SavedAdd your journal

Journals / Anadolu Kardiyoloji Dergisi / 2007 / Cilt: 7 - Sayı: 3

Antihipertansif tedavi alan normal koroner arterli hastalarda anjiyotensinojen M235T polimorfizminin sol ventrikül parametreleri ile ilişkisi

Angiotensinogen M235T polymorphism and left ventricular indices in treated hypertensive patients with normal coronary arteries

Ayhan OLCAY
Berrin UMMAN
Zehra BUĞRA
C.Gökhan EKMEKÇİ
Uğur ÖZBEK
Yılmaz NİŞANCI
Murat SEZER
Pages
257–261
Publication Date
2022-10-10
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Angiotensinogen M235T polymorphism was not useful to predict left ventricular mass, function, hypertrophy or dilatation in a small population of treatedTurkish hypertensive patients with normal coronary arteries. (Anadolu Kardiyol Derg 2007; 7: 257-61)

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Hypertension and left ventricular hypertrophy (LVH) are important causes of morbidity and mortality in the population.
📊
Key Findings & Data:Angiotensinogen (AGT) M235T polymorphism has been associated with LVH, left ventricular dimensions, coronary artery disease and antihypertensive drug response in previous studies.
💡
Conclusion & Impact:Conclusion: Angiotensinogen M235T polymorphism was not useful to predict left ventricular mass, function, hypertrophy or dilatation in a small population of treatedTurkish hypertensive patients with normal coronary arteries. (Anadolu Kardiyol Derg 2007; 7: 257-61)
🔬Design:Research Article
📍Scope:2007 Verileri
⚙️Variables:Domain Parameters

Abstract

Objective: Hypertension and left ventricular hypertrophy (LVH) are important causes of morbidity and mortality in the population. Angiotensinogen (AGT) M235T polymorphism has been associated with LVH, left ventricular dimensions, coronary artery disease and antihypertensive drug response in previous studies. We examined relationship between AGT M235T polymorphism and echocardiographic left ventricular indices in a Turkish population of treated hypertensive patients with normal coronary arteries.Methods: In this cross-sectional study a Turkish population of 92 hypertensive patients treated in our outpatient clinic were enrolled. All patients had normal coronary angiographic examinations. Genotypes for AGT M235T were determined from peripheral leukocytes. Left ventricular dimensions, mass and function indices, after adjustment for clinical covariates were analyzed by multiple regression analysis according to genotypes.Results: Genotype frequencies for AGT M235T were MM-24.7%, MT-52.8% and TT-22.5%. Left ventricular end systolic dimensions for AGT M235T MM, MT, TT genotypes were 17.9±4.2 mm, 19.4±6.2 mm, and 16.4±2.9 mm, respectively (p=0.08). Angiotensinogen M235T TT genotype showed a trend towards a lower LVES dimension but results were not statistically significant. Left ventricular ejection fractions for AGT M235T MM, MT, TT subgroups were 61.3±15.0%, 59.4±14.0%, and 67.8±8.5%, respectively (p=0.07). Angiotensinogen M235T TT genotype showed a tendency towards lower left ventricular mass index but results were not statistically significant. None of the AGT M235T genotypes predicted left ventricular dilatation, mass or function in treated hypertensive patients with normal coronary arteries. Conclusion: Angiotensinogen M235T polymorphism was not useful to predict left ventricular mass, function, hypertrophy or dilatation in a small population of treatedTurkish hypertensive patients with normal coronary arteries. (Anadolu Kardiyol Derg 2007; 7: 257-61)

