Left ventricular remodelling in post-myocardial infarction patients with left ventricular ejection fraction 40-50% vs 25-39%. influence of nisoldipine treatment? An echocardiographic substudy from the DEFIANT II study

Citation
Je. Otterstad et al., Left ventricular remodelling in post-myocardial infarction patients with left ventricular ejection fraction 40-50% vs 25-39%. influence of nisoldipine treatment? An echocardiographic substudy from the DEFIANT II study, SC CARDIOVA, 33(4), 1999, pp. 234-241
Citations number
15
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
SCANDINAVIAN CARDIOVASCULAR JOURNAL
ISSN journal
14017431 → ACNP
Volume
33
Issue
4
Year of publication
1999
Pages
234 - 241
Database
ISI
SICI code
1401-7431(1999)33:4<234:LVRIPI>2.0.ZU;2-F
Abstract
Objective: Left ventricular (LV) remodelling following acute myocardial inf arction has generally been studied in patients with LV ejection fraction (E F) < 40%, and it has been shown that this process can be attenuated by ACE inhibitors. Little is known regarding LV remodelling in patients with LVEF greater than or equal to 40% or the effects of treatment in this patient co hort. The DEFIANT II study (Doppler Flow and Echocardiography in Functional cardiac insufficiency) included 542 post-infarction patients with LVEF 25- 50% without overt heart failure within 13 days following acute myocardial i nfarction (AMI). They were then randomized to nisoldipine coat-core (CC) or placebo and followed up for 6 months. Design: Two-dimensional echoes were obtained after 8 (5-13) days and 6 months following AMI. Setting: LV end di astolic (ED) and end systolic (ES) volumes (V) were calculated in 503 patie nts with technically satisfactory paired echoes using the biplabe method of discs in a core laboratory. Subjects: Group A. 217 patients with baseline EF 40-50%, of whom 112 were randomized to nisoldipine and 104 to placebo (o ne patient was taken off study medication). Group B. 286 patients with EF 2 5-39%, of whom 145 were randomized to nisoldipine and 141 to placebo. Resul ts: LVEDV was 175 (+/- 45) ml in Group A vs 203 (+/- 49) ml in Group B (p = 0.001) at baseline and 184 (+/- 48) ml vs 213 (+/- 56) ml (p = 0.001), res pectively, at 6 months. LVESV at baseline was 97 (+/- 42) ml in Group A vs 133 (+/- 37) ml in Group B (p = 0.001), and 106 (+/- 34) ml vs 134 (+/- 45) ml (p = 0.001) at 6 months, respectively. The increase of LVESV was 9 (+/- 29) ml in Group A vs 2 (+/- 35) ml in Group B (p = 0.007). LVEF decreased by 2 (+/- 6)% in Group A vs an increase of 3 (+/- 6)% in Group B (p = 0.001 ). Treatment with nisoldipine had no influence on LV volumes in either of t he two groups or in the total study group. Conclusion. LV dilatation 6 mont hs following AMI in patients with EF 40-50% was similar in end diastole, bu t more pronouneced in end systole vs patients with EF 25-39%. LV remodellin g did not change significantly after nisoldipine treatment.