European Journal of Cardiovascular Medicine

Remote MI is diagnosed by presence of pathological q waves on 12 lead ECG but with better treatment options Q wave MI are decreasing with reciprocal increase (upto 2/3^rd) in Non Q WAVE MI. Q waves on a 12-lead ECG are markers of a prior myocardial infarction (MI). However, they may regress or even disappear over time, and there is no specific ECG sign of a non–Q-wave/ST wave MI and so depends mainly on cardiac biomarker levels.

Fragmented QRS complexes (fQRSs), which include various RSR′ patterns, without a typical bundle-branch block are markers of altered ventricular depolarization and myocardial conduction abnormalities owing to a prior myocardial scar in patients with coronary artery disease.

The reasons for documented association between fQRS and increased morbidity,mortality, sudden cardiac death and recurrent adverse cardiac events have been investigated in previous studies. In these studies, the main causative mechanism of fQRS was cardiac fibrosis. Additionally, fQRS may represent altered ventricular depolarization, which can be derived from mechanisms such as non-homogeneous activation of ischemic ventricles in the setting of STEMI.

Sometimes fQRS may be the only electrocardiographic marker of myocardial damage in patients with non-Q myocardial infarction and in patients with resolved Q wave. QRS complex fragmentations are frequently seen on surface electrocardiograms with narrow or wide QRS complex including paced rhythm, bundle branch block or ventricular pre- mature beats.

These fragmentations on surface ECG have been associated with increased adverse cardiovascular events in previous studies. Fragmented QRS may be important for stratifying patients at high risk on admission and after ST elevation myocardial infarction. fQRS on 12-lead electrocardiography occurs within 48 hours of presentation with NSTEMI as well as ST elevation MI and persists thereafter.(Yatuka et al.2012)

Kaplan-Meier survival analysis revealed that patients with fQRS had significantly decreased times to death compared to those without fQRS.

It was demonstrated that the fragmentation of QRS complexes represent myocardial scar in patients with suspected or known CAD in two major studies, one for narrow QRS complex (QRS duration < 120 ms) (DAS,KUMAR et.al 2006) and the other for wide QRS complex (QRS duration ≥ 120 ms)(DAS ,SURADI et.al 2008)

Sensitivity, specificity, and the negative predictive value for myocardial scar were 86%, 89%, and 93%, respectively, for the fQRS in the first study. And the second study showed a sensitivity, specificity, positive predictive value and negative predictive value of f-wQRS for myocardial scar were 87%, 93%, 92% and 88%, respectively

Fragmented QRS, T-wave inversion, and ST depression were independent predictors of mortality during a mean follow-up period of 34 ± 16 months.

In conclusion, fQRS on 12-lead electrocardiography is a moderately sensitive(55%and 50%) but highly specific sign(96%) for ST elevation MI and NSTEMI sensitivity [Y.TAKE and H.MORITA 2012]

AIMS AND OBJECTIVES

To determine association between QRS fragmentation and IHD in comparison with control group.

INCLUSION CRITERIA:

1. Patient willing to be a part of study
2. Known case of myocardial infarction
3. Newly diagnosed cases of myocardial infarction

EXCLUSION CRITERIA:

1. Patient not willing
2. Non Ischemic Cardiomyopathy
3. Rheumatic Heart Disease

METHODS

50 known cases of IHD and acute MI were included in study along with 100 controls.results obtained on basis of ECG criteria for QRS fragmentation with confirmation by 2D echo of IHD.

ECG CRITERIA-

1.Fragmentation of narrow complex QRS was defined by Das et al., as presence of a) an additional R wave (R’) or b) notching in the nadir of the S wave, orc) the presence of > 1 R’ in 2 contiguous leads, corresponding to a major coronary artery territory

2. Fragmentation of wide complex QRS (BBB and paced rhythms) was defined by Das et al.,

Various RSR patterns with or without a Q wave, with a)more than 2 R waves (R’) or b) more than 2 notches in the R wave, or c)more than 2 notches in the downstroke or upstroke of the S wave, in 2 contiguous leads corresponding to a major coronary artery territory.

