Impact of renin-angiotensin-aldosterone system polymorphisms on myocardial perfusion: Correlations with myocardial single photon emission computed tomography-derived parameters.
Adult
Aged
Aged, 80 and over
Angiotensinogen
/ genetics
Coronary Artery Disease
/ diagnostic imaging
Coronary Circulation
Female
Humans
Male
Middle Aged
Myocardial Perfusion Imaging
Peptidyl-Dipeptidase A
/ genetics
Polymorphism, Genetic
/ genetics
Receptors, Angiotensin
/ genetics
Renin
/ genetics
Renin-Angiotensin System
Tomography, Emission-Computed, Single-Photon
ACE
CAD
Renin
angiotensin ΙΙ receptors
angiotensinogen
Journal
Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology
ISSN: 1532-6551
Titre abrégé: J Nucl Cardiol
Pays: United States
ID NLM: 9423534
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
10
11
2017
accepted:
26
12
2017
pubmed:
19
1
2018
medline:
22
9
2020
entrez:
19
1
2018
Statut:
ppublish
Résumé
Renin-angiotensin-aldosterone system (RAAS) has an important role in atherosclerosis. We investigated the effects of six RAAS gene polymorphisms on myocardial perfusion. We examined 810 patients with known or suspected coronary artery disease (CAD) using stress-rest myocardial single-photon emission computed tomography. Summed stress score (SSS), summed rest score (SRS), summed difference score (SDS), transient ischemic dilation (TID), and lung/heart ratio (LHR) were recorded. The following gene polymorphisms were investigated: angiotensin-converting enzyme (ACE) insertion/deletion (I/D), angiotensinogen (AGT) M235T and T174M, angiotensin II type 1 receptor (AT1R) A1166C, renin (REN) C5312T, and angiotensin II type 2 receptor (AT2R) C3123A. The heterozygotes or homozygotes on ACE D allele were 7.54 times more likely to have abnormal SSS, while the AGT (T174M) heterozygotes were 5.19 times more likely to have abnormal SSS. The homozygotes of ACE D had significantly higher values on TID and LHR, while the AGT (T174M) heterozygotes had higher values on TID. The AT1R heterozygotes had greater odds for having SSS ≥ 3. The patients carried AT1R homozygosity of C allele had significantly higher values on TID, while heterozygotes of AT1R had significantly higher values on LHR. Among the polymorphisms investigated, ACE D allele had the strongest association with abnormal myocardial perfusion.
Sections du résumé
BACKGROUND
Renin-angiotensin-aldosterone system (RAAS) has an important role in atherosclerosis. We investigated the effects of six RAAS gene polymorphisms on myocardial perfusion.
METHODS AND RESULTS
We examined 810 patients with known or suspected coronary artery disease (CAD) using stress-rest myocardial single-photon emission computed tomography. Summed stress score (SSS), summed rest score (SRS), summed difference score (SDS), transient ischemic dilation (TID), and lung/heart ratio (LHR) were recorded. The following gene polymorphisms were investigated: angiotensin-converting enzyme (ACE) insertion/deletion (I/D), angiotensinogen (AGT) M235T and T174M, angiotensin II type 1 receptor (AT1R) A1166C, renin (REN) C5312T, and angiotensin II type 2 receptor (AT2R) C3123A. The heterozygotes or homozygotes on ACE D allele were 7.54 times more likely to have abnormal SSS, while the AGT (T174M) heterozygotes were 5.19 times more likely to have abnormal SSS. The homozygotes of ACE D had significantly higher values on TID and LHR, while the AGT (T174M) heterozygotes had higher values on TID. The AT1R heterozygotes had greater odds for having SSS ≥ 3. The patients carried AT1R homozygosity of C allele had significantly higher values on TID, while heterozygotes of AT1R had significantly higher values on LHR.
CONCLUSIONS
Among the polymorphisms investigated, ACE D allele had the strongest association with abnormal myocardial perfusion.
Identifiants
pubmed: 29344922
doi: 10.1007/s12350-017-1181-8
pii: 10.1007/s12350-017-1181-8
doi:
Substances chimiques
Receptors, Angiotensin
0
Angiotensinogen
11002-13-4
Peptidyl-Dipeptidase A
EC 3.4.15.1
Renin
EC 3.4.23.15
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1298-1308Commentaires et corrections
Type : CommentIn
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