Hipertansif Hastalarda Sol Ventrikül Hipertrofisini Öngörmede Yeni Bir Elektrokardiyografik Parametre: Ventriküler Aktivasyon Zamanı

Öz

Amaç: Hipertansiyon hastalarında elektrokardiyografik parametreler ile sol ventrikül hipertrofisi (SVH) arasındaki ilişkinin araştırılması ve özellikle ventriküler aktivasyon zamanının (VAT) tanısal değerinin değerlendirilmesi amaçlandı. Gereç ve Yöntem: Esansiyel hipertansiyonu olan 320 hasta (ortalama yaş 61,9±7,8 yıl, %57,5 erkek) çalışmaya dahil edildi. Tüm hastalara transtorasik ekokardiyografi ve 12 derivasyonlu yüksek çözünürlüklü EKG çekildi. Hastalar ekokardiyografide SVH varlığına göre iki gruba ayrıldı. Demografik, laboratuvar, ekokardiyografik ve elektrokardiyografik parametreler karşılaştırıldı. Çok değişkenli lojistik regresyon ve ROC analizleri ile bağımsız öngördürücü parametreler belirlendi. Bulgular: Hastaların 114’ünde (%35,6) SVH saptandı. SVH (+) grupta sol atriyum çapı, interventriküler septal kalınlık, arka duvar kalınlığı, sol ventrikül kütlesi ve kitle indeksi anlamlı olarak daha yüksekti (tümü p<0,001). Elektrokardiyografik parametrelerde P dalgası süresi (p=0,024), QRS süresi (p=0,009) ve VAT (p<0,001) SVH (+) grupta anlamlı derecede uzundu. Çok değişkenli analizde VAT (RR: 2,872; %95 GA: 1,151–7,169; p=0,021), sol ventrikül kütlesi (p=0,017) ve kitle indeksi (p=0,026) SVH için bağımsız öngördürücü bulundu. VAT ile sol ventrikül kütlesi arasında orta düzeyde pozitif korelasyon saptandı (r=0,594; p<0,001). ROC analizinde VAT >30 ms için %67 duyarlılık ve %59 özgüllük elde edildi (AUC=0,681; p<0,001). Sonuç: Hipertansif hastalarda VAT, sol ventrikül hipertrofisini öngörmede bağımsız bir parametredir. Kolay ölçülebilir ve ek maliyet gerektirmemesi nedeniyle, ekokardiyografiye ek olarak klinik uygulamada kullanılabilecek pratik bir belirteçtir. Daha geniş ve çok merkezli çalışmalarla tanısal ve prognostik değerinin doğrulanması gerekmektedir.

Anahtar Kelimeler

• Hipertansiyon
• Sol ventrikül hipertrofisi
• Ventriküler aktivasyon zamanı
• Elektrokardiyografi
• Ekokardiyografi

Destekleyen Kurum

Bu çalışma için herhangi bir finansal destek alınmamıştır.

Etik Beyan

Çalışma protokolü, Helsinki Bildirgesi ve İyi Klinik Uygulamalar kılavuzlarına dayanarak 15/11/2018 tarihinde Kartal Kosuyolu Yüksek İhtisas Eğitim ve Araştırma Hastanesi Girişimsel Olmayan Klinik Araştırmalar Etik Kurulu’ndan onay alınmıştır (Karar no: 2018.8/8-139). Tüm hastalardan yazılı bilgilendirilmiş onam ve yayın için izin alınmıştır.

Teşekkür

Çalışmamızın yapıldığı kliniğimizdeki çalışma arkadaşlarıma özel teşekkür ederiz.

A Novel Electrocardiographic Parameter for Predicting Left Ventricular Hypertrophy in Hypertensive Patients: Ventricular Activation Time

Öz

Objective: The aim of this study was to investigate the relationship between electrocardiographic parameters and left ventricular hypertrophy (LVH) in patients with hypertension, and to evaluate the diagnostic value of ventricular activation time (VAT). Material and Method: A total of 320 patients with essential hypertension (mean age 61.9±7.8 years, 57.5% male) were enrolled. All patients underwent transthoracic echocardiography and 12-lead high-resolution electrocardiography. Patients were divided into two groups according to the presence of LVH on echocardiography. Demographic, laboratory, echocardiographic, and electrocardiographic parameters were compared. Independent predictors were determined using multivariate logistic regression and ROC curve analysis. Results: LVH was detected in 114 patients (35.6%). The LVH (+) group had significantly larger left atrial diameter, interventricular septal thickness, posterior wall thickness, left ventricular mass, and mass index (all p<0.001). Electrocardiographically, P-wave duration (p=0.024), QRS duration (p=0.009), and VAT (p<0.001) were significantly longer in the LVH (+) group. In multivariate analysis, VAT (RR: 2.872; 95% CI: 1.151–7.169; p=0.021), left ventricular mass (p=0.017), and mass index (p=0.026) were identified as independent predictors of LVH. VAT showed a moderate positive correlation with left ventricular mass (r=0.594; p<0.001). ROC analysis demonstrated that VAT >30 ms predicted LVH with 67% sensitivity and 59% specificity (AUC=0.681; p<0.001). Conclusion: VAT is an independent predictor of left ventricular hypertrophy in hypertensive patients. Due to its ease of measurement and lack of additional cost, VAT may serve as a practical parameter in clinical practice alongside echocardiography. Larger, multicenter studies are warranted to further validate its diagnostic and prognostic value.

