PMID- 38158675
OWN - NLM
STAT- MEDLINE
DCOM- 20240104
LR  - 20240104
IS  - 1165-158X (Electronic)
IS  - 0145-5680 (Linking)
VI  - 69
IP  - 13
DP  - 2023 Dec 10
TI  - Correlation between the insertion-deletion variant of the angiotensin-converting 
      enzyme gene and various classes of heart failure.
PG  - 149-155
LID - 10.14715/cmb/2023.69.13.23 [doi]
AB  - The angiotensin-converting enzyme (ACE) genetic variation for insertion/deletion 
      (I/D) is located at the 16th intron of the ACE gene. A number of studies 
      investigated the homozygous deletion genotype of ACE and its association with 
      cardiovascular diseases. However, ACE's genetic variation and its association 
      with heart failure (HF) is yet to be confirmed. We examined the possibility of 
      the association between the ACE I/D gene variant with the severity of HF. The ACE 
      genotypes were determined by polymerase chain reactions using samples derived 
      from 150 patients with HF and 90 healthy subjects which were age and 
      gender-matched. These patients included those of all four of the New York Heart 
      Association (NYHA) classes. Echocardiography was performed on all HF patients and 
      ejection fraction (EF), left ventricular systolic and diastolic diameters were 
      measured. The HF patients were redistributed to systolic where EF is equal and 
      less than 45% and non-systolic HF where EF is more than 45%. We demonstrate a 
      statistically significant difference in DD genotype in NYHA class IV in 
      comparison to the control group. The values of odds ratio (OR) (95%CI) of the DD 
      genotype (DD vs ID and II) were 3.37 (1.01-11.19) (p value = 0.039) and the OR 
      (95%CI) of the D allele (D vs I) was 2.55 (0.98-6.65) (p value = 0.049). Higher 
      frequencies of D allele compared to I allele is linked to severity of HF. DD 
      variant of the ACE gene is associated with NYHA class IV heart failure. This 
      could have a profound impact on risk stratification and prognosis of HF in the 
      management of this condition.
FAU - Tawfeeq, Rawaz D
AU  - Tawfeeq RD
AD  - Department of Clinical Analysis, College of Pharmacy, Hawler Medical University. 
      Erbil, 44001, Iraq. rawaz.tawfeeq@hmu.edu.krd.
FAU - Ismael, Ava T
AU  - Ismael AT
AD  - Department of Pathology, College of Pharmacy, Hawler Medical University. Erbil, 
      44001, Iraq. ava.shexani@hmu.edu.krd.
FAU - Alwan, Mohammed H
AU  - Alwan MH
AD  - Medicine Department. College of Medicine, Hawler Medical University.Erbil, 44001, 
      Iraq. mohammed.hasan@hmu.edu.krd.
LA  - eng
PT  - Journal Article
DEP - 20231210
PL  - France
TA  - Cell Mol Biol (Noisy-le-grand)
JT  - Cellular and molecular biology (Noisy-le-Grand, France)
JID - 9216789
RN  - 0 (Angiotensins)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - EC 3.4.15.1 (ACE protein, human)
SB  - IM
MH  - Humans
MH  - Angiotensins/genetics
MH  - Gene Deletion
MH  - Genotype
MH  - *Heart Failure/genetics
MH  - Homozygote
MH  - *Peptidyl-Dipeptidase A/genetics
MH  - *Polymorphism, Genetic
MH  - Sequence Deletion/genetics
MH  - INDEL Mutation
EDAT- 2024/01/02 11:45
MHDA- 2024/01/03 09:42
CRDT- 2023/12/30 01:45
PHST- 2023/07/18 00:00 [received]
PHST- 2024/01/03 09:42 [medline]
PHST- 2024/01/02 11:45 [pubmed]
PHST- 2023/12/30 01:45 [entrez]
AID - 10.14715/cmb/2023.69.13.23 [doi]
PST - epublish
SO  - Cell Mol Biol (Noisy-le-grand). 2023 Dec 10;69(13):149-155. doi: 
      10.14715/cmb/2023.69.13.23.