Kardiyak Sendrom X Tanılı Hastalarda Artmış Ventriküler Aktivasyon Zamanı

Abstract

Giriş: Kardiyak sendrom X (KSX) noninvaziv stres testlerinde tespit edilebilen iskemi olmasına rağmen koroner anjiyografide koroner arter stenozu bulgularının olmadığı tipik anjina olarak tanımlanmaktadır. Bozulmuş koroner mikrosirkülasyon, inflamasyon ve endotel disfonksiyonu KSX için kabul edilmiş etyolojik faktörlerdir. Ventriküler aktivasyon zamanının (VAZ) miyokardiyal iskemi durumunda Purkinje liflerinde ve miyositlerdeki iletim yavaşlamasına bağlı olarak uzadığı bildirilmiştir. Bu çalışmada, KSX hastalarında aralarında VAZ’ın da bulunduğu elektrokardiyografik parametrelerin araştırılması amaçlanmıştır. Hastalar ve Yöntem: Çalışmaya KSX tanısı alan 120 hasta (ortalama yaş: 54.7 ± 8.6 yıl , erkek: 53) ile iskemisi olmayan 130 sağlıklı kontrol (ortalama yaş: 53.3 ± 8.9 yıl , erkek: 66) dahil edildi. Tüm hastalar elektrokardiyografi ve transtorasik ekokardiyografi ile değerlendirildi. VAZ elektrokardiyografide QRS kompleksinin başlangıcından R veya R’ dalgasının zirvesine kadar geçen zaman aralığı olarak tanımlandı. Bulgular: KSX hastaları ile kontrol grubu arasında demografik, laboratuvar ve ekokardiyografik parametreler açısından anlamlı bir fark izlenmedi. Elektrokardiyografik parametreler karşılaştırıldığında gruplar arasında kalp hızı, P dalga süresi, PR aralığı, QT ve düzeltilmiş QT aralığı açısından anlamlı fark yok iken, QRS süresi (95.1 ± 13.8 ve 90.4 ± 12.7 msn, p= 0.006) ve VAZ (34.8 ± 5.7 ve 29.2 ± 5.6 msn, p< 0.001) KSX grubunda anlamlı olarak daha uzun olarak tespit edildi. Sonuç: Bu çalışmada KSX hastalarında QRS süresi ve VAZ’ın anlamlı olarak uzadığı gösterilmiştir. Bu uzama KSX hastalarındaki bozulmuş mikrovasküler perfüzyon ve iskemiye bağlı iletim yavaşlamasına bağlı gelişmiş olabilir.

Increased Ventricular Activation Time in Patients with the Diagnosis of Cardiac Syndrome X

Abstract

Introduction: Cardiac syndrome X (CSX) is defined as typical angina with detectable ischaemia on noninvasive stress tests without any evidence of coronary artery stenosis during coronary angiography. Impaired coronary microcirculation, inflammation and endothelial dysfunction are accepted aetiological factors for CSX. The ventricular activation time (VAT) has been reported to be prolonged in myocardial ischaemia due to the conduction delay in the Purkinje fibres and the myocytes. In this study, we aimed to investigate the electrocardiographic parameters including VAT in patients with CSX. Patients and Methods: This study enrolled 120 patients (mean age, 54.7 ± 8.6 years; male, 53) diagnosed with CSX and 130 healthy controls (mean age, 53.3 ± 8.9; male, 66) without ischaemia. All patients underwent electrocardiography and transthoracic echocardiography. VAT was defined as the interval from the beginning of the QRS complex until the peak of the R or R’ wave. Results: There was no significant difference in terms of demographic, laboratory and echocardiographic parameters between CSX patients and controls. Comparison of electrocardiographic parameters yielded that there was no significant difference in terms of the heart rate, P-wave duration, PR interval, QT and corrected QT intervals between the groups. However, the QRS duration (95.1 ± 13.8 vs. 90.4 ± 12.7 msec; p= 0.006) and VAT (34.8 ± 5.7 vs. 29.2 ± 5.6 msec; p< 0.001) were significantly higher in patients with CSX. Conclusion: The present study demonstrated that QRS duration and VAT were prolonged significantly in patients with CSX. This prolongation may be due to the presence of impaired microvascular perfusion and ischaemia-induced conduction delay.

