PMID- 9562938
OWN - NLM
STAT- MEDLINE
DCOM- 19980609
LR  - 20200225
IS  - 0160-9289 (Print)
IS  - 1932-8737 (Electronic)
IS  - 0160-9289 (Linking)
VI  - 21
IP  - 4
DP  - 1998 Apr
TI  - Influence of tissue affinity of angiotensin-converting enzyme inhibitors on left 
      ventricular remodeling after myocardial infarction.
PG  - 277-85
AB  - BACKGROUND: The demonstration of local renin-angiotension systems has raised the 
      question of whether angiotensin-converting enzyme (ACE) inhibitors with different 
      tissue affinities differ with regard to their effects on postinfarction 
      remodeling. HYPOTHESIS: The study was undertaken to investigate the influence of 
      ACE inhibitors with different tissue affinity on morphology and function of the 
      infarcted left ventricle. METHODS: In all, 52 patients (17 women, 35 men, 38-73 
      years) with large acute myocardial infarction were randomized to receive either 
      25-75 mg/day captopril or 10-20 mg/day fosinopril beginning on the Day 7 after 
      infarction. Of these, 28 had anterior and 24 had posterior wall infarctions. 
      Infarct size was determined by the creatine kinase integral method. Fifty 
      patients were examined by cinemagnetic resonance imaging (CMRI) 1 and 26 weeks 
      after infarction. The following parameters were determined: left ventricular 
      end-diastolic and end-systolic volume index (LVEDVI, LVESVI), ejection fraction 
      (LVEF), infarct weight, and muscle mass (LVMM). The volume-to-mass ratio (VMR) 
      was calculated and the clinical status according to the guidelines of the New 
      York Heart Association (NYHA) was documented at each examination time. The 
      results were compared with those of a historical sample without ACE-inhibitor 
      therapy examined in an identical manner (n = 31, 10 women, 21 men, 36-75 years). 
      RESULTS: LVEDVI and LVESVI increased in the first 6 months after infarction by 
      24.9 and 36.6%, respectively, in the historical sample; by 11.0 and 7.8%, 
      respectively, under captopril; and by 13.1 and 10.7%, respectively, under 
      fosinopril. LVEF decreased by 14.9% in the untreated sample, by 3.7% under 
      captopril and by 5.0% under fosinopril. Infarct weight and LVMM increased by 12.7 
      and 15.3%, respectively, without ACE inhibition, by 5.7 and 10.1%, respectively, 
      in patients treated with captopril, and by 6.1 and 9.3%, respectively, in 
      patients treated with fosinopril. The VMR increased by 7.4% in the historical 
      sample, by 3.5% in the captopril group, and by 1.8% in the fosinopril group. The 
      NYHA clinical status improved by 18.2% without ACE inhibition, by 42.9% in the 
      captopril group, and by 26.3% in the fosinopril group. The differences between 
      the two ACE-inhibitor groups and the reference group were all significant, while 
      the differences between the captopril group and the fosinopril group were 
      significant only for VMR (p < 0.01) and NYHA class (p < 0.05). CONCLUSIONS: Both 
      captopril and fosinopril have a comparable positive influence on postinfarction 
      remodeling and on clinical status. Lipophilicity and tissue affinity do not seem 
      to play a clinically important role in ACE-inhibitor therapy after infarction.
FAU - Konermann, M
AU  - Konermann M
AD  - Medical Department, Ruhr University of Bochum, Marienhospital Herne, Kasse, 
      Germany.
FAU - Altmann, C
AU  - Altmann C
FAU - Laschewski, F
AU  - Laschewski F
FAU - Josephs, W
AU  - Josephs W
FAU - Odenthal, H J
AU  - Odenthal HJ
FAU - Horstmann, E
AU  - Horstmann E
FAU - Sanner, B
AU  - Sanner B
LA  - eng
PT  - Clinical Trial
PT  - Comparative Study
PT  - Journal Article
PT  - Randomized Controlled Trial
PL  - United States
TA  - Clin Cardiol
JT  - Clinical cardiology
JID - 7903272
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 9G64RSX1XD (Captopril)
RN  - EC 2.7.3.2 (Creatine Kinase)
RN  - R43D2573WO (Fosinopril)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Angiotensin-Converting Enzyme Inhibitors/*therapeutic use
MH  - Captopril/*therapeutic use
MH  - Creatine Kinase/blood
MH  - Female
MH  - Follow-Up Studies
MH  - Fosinopril/*therapeutic use
MH  - Heart Ventricles/drug effects/enzymology/pathology
MH  - Humans
MH  - Magnetic Resonance Imaging, Cine
MH  - Male
MH  - Middle Aged
MH  - Myocardial Contraction/drug effects
MH  - Myocardial Infarction/*drug therapy/pathology/physiopathology
MH  - Organ Size
MH  - Stroke Volume/drug effects
MH  - Treatment Outcome
MH  - Ventricular Function, Left/*physiology
PMC - PMC6655384
EDAT- 1998/05/01 00:00
MHDA- 1998/05/01 00:01
PMCR- 2009/02/03
CRDT- 1998/05/01 00:00
PHST- 1998/05/01 00:00 [pubmed]
PHST- 1998/05/01 00:01 [medline]
PHST- 1998/05/01 00:00 [entrez]
PHST- 2009/02/03 00:00 [pmc-release]
AID - CLC4960210409 [pii]
AID - 10.1002/clc.4960210409 [doi]
PST - ppublish
SO  - Clin Cardiol. 1998 Apr;21(4):277-85. doi: 10.1002/clc.4960210409.