most had detectable levels of cTn present at admission, and some patients developed cTn release during hospitalization. Because cTn release may be a marker for myocardial injury, this study raises the possibility that injury occurred in most patients admitted with AHFS. Therefore, the goal of therapy for AHFS should be not only to improve symptoms and hemodynamics but also to salvage myocardium. Accordingly, therapies for AHFS that are aimed at improving hemodynamics may affect long-term prognosis by either injuring or salvaging myocardium.
Gheorghiade
Mihai
M
Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA. m-gheorghiade@northwestern.edu
Gattis Stough
Wendy
W
Adams
Kirkwood F
KF
Jaffe
Allan S
AS
Hasselblad
Victor
V
O'Connor
Christopher M
CM
D000318:Adrenergic beta-Agonists / Q000008:administration & dosage; D000368:Aged; D015415:Biomarkers / Q000097:blood; D004280:Dobutamine / Q000008:administration & dosage; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy / Q000209:etiology; D006760:Hospitalization; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications; D045283:Natriuretic Agents / Q000008:administration & dosage; D020097:Natriuretic Peptide, Brain / Q000008:administration & dosage; D010865:Pilot Projects; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D016032:Randomized Controlled Trials as Topic; D019210:Troponin I / Q000097:blood*; D020107:Troponin T / Q000097:blood*
D000318:Adrenergic beta-Agonists; D015415:Biomarkers; D045283:Natriuretic Agents; D019210:Troponin I; D020107:Troponin T; D020097:Natriuretic Peptide, Brain; D004280:Dobutamine