P Wave Analysis in Patients with Sarcoidosis

Elias Gialafos, Elias Perros, Aggeliki Rapti, Theodore G. Papaioannou, Vassilios Kouranos, Ioannis Moyssakis, Konstantina Aggeli, Georgios Dimopoulos, Charalambos Kostopoulos, Eleftherios Stamboulis, John Gialafos, Christodoulos Stefanadis, Nikolaos Koulouris, Myron Mavrikakis

Department of Cardiology, University of Athens, Athens, Greece.
Department of Clinical Therapeutics, University of Athens, Athens, Greece.
Department of Clinical Therapeutics, University of Athens, Athens, Greece;.
Department of Criti- cal Care Medicine, University of Athens, Athens, Greece..
Department of Neurology, University of Athens, Athens, Greece.
Department of Neurology, University of Athens, Athens, Greece; Department of Pulmonology, University of Athens, Athens, Greece;.
Department of Pulmonology, University of Athens, Athens, Greece;.
Outpatient Department of Sarcoidosis, Chest Disease Hospital “Sotiria”, Athens, Greece;.

DOI: 10.4236/ijcm.2013.49070                

Abstract

Introduction: Atrial arrhythmias in patients with sarcoidosis (Sar) are not unusual and can occur due to either atrial myocardial fibrosis and/or due to autonomic nervous system imbalance. Electrocardiographic markers (ECG), like maximum and minimum P wave duration and P wave dispersion {Pdis = Pmax ﹣Pmin} reflect atrial depolarization inhomogeneity and can indicate patients prone to develop atrial arrhythmias while standard deviation of RR interval (SDNN) is an index of heart rate variability, reflecting autonomic nervous system (ANS) activity. Methods: 90 patients with sarcoidosis (41 males/49 females) enrolled in this multicenter prospective study underwent digital electrocardiography, echocardiography and pulmonary function tests (PFTs). Diastolic and systolic indices of right and left ventricle were measured echocardiographically including Doppler parameters while Pmax, Pmin, Pdis and SDNN were measured in a 5-minute duration digital electrocardiogram. All consecutive patients were compared to 65 healthy volunteers (30 males/35 females). Results: Although heart rate and the echocardiographic indices were similar among the two groups, the electrocardiographic indices were significantly prolonged in the patient group compared to controls. Maximum P wave duration was correlated with SDNN (p < 0.05, r = ﹣0.272) and the age of the patients (p < 0.05, r = 0.219) while Pdis was correlated with SDNN (p < 0.001, r = 0.350) and the heart rate (p < 0.005, r = 0.323). Multivariate analysis showed that Pmax and Pdis were independently correlated with SDNN. Conclusion: P wave dispersion is significantly increased in patients with systemic sarcoidosis compared to healthy persons while maximum P wave duration and P wave dispersion are negatively correlated with the standard deviation of RR, an index of heart rate variability implying imbalance of ANS function. Further studies are needed for the clarification of the significance of this correlation.

