Muzaffer Kahyaoğlu1, Çetin Geçmen2, Mehmet Çelik2, Yusuf Yılmaz3, Emrah Bayam2, Ender Özgün Çakmak2, Özkan Candan4, İbrahim Akın İzgi5, Cevat Kırma2

1Department of Cardiology, Abdulkadir Yuksel State Hospital, Gaziantep, Turkey
2Department of Cardiology, Kartal Koşuyolu High Specialization Training and Research Hospital, Istanbul, Turkey
3Department of Cardiology, Goztepe Training and Research Hospital, Istanbul, Turkey
4Department of Cardiology, Faculty of Medicine, University of Usak, Usak, Turkey
5Department of Cardiology, Faculty of Medicine, University of Abant Izzet Baysal, Bolu, Turkey

Keywords: Fragmented QRS; hypertension; left ventricular dysfunction; speckle tracking echocardiography.


Introduction: In hypertensive patients, the early detection of subclinical left ventricular dysfunction could prevent or delay patients from heart failure by aggressive risk factor control and rigorous medical management. Fragmented QRS (fQRS) is a marker of myocardial fibrosis, and myocardial fibrosis causes left ventricular dysfunction in hypertensive patients. In this study, we aimed to assess the association between the presence of fQRS and LV function at hypertensive patients using the speckle tracking echocardiography method.

Patients and Methods: The study included a total of 95 hypertensive patients. Detailed anamnesis, physical examination, laboratory tests, 12-lead electrocardiography, and conventional echocardiography were administered to all patients. The participating patients were divided into two groups as fQRS (+) (n= 33) and fQRS (-) (n= 62).

Results: Compared to the fQRS (-) group, the fQRS (+) group had older age, the average duration of hypertension was longer, and had a higher hemoglobin level. In the fQRS (+) group, interventricular septum thickness, posterior wall thickness, left ventricular mass index, relative wall thickness, deceleration time, and E/Em were significantly higher while left ventricular global longitudinal strain values were lower compared to fQRS (-) group. In the multiple linear regression analysis, fQRS and duration of hypertension were identified as independent predictors of LV-GLS.

Conclusion: In this study, we demonstrated that subclinical left ventricular dysfunction developing secondary to myocardial fibrosis could be predicted by fQRS, a simple marker in 12-lead electrocardiography.


Essential hypertension is a serious public health problem which is one of the leading causes of mortality and morbidity worldwide(1). Hypertension is associated with a significant increase in the risk of adverse cardiovascular and renal outcomes such as left ventricular hypertrophy, heart failure, ischemic and hemorrhagic stroke, ischemic heart disease, or chronic kidney disease(1). Hypertension creates a chronic pressure load on the heart, causing structural changes on the left ventricle (LV) and left atrium, which leads to impaired left ventricular systolic and diastolic functions. Longstanding pressure and volume overload cause left ventricular hypertrophy which plays a significant role in the pathophysiology of heart failure with both reduced and preserved ejection fraction (EF)(2). Chronic pressure load due to hypertension also causes various abnormalities in electrocardiography (ECG). Previous studies have shown that fragmented QRS (fQRS) is a more common finding in hypertensive patients than normotensive patients, and it is associated with LV hypertrophy, increased epicardial adipose tissue, non-dipper status, diastolic dysfunction, and increased arterial stiffness(3-6). Secondary to hypertension, myocardial fibrosis caused by myocardial hypertrophy and excessive collagen accumulation in interstitial tissue could be one crucial early mechanism in the transition from hypertension to heart failure(2). Based on this information, we think that fQRS, which is shown as an indirect indicator of the myocardial fibrotic burden on ECG in hypertensive patients, may also be an indicator of left ventricular subclinical systolic dysfunction. In this study, we aimed to assess the association between the presence of fQRS and LV function at hypertensive patients using the speckle tracking echocardiography method.

