PMID- 19050458
OWN - NLM
STAT- MEDLINE
DCOM- 20090106
LR  - 20160803
IS  - 1081-5589 (Print)
IS  - 1081-5589 (Linking)
VI  - 56
IP  - 8
DP  - 2008 Dec
TI  - ACE insertion/deletion, but not -240A>T polymorphism, modulates the severity in 
      heart failure.
PG  - 1004-10
LID - 10.2310/JIM.0b013e31818e8028 [doi]
AB  - OBJECTIVE: : ACE gene is reported to be a candidate gene in heart failure. The 
      insertion/deletion (I/D) polymorphism has been observed to be a predictor of 
      mortality in this disease, but no data are available concerning the role of ACE 
      -240A>T polymorphism. In this study, we investigated the role of ACE I/D and 
      -240A>T polymorphisms in influencing both severity and clinical outcomes in 
      patients with heart failure, according to New York Heart Association (NYHA) 
      class. PATIENTS: : We studied 323 patients with heart failure (258 men/65 women; 
      age, 70.8 +/- 11.5 years) followed-up for 11.9 +/- 6.6 months. RESULTS: : The ACE 
      D and -240T allele frequency significantly increased according to the NYHA 
      functional class (P = 0.0002 and P < 0.0001, respectively).No significant 
      difference in ACE polymorphism genotype distribution and allele frequency 
      according to N-terminal pro-brain natriuretic peptide tertiles was observed. At 
      multinomial regression analysis, ACE D but not -240T allele has been evidenced to 
      be a significant and independent predictor of severity for both NYHA III and IV 
      classes (P = 0.01 and P = 0.004, respectively). The ACE D allele prevalence was 
      higher, even if not significantly in both death and rehospitalization groups in 
      comparison with survivors and nonrehospitalized (P = 0.6 and P = 0.9, 
      respectively). No difference in -240T allele frequency has been observed for the 
      ACE -240A>T polymorphism, in relation to both death and rehospitalization (P = 
      0.1 and P = 0.6, respectively). CONCLUSIONS: : This study suggests that ACE I/D 
      polymorphism might represent a predisposing factor to severe heart failure, 
      independently of well-known prognostic markers.
FAU - Fatini, Cinzia
AU  - Fatini C
AD  - Department of Medical and Surgical Critical Care, Thrombosis Centre and Centre 
      for the Study at Molecular and Clinical Level of Chronic, University of Florence, 
      Italy. cinzia.fatini@unifi.it
FAU - Sticchi, Elena
AU  - Sticchi E
FAU - Marcucci, Rossella
AU  - Marcucci R
FAU - Said, Abdihakim Abdullahi
AU  - Said AA
FAU - Del Pace, Stefano
AU  - Del Pace S
FAU - Verdiani, Valerio
AU  - Verdiani V
FAU - Nozzoli, Carlo
AU  - Nozzoli C
FAU - Gensini, Gian Franco
AU  - Gensini GF
FAU - Abbate, Rosanna
AU  - Abbate R
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Investig Med
JT  - Journal of investigative medicine : the official publication of the American 
      Federation for Clinical Research
JID - 9501229
RN  - 0 (Peptide Fragments)
RN  - 0 (pro-brain natriuretic peptide (1-76))
RN  - 114471-18-0 (Natriuretic Peptide, Brain)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Female
MH  - *Gene Deletion
MH  - Genotype
MH  - Heart Failure/*genetics
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Mutagenesis, Insertional
MH  - Natriuretic Peptide, Brain/analysis
MH  - Peptide Fragments/analysis
MH  - Peptidyl-Dipeptidase A/*genetics
MH  - *Polymorphism, Genetic
EDAT- 2008/12/04 09:00
MHDA- 2009/01/07 09:00
CRDT- 2008/12/04 09:00
PHST- 2008/12/04 09:00 [pubmed]
PHST- 2009/01/07 09:00 [medline]
PHST- 2008/12/04 09:00 [entrez]
AID - 10.2310/JIM.0b013e31818e8028 [doi]
PST - ppublish
SO  - J Investig Med. 2008 Dec;56(8):1004-10. doi: 10.2310/JIM.0b013e31818e8028.