Keywords

P Wave Analysis; Systemic Sarcoidosis; Autonomic Nervous System

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1]	Joint Statement of the American Thoracic Society (ATS), the European Respiratory Society (ERS) and the World Association of Sarcoidosis and Other Granulomatous Disorders (WASOG) adopted by the ATS Board of Directors and by the ERS Executive Committee, “Statement on Sarcoidosis,” American Journal of Respiratory and Critical Care Medicine, Vol. 160, No. 2, 1999, pp. 736-755. doi:10.1164/ajrccm.160.2.ats4-99
[2]	D. Mehta, S. A. Lubitz, Z. Frankel, et al., “Cardiac Involvement in Patients with Sarcoidosis: Diagnostic and Prognostic Value of Outpatient Testing,” Chest, Vol. 133, No. 6, 2008, pp. 1426-1435. doi:10.1378/chest.07-2784
[3]	M. R. Patel, P. J. Cawley, J. F. Heitner, et al., “Detection of Myocardial Damage in Patients with Sarcoidosis,” Circulation, Vol. 120, No. 20, 2009, pp. 1969-1977.
[4]	A. Perry and F. Vuitch, “Causes of Death in Patients with Sarcoidosis. A Morphologic Study of 38 Autopsies with Clinicopathologic Correlations,” Archives of Pathology & Laboratory Medicine, Vol. 119, No. 2, 1995, pp. 167-172.
[5]	J. C. Deng, R. P. Baughman and J. P. Lynch, “Cardiac Involvement in Sarcoidosis,” Seminars in Respiratory and Critical Care Medicine, Vol. 23, No. 6, 2002, pp. 513-527. doi:10.1055/s-2002-36516
[6]	B. Pierre-Louis, A. Prasad and W. H. Frishman, “Cardiac Manifestations of Sarcoidosis and Therapeutic Options,” Cardiology in Review, Vol. 17, No. 4, 2009, pp. 153-158. doi:10.1097/CRD.0b013e3181a1f763
[7]	K. Aytemir, N. Ozer, E. Atalar, et al., “P Wave Dispersion on 12-Lead Electrocardiography in Patients with Paroxysmal Atrial Fibrillation,” Pacing and Clinical Electrophysiology, Vol. 23, No. 7, 2000, pp. 1109-1112. doi:10.1111/j.1540-8159.2000.tb00910.x
[8]	P. E. Dilaveris, E. J. Gialafos, S. K. Sideris, et al., “Simple Electrocardiographic Markers for the Prediction of Paroxysmal Idiopathic Atrial Fibrillation,” American Heart Journal, Vol. 135, No. 5, 1998, pp. 733-738. doi:10.1016/S0002-8703(98)70030-4
[9]	P. E. Dilaveris, G. K. Andrikopoulos, G. Metaxas, et al., “Effects of Ischemia on P Wave Dispersion and Maximum P Wave Duration during Spontaneous Anginal Episodes,” Pacing and Clinical Electrophysiology, Vol. 22, No. 11, 1999, pp. 1640-1647. doi:10.1111/j.1540-8159.1999.tb00384.x
[10]	A. Dogan, M. Ozaydin, C. Nazli, et al., “Does Impaired Left Ventricular Relaxation Affect P Wave Dispersion in Patients with Hypertension?” Annals of Noninvasive Electrocardiology, Vol. 8, No. 3, 2003, pp. 189-193. doi:10.1046/j.1542-474X.2003.08304.x
[11]	F. Ozmen, E. Atalar, K. Aytemir, et al., “Effect of Balloon-Induced Acute Ischaemia on P Wave Dispersion during Percutaneous Transluminal Coronary Angioplasty,” Europace, Vol. 3, No. 4, 2001, pp. 299-303. doi:10.1053/eupc.2001.0187
[12]	H. Turhan, E. Yetkin, R. Atak, et al., “Increased P-Wave Duration and P-Wave Dispersion in Patients with Aortic Stenosis,” Annals of Noninvasive Electrocardiology, Vol. 8, No. 1, 2003, pp. 18-21. doi:10.1046/j.1542-474X.2003.08104.x
[13]	J. Sztajzel, “Heart Rate Variability: A Noninvasive Electrocardiographic Method to Measure the Autonomic Nervous System,” Swiss Medical Weekly, Vol. 134, No. 35-36, 2004, pp. 514-522
[14]	J. Habersberger, V. Manins and A. J. Taylor, “Cardiac Sarcoidosis,” Internal Medicine Journal, Vol. 38, No. 4, 2008, pp. 270-277. doi:10.1111/j.1445-5994.2007.01590.x
[15]	F. Tavora, N. Cresswell, L. Li, et al., “Comparison of Necropsy Findings in Patients with Sarcoidosis Dying Suddenly from Cardiac Sarcoidosis versus Dying Suddenly from Other Causes,” American Journal of Cardiology, Vol. 104, No. 4, 2009, pp. 571-577. doi:10.1016/j.amjcard.2009.03.068
[16]	H. Hiraga, K. Yuwai, M. Hiroe, et al., “Guidelines for the Diagnosis of Cardiac Sarcoidosis: Study Report of Diffuse Pulmonary Diseases,” Japanese Ministry of Health and Welfare, Tokyo, 1993, pp. 23-24.
[17]	G. W. Hunninghake, U. Costabel, M. Ando, et al., “ATS/ ERS/WASOG Statement on Sarcoidosis,” Sarcoidosis, Vasculitis and Diffuse Lung Diseases, Vol. 16, No. 2, 1999, pp. 149-173.
[18]	K. Sugisaki, T. Yamaguchi, S. Nagai, et al., “Clinical Characteristics of 195 Japanese Sarcoidosis Patients Treated with Oral Corticosteroids,” Sarcoidosis, Vasculitis and Diffuse Lung Diseases, Vol. 20, No. 3, 2003, pp. 222-226.