Materials and Methods

This study was designed as a prospective single-center, non-randomized observational study. We recruited 95 cardiology outpatients with hypertension who meets the inclusion criteria, between January 2021 and March 2021. Hypertension is defined as office systolic blood pressure (SBP) values ≥ 140 mmHg, diastolic BP (DBP) values ≥ 90 mmHg, or the use of antihypertensive medicine(7). Exclusion criteria were the presence of coronary artery disease, objective signs of myocardial ischemia detected with exercise test or single photon emission computerized tomography (SPECT), a moderate or severe valvular disease, secondary hypertension, heart failure, atrial fibrillation, chronic renal and liver disease, poor quality echocardiographic images, and the presence of left or right bundle branch block with QRS width > 120 ms. Detailed anamnesis, physical examination, laboratory tests, 12-lead ECG, and conventional echocardiography were administered to all patients. The patients were separated into two groups as those with and without fQRS complexes on ECG. The following characteristics were recorded for each participant: Age, gender, duration of hypertension, history of smoking, history of diabetes mellitus, body mass index, and blood measurements were taken of 12-hour fasting glucose, creatinine, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, total cholesterol, hemoglobin, white blood cell count and albumin. The study was approved by the local ethics committee, and all participants gave written and oral informed consent.


In this study, the presence of fQRS in all patients was analyzed with superficial 12-lead resting ECG (filter interval: 0.5-150 Hz; AC filter: 60 Hz; 25 mm/s, 10 mm/mV). The fQRS was defined as the presence of an additional R wave (R’), notching of the R or S wave, or the presence of fragmentation (more than one R’) without a typical bundle-branch block in two contiguous leads corresponding to a major coronary artery(8). All ECGs were evaluated by two cardiologists who did not know the patients’ echocardiographic data and the study protocol. Figure 1 demonstrates an example of fQRS.


Echocardiographic examinations were performed with an ultrasound platform (Epiq; Philips Healthcare, Andover, Massachusetts, USA) equipped with a 5-1 MHz transthoracic transducer (X5-1; Philips Healthcare). Offline analyses were performed by using the QLAB advanced quantification software version 7.1 (Philips, Amsterdam, The Netherlands). All echocardiographic examinations were performed by two cardiologists who were blinded to the clinical two-dimensional and Doppler measurements (including tissue Doppler measurements) and evaluated according to the guidelines of the American Society of Echocardiography(9). All variables were measured 3 times, and an average of these measurements was used in the statistical analysis.

The interventricular septum (IVS) thickness, posterior wall (PW) thickness, left atrium, ascending aorta, and LV dimensions were measured in M-mode at end-diastole from the parasternal long-axis view according to the current guidelines(9). LA maximum volume was obtained using a biplane area-length method at end-systole before mitral valve opening. LV ejection fraction (LVEF) was obtained by using Simpson’s rule(10). LV mass was calculated using the ASE formula and was indexed to body surface area(10). Relative wall thickness (RWT) was calculated using the ASE formula: RWT = 2 x posterior wall thickness/left ventricular dimension in diastole(10).

Mitral inflow velocities were measured from the apical four-chamber view by placing the pulsed-wave Doppler sample volume to the leaflet tips. Mitral early diastolic velocity (E, cm/s), late diastolic velocity (A, cm/s), E/A ratio, and deceleration time (DT) were determined. Tissue Doppler imaging echocardiography was performed with a 3.5 to a 4.0-MHz transducer, adjusting the Doppler pulse repetition frequency until a Nyquist limit of 15-20 cm/s was reached, and using the minimal optimal gain. The monitor sweep speed was set at 50-100 mm/s to optimize the spectral display of myocardial velocities. Myocardial peak systolic (Sm, cm/s), early (Em, cm/s), late (Am, cm/s) diastolic velocities and isovolumetric contraction time (IVCT), isovolumetric relaxation time (IVRT) were obtained by placing the tissue Doppler sample volume in the basal segments of lateral and septal walls of the LV. Also, the E/Em ratio was calculated.

For left ventricular speckle-tracking analysis, three cycles were recorded at the rate of 50 to 80 frames per second, and the mean values calculated for the strain analysis. The aortic valve opening and closing times were measured with the LV outflow Doppler profile and were integrated into the speckletracking strain profile to exclude the post systolic components. LV endocardial borders were automatically detected by the software in apical views with the help of three manually selected landmark points (lateral and septal mitral annulus and LV apex). Finally, automatic tracking of myocardial speckles was performed throughout the cardiac cycle. Manual correction of the border tracings was avoided as much as possible. Global longitudinal strains (GLS) were obtained for apical 4-chamber, 3-chamber, and 2-chamber views, including all LV myocardial segments (six segments per view). LV global longitudinal strain (LV-GLS) was calculated as the arithmetic mean of the three values.