Keywords

• Cardiac syndrome X,electrocardiography,ventricular activation time

References

1. 1. Melikian N, De Bruyne B, Fearon WF, MacCarthy PA. The pathophysiology and clinical course of the normal coronary angina syndrome (cardiac syndrome X). Prog Cardiovasc Dis 2008;50:294-310.
2. 2. Phan A, Shufelt C, Merz CN. Persistent chest pain and no obstructive coronary artery disease. JAMA 2009;301:1468-74.
3. 3. Singh M, Singh S, Arora R, Khosla S. Cardiac syndrome X: current concepts. Int J Cardiol 2010;142:113-9.
4. 4. Hurst T, Olson TH, Olson LE, Appleton CP. Cardiac syndrome X and endothelial dysfunction: new concepts in prognosis and treatment. Am J Med 2006;119:560-6.
5. 5. Cannon RO. Microvascular angina and the continuing dilemma of chest pain with normal coronary angiograms. J Am Coll Cardiol 2009;54:877-85.
6. 6. Chen C, Wei J, AlBadri A, Zarrini P, Bairey Merz CN. Coronary microvascular dysfunction- epidemiology, pathogenesis, prognosis, diagnosis, risk factors and therapy. Circ J 2016;81:3-11.
7. 7. MacLeod AG, Wilson FN, Barker PS. The form of the electrocardiogram. I. intrinsicoid electrocardiographic deflections in animals and man. Exp Biol Med 1930;27:586-7.
8. 8. Pérez-Riera AR, de Abreu LC, Barbosa-Barros R, Nikus KC, Baranchuk A. R-peak time: an electrocardiographic parameter with multiple clinical applications. Ann Noninvasive Electrocardiol 2016;21:10-9.

9. 9. Holland RP, Brooks H. The QRS complex during myocardial ischemia. An experimental analysis in the porcine heart. J Clin Invest 1976;57:541-50.
10. 10. Çağdaş M, Karakoyun S, Rencüzoğullari İ, Karabağ Y, Yesin M, Uluganyan M, et al. Relationship between R-wave peak time and no-reflow in ST elevation myocardial infarction treated with a primary percutaneous coronary intervention. Coron Artery Dis 2017;28:326-31.
11. 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;18:499-502.
12. 12. Lanza GA, Crea F. Primary coronary microvascular dysfunction clinical presentation, pathophysiology, and management. Circulation 2010;121:2317-25.
13. 13. Iacobellis G, Corradi D, Sharma AM. Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med 2005;2:536-43.
14. 14. Savard P, Rouleau JL, Ferguson J, Poitras N, Morel P, Davies RF, et al. Risk stratification after myocardial infarction using signal-averaged electrocardiographic criteria adjusted for sex, age, and myocardial infarction location. Circulation 1997;96:202-13.
15. 15. Shenkman HJ, Pampati V, Khandelwal AK, McKinnon J, Nori D, Kaatz S, et al. Congestive heart failure and QRS duration: establishing prognosis study. Chest 2002;122:528-34.
16. 16. Grant RP, Dodge HT. Mechanisms of QRS complex prolongation in man; left ventricular conduction disturbances. Am J Med 1956;20:834-52.
17. 17. Hamilin RL, Pipers FS, Hellerstein HK, Smith CR. QRS alteration immediately following production of left ventricular free wall ischemia in dogs. Am J Physiol 1968;215:1032-40.
18. 18. Rencüzoğulları İ, Çağdaş M, Karakoyun S, Karabağ Y, Yesin M, Artaç İ, et al. The association between electrocardiographic R wave peak time and coronary artery disease severity in patients with non-ST segment elevation myocardial infarction and unstable angina pectoris. J Electrocardiol 2018;51:230-5.
19. 19. Bendary A, El-Husseiny M, Aboul Azm T, Abdoul Moneim A. The predictive value of R-wave peak time on no-reflow in patients with ST-elevation myocardial infarction treated with a primary percutaneous coronary intervention. Egypt Heart J 2018;70:415-9.