Wall involvement

• 52% OF IHD CASES had Anterior wall involvement;
• 34 % had posterior wall involvement
• 14 % had multiple involvement

QRS FRAGMENTATION

• Q wave MI were 46% while non Q MI were 54;
• Out of those Q wave MI 65.2% had fragmentation of QRS
• Out of non q wave MI 48.1 % had fragmentation of QRS
• So,in both type of MI combined 56% had QRS fragmentation.
• And out of 100 controls ,5 had qrs fragmentation i.e. 5%.
• AGE DISTRIBUTION
• 18% cases and 22% controls were in age group 40-49
• 42% of cases and 40%of controls were in 50-59 age group
• 28% of cases and 32%of controls were in 60-69 age group
• 10% of cases and 4 % of controls were in 70-79 age group
• 2% cases as wall as controls in 80-89 age group
• 72 % cases and 66 % controls were male.
• RISK FACTORS
• 50% of cases were smokers while 26 % of cases were smokers
• 38% cases and 10% controls were alcoholic
• 30% cases and 8% controls suffered from DM
• 30% cases had family history of CAD

Table 1

Figure 1

Table 2

Figure 2

Table 3

Test Chi square applied to see association between fqrs and MI (q wave and non q wave)

Statistically significant association found with both type of MI.

Figure 3

Table 4

It has been shown in some studies that abnormality within the QRS complex can represent conduction disturbance and myocardial scar. Injured tissue around an infarct scar resulted in the RSR’ pattern of the QRS complex. However, the diagnostic and prognostic values of these subtle abnormalities within the QRS complex were not clarified in prior studies.

In 2006, Das et al. proved that, fragmented QRS complex in patients with coronary artery disease (CAD) was associated with myocardial conduction block due to myocardial scar detected by myocardial single photon emission tomography (SPECT). fQRS improved identification of prior myocardial infarction in patients who are being evaluated for CAD.

As fQRS represents prior occurrence of myocardial infarction, further studies are directed to its role in identifying the risk of subsequent occurrence of ischemic events, its correlation to ventricular dysfunction and occurrence of congestive heart failure. Das et al. demonstrated that fQRS is an independent predictor of cardiac events in patients with CAD. Other studies confirmed a relation between fQRS and LV dysfunction.

Myocardial scar is also a substrate for reentrant ventricular tachyarrhythmia. Signal averaged electrocardiogram (SAECG) reveals the presence of late potential that indicates low-amplitude high-frequency potentials out- side the terminal QRS complex. Abnormal late potential represents a slow conduction zone with damaged myo- cardium around the fibrosis of healed myocardial infarction. The presence of late potential has been used for risk stratification of sudden cardiac death or lethal arrhythmic events.

As well as SAECG, fQRS also can reflect intra-cardiac conduction abnormality and will represent a substrate for ventricular arrhythmia. There has been only one study in which the correlation between fQRS and late potential detected by SAECG was investigated. This study dem- onstrated that the existence of fQRS appeared independently from the existence of late potential in patients with Brugada syndrome, but it is still unknown whether there is a correlation between fQRS and late potential in other diseases such as CAD and various cardiomyopathies.

fQRS in Coronary Artery Disease (CAD)

It was demonstrated that the fragmentation of QRS complexes represent myocardial scar in patients with suspected or known CAD in two major studies, one for narrow (QRS duration < 120 ms) [5] and the other for wide (QRS duration ≥ 120 ms). Sensitivity, specificity, and the negative predictive value for myocardial scar were 86%, 89%, and 93%, respectively, for the fQRS in the first study. And the second study was on 879 patients showed a sensitivity, specificity, positive predictive value and negative predictive value of f-wQRS for myocardial scar were 87%, 93%, 92% and 88%, respectively.