Statistical Analysis

Statistical analyses were performed by using the IBMSPSS 22.0 statistical software package (IBM, Armonk, NY). Continuous variables were expressed as mean ± SD, while categorical variables were presented as numbers and percentages. The Chi-squared and Fisher’s exact tests were used for the comparison of categorical variables, while the Student’s t-test and Mann-Whitney U tests were used to compare parametric and non-parametric continuous variables, respectively. The correlation of continuous variables was analyzed by Spearman’s and Pearson’s correlation analyses. Values of p< 0.05 were considered statistically significant. Finally, multiple linear regression analysis was applied to identify independent predictors of the severity of GLS.


A total of 95 patients were included in this study. The participating patients were divided into two groups based on the 12-lead ECG, thirty-three patients had fQRS on their ECGs [fQRS (+) group], 62 patients did not have fQRS on their ECGs [fQRS (-) group]. The clinical and demographic characteristics and laboratory findings of the patients were summarized in Table 1. Compared to fQRS (-) group, the fQRS (+) group had older age, the average duration of hypertension was longer, and had a higher hemoglobin level.

The echocardiographic parameters of the fQRS (+) and fQRS (-) groups are presented in Table 2. In fQRS (+) group, IVS (1.23 ± 0.17 vs. 1.11 ± 0.13; p= 0.001), PW (1.12 ± 0.13 vs. 1.02 ± 0.9; p< 0.001), left ventricular mass index (95.6 ± 17.5 vs. 83.7 ± 14.7; p= 0.001), RWT (0.51 ± 0.05 vs. 0.48 ± 0.05; p= 0.001), DT (215.9 ± 47.2 vs. 189.4 ± 44.1; p= 0.01) and E/ Em (9.8 ± 3.3 vs. 8.2 ± 1.8; p= 0.004) were significantly higher while LV-GLS (-16.6 ± 2.4 vs. -19.3 ± 2.4; p< 0.001), were lower compared to fQRS (-) group.

We performed univariate and multivariate analyses to identify independent predictors of GLS and in the multiple linear regression analysis, fQRS (β= -2.057, p< 0.001) and duration of hypertension (β= -0.132, p= 0.016) were identified as independent predictors of LV-GLS (Table 3).


In this study, we showed that fQRS and duration of hypertension had a predictive value for subclinical LV dysfunction detected with speckle tracking echocardiography in patients with hypertension.

Hypertension is one of the leading causes of cardiovascular mortality and morbidity and it is well known to be associated with deterioration in LV systolic and diastolic functions by the way that causing myocardial fibrosis(2,11,12). The adaptive mechanisms for increased afterload, such as myocyte hypertrophy, myocardial fibrosis, endothelial dysfunction, could cause functional and structural left ventricular dysfunction(13). Myocardial fibrosis plays a prominent role in left ventricular systolic dysfunction(2). However, overt LV failure may not occur until the late stages. Furthermore, subendocardial fibers are more vulnerable to injury and the first to be affected by interstitial and perivascular fibrosis(14). Thus, longitudinal fibers, which are predominantly located sub-endocardial, are more prone to fibrosis and hemodynamic alterations, so that primarily due to these subendocardial fibers being affected would probably result in a subtle decline in LV function that could not be detected by conventional echocardiographic techniques(14). With speckle tracking echocardiography these subtle changes in myocardial deformation can be detected before the more extensive impairment of the LV, that is detectable by changes in conventional echocardiographic parameters. It is showed that decreased LV global longitudinal strain values obtained by speckle-tracking echocardiography were defined as subclinical LV dysfunction in many different pathologies such as diabetes mellitus, hypertrophic cardiomyopathy, hypertensive patients(15-17). Similarly, in our study, LV GLS values were found to be lower, and the decrease in GLS values seems more pronounced, especially in the fQRS (+) group.