Özet

Amaç: Hipertansiyon ve sol ventrikül hipertrofisi (SVH) toplumda önemli bir morbidite ve mortalite sebebidir. Daha önce yapılan çalışmalarda anjiyotensinojen (AGT) M235T hipertrofisi SVH, sol ventrikül çapları, koroner arter hastalığı ve antihipertansif tedaviye yanıt ile ilişkili bulunmuştur. Çalışmamızda antihipertansif tedavi alan normal koroner arterli hastalarda AGT M235T polimorfizmi ile ekokardiyografik sol ventrikül parametreleri arasındaki ilişkiyi inceledik. Yöntemler: Bu kros-seksiyonel çalışmaya 92 hasta dahil edildi ve periferik lökositlerden AGT M235T genotiplemesi yapıldı. Çalışmaya alınan tüm hastaların daha önce yapılan koroner anjiografileri normal idi. Sol ventrikül çapları, kitlesi ve fonksiyonu ile ilgili indeksler genotiplere göre çoklu regresyon analizleri ile incelendi. Bulgular: Genotip dağılımı MM-%24.7, MT-%52.8 ve TT-%22.5 şeklinde idi. Sol ventrikül sistol sonu çapları AGT M235T MM, MT, TT tipleri için sırası ile 17.9±4.2 mm, 19.4±6.2 mm, 16.4±2.9 mm ve p=0.08 idi. Sol ventrikül ejeksiyon fraksiyonları AGT M235T MM, MT, TT grupları için sırası ile %61.3±15.0, %59.4±14.0, %67.8±8.5 ve p=0.07 idi. Anjiyotensin M235T TT genotipi daha düşük sol ventrikül kitle indeksi göstermeye eğilimli idi fakat sonuç istatistik anlamlı bulunmadı.Sonuç: Tedavi edilmiş hipertansif normal koroner arterli hastalarda AGT M235T genotiplerinden hiçbiri sol ventrikül dilatasyonu, fonksiyonu veya kitlesi ile ilişkili bulunmamıştır. (Anadolu Kardiyol Derg 2007; 7: 257-61)

🔖

Cite This Article

OLCAY, A., UMMAN, B., BUĞRA, Z., EKMEKÇİ, C., ÖZBEK, U., NİŞANCI, Y., SEZER, M. (2022). Antihipertansif tedavi alan normal koroner arterli hastalarda anjiyotensinojen M235T polimorfizminin sol ventrikül parametreleri ile ilişkisi. Anadolu Kardiyoloji Dergisi, Cilt: 7 - Sayı: 3, 257–261. https://ajindex.com/articles/437149

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J, et al. Blood pressure, stroke and coronary heart disease: part 1, prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet 1990; 335: 765-74
  2. Ward R. Familial Aggregation and genetic epidemiology of blood pressure. New York: Raven Pres; 1995
  3. Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, et al. A chimeric 11b-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature 1992; 355: 262-5
  4. Shimkets RA, Warnock DG, Bositis CM, Nelson-Williams C, Hansson JH, Shambelan M, et al. Liddle’s syndrome: Heritable human hypertension caused by mutations in the b subunit of the epithelial sodium channel. Cell 1994; 79: 407-14
  5. Mune T, Rogerson FM, Nikkila H, Agarwal AK, White PC. Human hypertension caused by mutations in the kidney isozyme of 11b-hydroxysteroid dehydrogenase. Nat Genet 1995; 10: 394-9
  6. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 1991; 114: 345-52
  7. Bikkina M, Levy D, Evans JC, Larson MG, Benjamin EJ, Wolf PA. Left ventricular mass and risk of stroke in an elderly cohort. The Framingham Heart Study. JAMA 1994; 272: 33-6
  8. Schillaci G, Verdecchia P, Reboldi G, Pede S, Porcellati C. Continuous relation between left ventricular mass and cardiovascular risk in essential hypertension. Hypertension 2000; 35: 580-6
  9. Adams TD, Yanowitz FG, Fisher AG, Ridges JD, Nelson AG, Hagan AD, et al. Heritability of cardiac size: echocardiographic and electrocardiographic study of monozygotic and dizygotic twins. Circulation 1985; 71: 39-44
  10. Allemann Y, Aeschbacher B, Zwyssig P, Ferrari P, Hopf M, Shaw S, et al. Left ventricular structure and determinants in normotensive offsprings of essential hypertensive patients. J Hypertens 1992; 10. 1257-64
  11. Schunkert H, Brockel U, Hengstenberg C, Luchner A, Muscholl MW, Kurzidim K, et al. Familial predisposition to left ventricular hypertrophy. J Am Coll Cardiol 1999; 33: 1685-91
  12. Post WS., Larson MG., Myers RH. Heritability of left ventricular mass: The Framingham Heart Study. Hypertension 1997; 30: 1025-8
  13. Levy D, Salomon M, D’Agostino RB, Belanger AJ, Kannel WB. Prognostic implications of baseline electrocardiographic features and their serial changes in subje