[19]	M. Tahir, S. K. Sharma, S. Ashraf and H. K. Mishra, “Angiotensin Converting Enzyme Genotype Affects Development and Course of Sarcoidosis in Asian Indians,” Sarcoidosis, Vasculitis and Diffuse Lung Diseases, Vol. 24, No. 2, 2007, pp. 106-112.
[20]	N. B. Schiller, P. M. Shah, M. Crawford, et al., “Recommendations for Quantitation of the Left Ventricle by Two-Dimensional Echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms,” Journal of the American Society of Echocardiography, Vol. 2, No. 5, 1989, pp. 358-367.
[21]	P. E. Dilaveris, E. J. Gialafos, D. Chrissos, et al., “Detection of Hypertensive Patients at Risk for Paroxysmal Atrial Fibrillation during Sinus Rhythm by Computer-Assisted P Wave Analysis,” Journal of Hypertension, Vol. 17, No. 10, 1999, pp. 1463-1470. doi:10.1097/00004872-199917100-00015
[22]	S. F. Nagueh, “Echocardiographic Assessment of Left Ventricular Relaxation and Cardiac Filling Pressures,” Current Heart Failure Reports, Vol. 6, No. 3, 2009, pp. 154-159. doi:10.1007/s11897-009-0022-8
[23]	S. Lucreziotti, A. Gavazzi, L. Scelsi, et al., “Five-Minute Recording of Heart Rate Variability in Severe Chronic Heart Failure: Correlates with Right Ventricular Function and Prognostic Implications,” American Heart Journal, Vol. 139, No. 6, 2000, pp. 1088-1095. doi:10.1067/mhj.2000.106168
[24]	K. Senen, H. Turhan, A. Riza Erbay, et al., “P-Wave Duration and P-Wave Dispersion in Patients with Dilated Cardiomyopathy,” European Journal of Heart Failure, Vol. 6, No. 5, 2004, pp. 567-569.
[25]	J. Boineau, “The Prolonged P Wave and Interatrial Block. Time to Consider a Broader Concept and Different Terminology,” Journal of Electrocardiology, Vol. 38, No. 4, 2005, pp. 327-329. doi:10.1016/j.jelectrocard.2005.05.002
[26]	O. Turgut, I. Tandogan, M. B. Yilmaz, et al., “Association of P Wave Duration and Dispersion with the Risk for Atrial Fibrillation: Practical Considerations in the Setting of Coronary Artery Disease,” International Journal of Cardiology, Vol. 144, No. 2, 2010, pp. 322-324. doi:10.1016/j.ijcard.2009.03.023
[27]	R. L. Verrier and C. Antzelevitch, “Autonomic Aspects of Arrhythmogenesis: The Enduring and the New,” Current Opinion in Cardiology, Vol. 19, No. 1, 2004, pp. 2-11. doi:10.1097/00001573-200401000-00003
[28]	A. N. Cheema, M. W. Ahmed, A. H. Kadish and J. J. Goldberger, “Effects of Autonomic Stimulation and Blockade on Signal-Averaged P Wave Duration,” Journal of the American College of Cardiology, Vol. 26, No. 2, 1995, pp. 497-502. doi:10.1016/0735-1097(95)80028-F
[29]	T. Tukek, V. Akkaya, S. Demirel, et al., “Effect of Valsalva Maneuver on Surface Electrocardiographic P-Wave Dispersion in Paroxysmal Atrial Fibrillation,” American Journal of Cardiology, Vol. 85, No. 7, 2000, pp. 896-899. doi:10.1016/S0002-9149(99)00891-7
[30]	R. Ramaraj, “Role of the Renin-Angiotensin System in the Promotion of Atrial Fibrillation,” Acta Cardiologica, Vol. 64, No. 6, 2009, p. 843. doi:10.2143/AC.64.6.2044757
[31]	K. Mizuno, M. Gotoh, J. Matsui, et al., “Acute Effects of Captopril on Serum Angiotensin-Converting Enzyme Activity, the Renin-Aldosterone System and Blood Pressure in Patients with Sarcoidosis,” The Tohoku Journal of Experimental Medicine, Vol. 140, No. 1, 1983, pp. 107-108. doi:10.1620/tjem.140.107
[32]	N. Asad, V. M. Johnson and D. H. Spodick, “Acute Right Atrial Strain: Regression in Normal as Well as Abnormal P-Wave Amplitudes with Treatment of Obstructive Pulmonary Disease,” Chest, Vol. 124, No. 2, 2003, pp. 560-564. doi:10.1378/chest.124.2.560
[33]	O. A. Centurion, “Clinical Implications of the P Wave Duration and Dispersion: Relationship between Atrial Conduction Defects and Abnormally Prolonged and Fractionated Atrial Endocardial Electrograms,” International Journal of Cardiology, Vol. 134, No. 1, 2009, pp. 6-8. doi:10.1016/j.ijcard.2008.12.072
[34]	Y. Yazaki, M. Isobe, M. Hiroe, et al., “Prognostic Determinants of Long-Term Survival in Japanese Patients with Cardiac Sarcoidosis Treated with Prednisone,” American Journal of Cardiology, Vol. 88, No. 9, 2001, pp. 1006-1010. doi:10.1016/S0002-9149(01)01978-6
[35]	V. V. Suranagi, P. R. Malur and H. B. Bannur, “Cardiac Sarcoidosis Causing Sudden Death,” Indian Journal of Pathology and Microbiology, Vol. 52, No. 4, 2009, pp. 566-567. doi:10.4103/0377-4929.56170
[36]	A. Uemura, S. Morimoto, S. Hiramitsu, et al., “Histologic Diagnostic Rate of Cardiac Sarcoidosis: Evaluation of Endomyocardial Biopsies,” American Heart Journal, Vol. 138, No. 2, 1999, pp. 299-302. doi:10.1016/S0002-8703(99)70115-8