August 2024 Issue
ISSN 2689-291X
ISSN 2689-291X
QRS Fragmentation:
Squiggly Curiosities!
Description
The above electrocardiograms (ECGs) have variable degrees of QRS fragmentation (inserts). Figure A demonstrates fragmented QRS only in lead III. Figure B fragmentation of the QRS is seen predominantly in Leads III and aVL, with rSr’ pattern in leads V1 and V2. Figure C reveals widespread QRS fragmentation, predominantly in leads III, V1 and V2, and to a lesser extent in leads aVL and aVF. The QRS duration in all ECGs is less than 110 milliseconds, and therefore does not meet criteria for an intraventricular conduction delay (IVCD).
All ECGs belong to young patients with sickle cell disease who had previous hospital admissions with chest pain and dyspnea. They all had mild to moderate increase in LV wall thickness measurements by 2-dimensional (2-D) echocardiography. They also all had documentation of either troponin I or NT-proBNP level elevations at some point in their care. They all suffered significant anemia expected of sickle cell disease. None of the patients manifested any specific tachy- or brady- arrhythmia beyond nonspecific isolated ectopy.
Discussion
QRS Fragmentation on the ECG has been known for many decades, previously described as high frequency components attributed to ventricular enlargement and infarction [1]. It has been defined as presence of extra R wave (R′) or notching in the S wave nadir in the setting of a narrow QRS complex [2]. It is an important marker of arrhythmia and mortality in several cardiac conditions [3].
Sickle cell patients have higher odds of an abnormal ECG, especially nonspecific ST-T changes, left ventricular hypertrophy, T-wave abnormalities, long QTc interval, and ischemia [4]. They are also prone to having myocardial damage due to repetitive microvascular injury [5], and as a result are likely to manifest QRS fragmentation on ECG, as the three ECGs discussed above demonstrate. This perhaps would be a worthwhile correlation to look into with further studies to help elucidate the prevalence and impact of QRS fragmentation on the risk of ventricular arrhythmia and sudden cardiac death in sickle cell patients [6].
References
The above electrocardiograms (ECGs) have variable degrees of QRS fragmentation (inserts). Figure A demonstrates fragmented QRS only in lead III. Figure B fragmentation of the QRS is seen predominantly in Leads III and aVL, with rSr’ pattern in leads V1 and V2. Figure C reveals widespread QRS fragmentation, predominantly in leads III, V1 and V2, and to a lesser extent in leads aVL and aVF. The QRS duration in all ECGs is less than 110 milliseconds, and therefore does not meet criteria for an intraventricular conduction delay (IVCD).
All ECGs belong to young patients with sickle cell disease who had previous hospital admissions with chest pain and dyspnea. They all had mild to moderate increase in LV wall thickness measurements by 2-dimensional (2-D) echocardiography. They also all had documentation of either troponin I or NT-proBNP level elevations at some point in their care. They all suffered significant anemia expected of sickle cell disease. None of the patients manifested any specific tachy- or brady- arrhythmia beyond nonspecific isolated ectopy.
Discussion
QRS Fragmentation on the ECG has been known for many decades, previously described as high frequency components attributed to ventricular enlargement and infarction [1]. It has been defined as presence of extra R wave (R′) or notching in the S wave nadir in the setting of a narrow QRS complex [2]. It is an important marker of arrhythmia and mortality in several cardiac conditions [3].
Sickle cell patients have higher odds of an abnormal ECG, especially nonspecific ST-T changes, left ventricular hypertrophy, T-wave abnormalities, long QTc interval, and ischemia [4]. They are also prone to having myocardial damage due to repetitive microvascular injury [5], and as a result are likely to manifest QRS fragmentation on ECG, as the three ECGs discussed above demonstrate. This perhaps would be a worthwhile correlation to look into with further studies to help elucidate the prevalence and impact of QRS fragmentation on the risk of ventricular arrhythmia and sudden cardiac death in sickle cell patients [6].
References
- Flowers NC, Horan LG, Thomas JR, Tolleson WJ. The anatomic basis for high-frequency components in the electrocardiogram. Circulation. 1969 Apr;39(4):531-9.
- Pietrasik G, Zaręba W. QRS fragmentation: diagnostic and prognostic significance. Cardiol J. 2012;19(2):114-21.
- Supreeth RN, Francis J. Fragmented QRS - Its significance. Indian Pacing Electrophysiol J. 2020 Jan-Feb;20(1):27-32.
- Taherifard E, Movahed H, Taherifard E, Sadeghi A, Dehdari Ebrahimi N, Ahmadkhani A, Kheshti F, Movahed H. Electrocardiographic abnormalities in patients with sickle cell disease: A systematic review and meta-analysis. Pediatr Blood Cancer. 2024 May;71(5):e30916.
- Kaur K, Huang Y, Raman SV, Kraut E, Desai P. Myocardial injury and coronary microvascular disease in sickle cell disease. Haematologica. 2021 Jul 1;106(7):2018-2021.
- d'Humières T, Saba J, Savale L, Dupuy M, Boyer L, Guillet H, Alassaad L, de Luna G, Iles S, Pham Hung d'Alexandry d'Orengiani AL, Zaouali Y, Boukour N, Pelinski Y, Messonnier L, Audureau E, Derbel H, Habibi A, Lellouche N, Derumeaux G, Bartolucci P. Determinants of ventricular arrhythmias in sickle cell anemia: toward better prevention of sudden cardiac death. Blood. 2023 Aug 3;142(5):409-420.
Authors:
Hajira Malik, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Brent Ruiz, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Celestine Odigwe, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Mustafeez Ur Rahman, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Mariam Riad, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Alexis Parks, D.O.
Cardiology Fellow
University of South Alabama
Mobile, AL
Sanchitha Nagaraj, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Mohammad As Sayaideh, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Christopher Malozzi, D.O.
Associate Professor of Cardiology
University of South Alabama
Mobile, AL
Bassam Omar, M.D., Ph.D.
Professor of Cardiology
University of South Alabama
Mobile, AL
Hajira Malik, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Brent Ruiz, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Celestine Odigwe, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Mustafeez Ur Rahman, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Mariam Riad, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Alexis Parks, D.O.
Cardiology Fellow
University of South Alabama
Mobile, AL
Sanchitha Nagaraj, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Mohammad As Sayaideh, M.D.
Cardiology Fellow
University of South Alabama
Mobile, AL
Christopher Malozzi, D.O.
Associate Professor of Cardiology
University of South Alabama
Mobile, AL
Bassam Omar, M.D., Ph.D.
Professor of Cardiology
University of South Alabama
Mobile, AL