Giriş:
Koroner arter ektazi (KAE)’den sorumlu olan
etyolojik ve patojenik etmenler belirgin değildir. Bizler KAE’si olan ve
olmayan olguları resistin düzeyleri açısından kıyaslamayı, böylelikle
resistinin KAE patogenezinde bir rolü olup olmadığını saptamayı amaçladık.
Hastalar
ve Yöntem: Çalışma 81 olgudan
oluşmaktaydı. Olguların 42’sinde (15’i kadın, ortalama yaş 60.4 ± 9.0 yıl), KAE
mevcut olup, 39 olguda (22’si kadın, ortalama yaş 56.2 ± 10.7 yıl) ise normal
koroner arter anatomisi vardı. Normal komşu segmentlere kıyasla en az 1.5 kat
koroner arter dilatasyonu mevcut olgular KAE olarak kabul edildiler. Koroner
anjiyografinin gerçekleştirildiği gün alınan kan örneklerinde resistin
düzeyleri ölçüldü.
Bulgular:
Her iki grubun referans özellikleri benzerdi. Serum
resistin düzeyi KAE grubunda [ortalama 703.5 ± 828.2 ng/L, ortanca 379.5
(40-492) ng/L] kontrol grubuna göre (ortalama 313.5 ± 252.6 ng/L, ortanca 256
(30-1244) ng/L] anlamlı şekilde daha yüksek saptandı (p= 0.001).
Introduction:
The etiological and pathogenic factors responsible
for coronary artery ectasia (CAE) are unclear. Therefore, we aimed to compare
subjects with and without CAE with respect to resistin levels and determine
whether resistin plays a role in the aetiology or pathogenesis of CAE.
Patients
and Methods: This study enrolled a total of 81 subjects,
of whom 42 had CAE [15 female (F), mean age 60.4 ± 9.0 years] and 39 had a
normal coronary anatomy (22 F, mean age 56.2 ± 10.7 years). Using coronary
artery diameters of the control group as reference, subjects having coronary
artery dilatation that was at least 1.5 times larger than the normal adjacent
segments were considered to have CAE. Resistin levels were measured from blood
samples obtained on the day of the coronary angiography.
Results: Both
the groups had similar baseline characteristics. Serum resistin levels were
significantly higher in the CAE group [mean 703.5 ± 828.1 ng/L, median 379.5
(40-4092) ng/L] than in the control group [mean 313.5 ± 252.6 ng/L, median 256
(30-1244) ng/L] (p= 0.001).
Conclusion:
CAE and atherosclerosis share common
histopathological and clinical characteristics. Resistin, a polypeptide with a
known role in the development and clinical presentation of atherosclerosis, may
also mediate the formation of CAE. There is a need for future studies with a
larger sample size to better delineate the effect of resistin on the
development of CAE.
Primary Language | English |
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Subjects | Clinical Sciences |
Journal Section | Original Investigations |
Authors | |
Publication Date | December 1, 2016 |
Published in Issue | Year 2016 Volume: 19 Issue: 3 |