fQRS is a useful parameter that can be easily determined on the surface ECG, and it has been shown in previous studies that its frequency is increased in many cardiovascular and non-cardiovascular pathologies such as myocardial infarction, hypertrophic cardiomyopathy, chronic renal failure, cardiac sarcoidosis, metabolic syndrome, diabetes mellitus, androgenic steroid users, acromegaly(15,18-24). Its accuracy and clinical usefulness have been reported in these studies and it was emphasized that the presence of fQRS is a reliable sign of scar and fibrosis in the myocardium. Also, in many studies, It has been shown that fQRS is associated with increased arterial stiffness, complex ventricular arrhythmia, diastolic dysfunction, left ventricular hypertrophy and increased epicardial adipose tissue thickness in hypertensive patients(3,4,6,12,25). In our study, we detected lower GLS values in hypertensive patients with fQRS. The pathogenesis of fQRS and myocardial dysfunction is similar. Increase fibrotic areas in the myocardium may delay and impair homogeneity of electrical stimuli conduction, so this situation appears as fQRS in ECG. Similarly, increased fibrotic tissue in the myocardium contributes to left ventricular dysfunction by disrupting the myocardial contraction mechanism. In other words, it would not be wrong to say that as myocardial fibrotic tissue increases, the frequency of fQRS increases in ECG, and at the same time, there is an increase in left ventricular systolic dysfunction. In our study, the significant association between the presence of fQRS and subclinical LV dysfunction may be related to these mechanisms.

Myocardial fibrosis was demonstrated with cardiac magnetic resonance imaging (CMR), SPECT, circulating biomarkers, and animal-based experimental studies in hypertension and many other diseases(8,26-28). However, this condition of myocardial fibrosis, which consists of an increase in the size of myofibrils and an accumulation of collagen in the extracellular matrix, in an adaptive response to increased load in hypertensive patients may not be diffuse in every patient. In SPECT and CMR-based studies, it has been detected focal and regionally(8,26). Therefore, it may not be possible to see overt left ventricular dysfunction in the early period since there is no diffuse fibrosis condition. And also, previous studies have shown that a decrease in LV longitudinal deformation parameters has been detected even in patients with mild to moderate hypertension or newly diagnosed(29). So, even in uncomplicated hypertension, we may see left ventricular global longitudinal strain impairment as an early sign of this myocardial fibrosis. Therefore, detection of early subclinical cardiac dysfunction in patients with hypertension is essential that aggressive risk factor control and medical management of hypertension could prevent or delay heart failure. Detection of this risky group can be evaluated with fQRS. In previous MR-based studies, fQRS was shown as a reliable marker in detecting myocardial scar tissue in coronary and non-coronary artery diseases, and various studies have highlighted the potential importance of fQRS about subclinical LV dysfunction in different pathologies such as coronary artery disease, dilated cardiomyopathy, metabolic syndrome, anabolic steroid users, acromegaly(18-24,30-32). Consistent with previous studies’ findings, in our study, we detected that the use of fQRS is a predictive marker in identifying patients with subclinical LV systolic dysfunction.

The present study has several limitations. The primary limitation was that our study was non-randomized, has a crosssectional design, and a single-center study with a relatively small number of patients. Second, even if coronary artery disease is tried to be ruled out by exercise test or SPECT, patients with possible subclinical coronary artery disease may have been included in this study, as coronary angiography is not used as a gold standard diagnostic method. Third, myocardial fibrosis was not be verified using imaging modalities such as CMR or SPECT. Fourth, our study population consists of selected hypertensive patients. Therefore, our results cannot be generalized to the general population. Lastly, the lack of prognostic information due to the absence of clinical follow-up was another limitation.


The result of our study demonstrated that fQRS was associated with subclinical LV dysfunction, which was assessed by speckle-tracking echocardiography in hypertensive patients. Myocardial fibrosis is one of the major myocardial structural alterations in patients with hypertension and may eventually lead to both overt or subclinical LV dysfunction. The assessment of fQRS by 12-lead ECG gives new insight into myocardial function in hypertension that might improve pathophysiologic understanding and identifying patients at high risk of LV systolic dysfunction. In daily practice, this inexpensive, easily accessible, and useful parameter may identify individuals who are required to follow closely and pursue more rigorous blood pressure control. All these findings strongly support the need for physicians to integrate in their daily practice the identification of fQRS when evaluating ECG in hypertensive patients.

Ethics Committee Approval

The approval for this study was obtained from Kartal Koşuyolu High Speciality Training and Research Hospital Ethics Committee (Decision no: 2021/1/435, Date: 12.01.2021).

Peer Review

Externally peer-reviewed.

Author Contributions

Concept/Design - MK, ÇG; Analysis/Interpretation - MK, ÖC; Data Collection - MÇ, YY; Writing - MK, EB; Critical Revision - İİ, CK; Statistical Analysis - MK, ÇG; Overall Responsibility - MK, ÇG; Final Approval - All of authors.