Anahtar Kelimeler

• Hypertension
• Left ventricular hypertrophy
• Ventricular activation time
• Electrocardiography
• Echocardiography

Destekleyen Kurum

No financial funding was received for this study.

Etik Beyan

Approval for the study was obtained from the Kartal Kosuyolu High Specialization Training and Research Hospital Non-Interventional Clinical Research Ethics Committee on 15/11/2018 (Decision no: 2018.8/8-139) based on the Declaration of Helsinki and Good Clinical Practice guidelines . Written informed consent and permission for publication were obtained from all patients.

Teşekkür

We would like to extend our special thanks to our colleagues in the clinic where our study was conducted

Kaynakça

1. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990;322(22):1561–1566.
2. Vakili BA, Okin PM, Devereux RB. Prognostic implications of left ventricular hypertrophy. Am Heart J 2001;141(3):334–341.
3. Díez J. Mechanisms of cardiac fibrosis in hypertension. J Clin Hypertens (Greenwich) 2007;9(7):546-550.
4. Schmieder RE. Mechanisms for the clinical benefits of angiotensin II receptor blockers. Am J Hypertens 2005;18(5):720–730.
5. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography. Eur Heart J Cardiovasc Imaging 2015;16(3):233–270.
6. Surawicz B, Childers R, Deal BJ, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part III: intraventricular conduction disturbances: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2009;53(11):976-981.
7. Okin PM, Devereux RB, Nieminen MS, et al. Electrocardiographic strain pattern and prediction of cardiovascular morbidity and mortality in hypertensive patients. Hypertension 2004;44(1):48–54.
8. Özmen Yıldız P. Association between left ventricular hypertrophy and the peak times of the R and P waves in hypertensive patients. Cukurova Med J 2024;49(3):665-672.

9. Narayanan K, Reinier K, Uy-Evanado A, et al. Electrocardiographic versus echocardiographic left ventricular hypertrophy and sudden cardiac arrest in the community. Heart Rhythm 2014;11(6):1040–1046.
10. Lovic D, Erdine S, Catakoğlu AB. How to estimate left ventricular hypertrophy in hypertensive patients. Anatol J Cardiol 2014;14(4):389–395.
11. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18(6):499–502.
12. Verdecchia P, Schillaci G, Borgioni C, et al. Prognostic significance of serial changes in left ventricular mass in essential hypertension. Circulation 1998;97(1):48–54.
13. 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(5):345–352.
14. Levy D, Salomon M, D’Agostino RB, Belanger AJ, Kannel WB. Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy. Circulation 1994;90(4):1786–1793.
15. Cuspidi C, Sala C, Tadic M, Gherbesi E, Grassi G, Mancia G. Clinical and prognostic significance of left ventricular hypertrophy in hypertension. Curr Hypertens Rep 2019;21(2):12.
16. Kis M, Dogan Y, Yildirim A, et al. Evaluation of demographic, clinical, and aetiological data of patients admitted to cardiology clinics and diagnosed with left ventricular hypertrophy in Turkish population (LVH-TR). Acta Cardiol 2022;77(9):836-845.
17. Rautaharju PM, Surawicz B, Gettes LS, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U waves, and the QT interval: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2009;53(11):982-991.
18. Peguero JG, Lo Presti S, Perez J, Issa O, Brenes JC, Tolentino A. Electrocardiographic criteria for the diagnosis of left ventricular hypertrophy. J Am Coll Cardiol 2017;69(13):1694–1703.
19. Vancheri F, Vancheri S, Henein M. Relationship between QRS measurements and left ventricular morphology and function in asymptomatic individuals. Echocardiography 2018;35(3):301-307.
20. Bacharova L, Ugander M. Left ventricular hypertrophy: the relationship between electrocardiography and magnetic resonance imaging. Ann Noninvasive Electrocardiol 2014;19(6):524–533.
21. Bacharova L. Electrical and structural remodeling in left ventricular hypertrophy-a substrate for a decrease in QRS voltage? Ann Noninvasive Electrocardiol 2007;12(3):260-273.
22. Iyer NR, Le TT, Kui MSL, et al. Markers of Focal and Diffuse Nonischemic Myocardial Fibrosis Are Associated With Adverse Cardiac Remodeling and Prognosis in Patients With Hypertension: The REMODEL Study. Hypertension 2022;79(8):1804-1813.
23. Díez J, González A, López B, Querejeta R, Varo N, Laviades C. Mechanisms of disease: pathologic structural remodeling is more than adaptive hypertrophy in hypertensive heart disease. Nat Clin Pract Cardiovasc Med 2005;2(4):209–216.
24. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Fibrosis and renin–angiotensin–aldosterone system. Circulation 1991;83(6):1849–1865.