Conflict of Interest

The authors have no conflicts of interest to declare.

Financial Disclosure

The authors declared that this study has received no financial support.


  1. Mills KT, Bundy JD, Kelly TN, Reed JE, Kearney PM, Reynolds K, et al. Global disparities of hypertension prevalence and control: a systematic analysis of population-based studies from 90 countries. Circulation 2016;134:441-50. [Crossref]
  2. Ekström M, Hellman A, Hasselström J, Hage C, Kahan T, Ugander M, et al. The transition from hypertension to hypertensive heart disease and heart failure: the PREFERS Hypertension study. ESC Heart Fail 2020;7:737-46. [Crossref]
  3. Zhang B, Zhen Y, Shen D, Zhang G. Significance of fragmented QRS complexes for identifying left ventricular hypertrophy in patients with hypertension. Ann Noninvasive Electrocardiol 2015;20:175-80. [Crossref]
  4. Yaman M, Arslan U, Bayramoglu A, Bektas O, Gunaydin ZY, Kaya A. The presence of fragmented QRS is associated with increased epicardial adipose tissue and subclinical myocardial dysfunction in healthy individuals. Rev Port Cardiol 2018;37:469-75. [Crossref]
  5. Eyuboglu M. Fragmented QRS as a marker of myocardial fibrosis in hypertension: a systematic review. Curr Hypertens Rep 2019;21:73. [Crossref]
  6. Korkmaz L, Hatem E, Erkan H, Ata Korkmaz A, Dursun I. Fragmented QRS may predict increased arterial stiffness in asymptomatic hypertensive patients. Blood Press Monit 2015;20:16-9. [Crossref]
  7. Williams B, Mancia G, Spiering W, Agabiti Rosei E, Azizi M, Burnier M, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J 2018;39:3021-104. [Crossref]
  8. Das MK, Khan B, Jacob S, Kumar A, Mahenthiran J. Significance of a fragmented QRS complex versus a Q wave in patients with coronary artery disease. Circulation 2006;113:2495-501. [Crossref]
  9. Mitchell C, Rahko PS, Blauwet LA, Canaday B, Finstuen JA, Foster MC, et al. Guidelines for performing a comprehensive transthoracic echocardiographic examination in adults: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr 2019;32:1-64. [Crossref]
  10. Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2015;16:233-70. [Crossref]
  11. Plaksej R, Kosmala W, Frantz S, Herrmann S, Niemann M, Störk S, et al. Relation of circulating markers of fibrosis and progression of left and right ventricular dysfunction in hypertensive patients with heart failure. J Hypertens 2009;27:2483-91. [Crossref]
  12. Kadı H, Demir AK, Ceyhan K, Damar İH, Karaman K, Zorlu Ç. Association of fragmented QRS complexes on ECG with left ventricular diastolic function in hypertensive patients. Turk Kardiyol Dern Ars 2015;43:149-56. [Crossref]
  13. Ivanovic BA, Tadic MV, Celic VP. To dip or not to dip? The unique relationship between different blood pressure patterns and cardiac function and structure. J Hum Hypertens 2013;27:62-70. [Crossref]
  14. Kosmala W, Plaksej R, Strotmann JM, Weigel C, Herrmann S, Niemann M, et al. Progression of left ventricular functional abnormalities in hypertensive patients with heart failure: an ultrasonic two-dimensional speckle tracking study. J Am Soc Echocardiogr 2008;21:1309-17. [Crossref]
  15. Bayramoğlu A, Taşolar H, Kaya Y, Bektaş O, Kaya A, Yaman M, et al. Fragmented QRS complexes are associated with left ventricular dysfunction in patients with type-2 diabetes mellitus: a two-dimensional speckle tracking echocardiography study. Acta Cardiol. 2018;73:449-56. [Crossref]
  16. Prinz C, van Buuren F, Faber L, Bitter T, Bogunovic N, Burchert W, et al. Myocardial fibrosis is associated with biventricular dysfunction in patients with hypertrophic cardiomyopathy. Echocardiography 2012;29:438-44. [Crossref]
  17. Shehata IE, Eldamanhory AS, Shaker A. Early predictors of left ventricular dysfunction in hypertensive patients: comparative cross-section study. Int J Cardiovasc Imaging 2020;36:1031-40. [Crossref]
  18. Lee DC, Albert CM, Narula D, Kadish AH, Panicker GK, Wu E, et al. Estimating myocardial infarction size with a simple electrocardiographic marker score. J Am Heart Assoc 2020;9:e014205. [Crossref]
  19. Bi X, Yang C, Song Y, Yuan J, Cui J, Hu F, et al. Quantitative fragmented QRS has a good diagnostic value on myocardial fibrosis in hypertrophic obstructive cardiomyopathy based on clinical-pathological study. BMC Cardiovasc Disord 2020;20:298. [Crossref]
  20. Ulusoy S, Ozkan G, Adar A, Bektaş H, Kırış A, Celik S. Relationship between fragmented QRS complex and left ventricular systolic and diastolic function in kidney transplant patients. Prog Transplant 2014;24:146-51. [Crossref]
  21. Homsi M, Alsayed L, Safadi B, Mahenthiran J, Das MK. Fragmented QRS complexes on 12-lead ECG: a marker of cardiac sarcoidosis as detected by gadolinium cardiac magnetic resonance imaging. Ann Noninvasive Electrocardiol 2009;14:319-26. [Crossref]
  22. Bayramoğlu A, Taşolar H, Bektaş O, Yaman M, Kaya Y, Özbilen M, et al. Association between metabolic syndrome and fragmented QRS complexes: speckle tracking echocardiography study. J Electrocardiol 2017;50:889-93. [Crossref]
  23. Kaya Ü, Eren H, Öcal L, İnanır M, Balaban İ. Association between fragmented QRS complexes and left-ventricular dysfunction in anabolic androgenic steroid users. Acta Cardiol 2020;75:244-53. [Crossref]
  24. Dereli S, Özer H, Özer N, Bayramoğlu A, Kaya A. Association between fragmented QRS and left ventricular dysfunction in acromegaly patients. Acta Cardiol 2020;75:435-41. [Crossref]
  25. Bekar L, Kalçık M, Kilci H, Çelik O, Yetim M, Doğan T, et al. Presence of fragmented QRS may be associated with complex ventricular arrhythmias in patients with essential hypertension. J Electrocardiol 2019;55:20-5. [Crossref]
  26. Mahenthiran J, Khan BR, Sawada SG, Das MK. Fragmented QRS complexes not typical of a bundle branch block: a marker of greater myocardial perfusion tomography abnormalities in coronary artery disease. J Nucl Cardiol 2007;14:347-53. [Crossref]
  27. Gyongyosi M, Winkler J, Ramos I, Do QT, Firat H, McDonald K, et al. Myocardial fibrosis: biomedical research from bench to bedside. Eur J Heart Fail 2017;19:177-91. [Crossref]
  28. Ishizu T, Seo Y, Kameda Y, Kawamura R, Kimura T, Shimojo N, et al. Left ventricular strain and transmural distribution of structural remodeling in hypertensive heart disease. Hypertension 2014;63:500-6. [Crossref]
  29. Atilgan D, Bilge AK, Onur I, Pamukçu B, Ozcan M, Adalet K. Assessment of longitudinal left ventricular systolic function by different echocardiographic modalities in patients with newly diagnosed mildto-moderate hypertension. Anadolu Kardiyol Derg 2010;10:247-52. [Crossref]
  30. Yooprasert P, Vathesatogkit P, Thirawuth V, Prasertkulchai W, Tangcharoen T. Fragmented QRS in prediction of ischemic heart disease diagnosed by stress cardiovascular magnetic resonance imaging. Ann Noninvasive Electrocardiol 2020;25:e12761. [Crossref]
  31. Ahn MS, Kim JB, Joung B, Lee MH, Kim SS. Prognostic implications of fragmented QRS and its relationship with delayed contrast-enhanced cardiovascular magnetic resonance imaging in patients with non-ischemic dilated cardiomyopathy. Int J Cardiol 2013;167:1417-22. [Crossref]
  32. Park CH, Chung H, Kim Y, Kim JY, Min PK, Lee KA, et al. Electrocardiography based prediction of hypertrophy pattern and fibrosis amount in hypertrophic cardiomyopathy: comparative study with cardiac magnetic resonance imaging. Int J Cardiovasc Imaging 2018;34:1619-28. [Crossref]

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