65.2% of q wave MI had fragmented qrs while 48% of non q wave MI had fragmentation of qrs

1. Das MK, Khan B, Jacob S, Kumar A, Mahenthiran J. Significance of a fragmented QRS complex vs a Q wave in patients with coronary artery disease. Circulation. 2006;113:2495 – 2501.
2. Michael MA, El Masry H, Khan BR, Das MK. Electrocardio- graphic signs of remote myocardial infarction. Prog Cardiovasc Dis. 2007;50(3):198 – 208.
3. 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(3):347 – 353.
4. Das MK, Saha C, El Masry H, et al. Fragmented QRS on a 12-lead ECG: a predictor of mortality and cardiac events in patients with coronary artery disease. Heart Rhythm. 2007;4(11): 1385 – 1392.
5. Das MK, Michael MA, Hussam S, et al. Usefulness of fragmented QRS on a12-lead electrocardiogram in acute coronary syndrome for predicting mortality. Am J Cardiol. In press.
6. Pietrasik G, Goldenberg I, Zdzienicka J, et al. Prognostic significance of fragmented QRS complex for predicting the risk of recurrent cardiac events in patients with Q-wave myocardial infarction. Am J Cardiol. 2007;100(4):583 – 586.
7. Oeff M, Go¨dde P, Agrawal R, et al. Magnetcardiographic detection of abnormal intraventricular activation in patients with ischemic heart disease with and without tachycardia [in German]. Herzschrittmacherther Elektrophysiol. 1997;8(3):195 – 204.
8. Stroink G, Meeder RJ, Elliott P, et al. Arrhythmia vulnerability assessment using magnetic field maps and body surface potential maps. Pacing Clin Electrophysiol. 1999;22(12):1718 – 1728.
9. Ouyang F, Ba¨nsch D, Schaumann A, et al. Catheter ablation of subepicardial ventricular tachycardia using electroanatomic mapping. Herz. 2003;28(7):591 – 597.
10. Das MK, Zipes DP. Fragmented QRS: a predictor of mortality and sudden cardiac death. Heart Rhythm. 2009;6(suppl 3):S8 – S14.
11. Morita H, Kusano KF, Miura D, et al. Fragmented QRS as a marker of conduction abnormality and a predictor of prognosis of Brugada syndrome. Circulation. 2008;118(17):1697 – 1704.
12. Ha¨ı ssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med. 2008;358: 2016 – 2023.
13. Wellens HJ. Early repolarization revisited. N Engl J Med. 2008; 358:2063 – 2065.
14. Peters S, Tru¨mmel M, Koehler B. QRS fragmentation in standard ECG as a diagnostic marker of arrhythmogenic right ventricular dysplasia-cardiomyopathy. Heart Rhythm. 2008;5(10): 1417 – 1421.
15. Kusano KF, Emori T, Morita H, Ohe T. Ablation of ventricular tachycardia by isolating the critical site in a patient with arrhythmogenic right ventricular cardiomyopathy. J Cardiovasc Electrophysiol. 2000;11(1):102 – 105.
16. Reddy CV, Cheriparambill K, Saul B, et al. Fragmented left sided QRS in absence of bundle branch block: sign of left ventricular aneurysm. Ann Noninvasive Electrocardiol. 2006;11(2):132 – 138.
17. Ogawa M, Miyoshi K, Morito N, et al. Successful catheter ablation of ventricular tachycardia originating from the idiopathic saccular apical left ventricular aneurysm. Int J Cardiol. 2004;93(2 – 3): 343 – 346.
18. Maehara K, Kokubun T, Awano N, et al. Detection of abnormal high-frequency components in the QRS complex by the wavelet transform in patients with idiopathic dilated cardiomyopathy. Jpn Circ J. 1999;63(1):25 – 32.
19. Homsi M, Alsayed L, Vaz D, Das MK, Mahenthiran J. 2064 fragmented QRS complexes on 12-lead ECG as a marker of greater myocardial infiltration by cardiac magnetic resonance gadolinium- delayed enhancement images in patients with sarcoidosis. J Cardio Mag Res. 2008;10(Suppl. 1suppl 1):A333.
20. Goernig M, DiPietroPaolo D, Haueisen J, Erne´ SE. Biomagnetic risk stratification by QRS fragmentation in patients with implanted cardioverter defibrillators. 4th European Conference of the International Federation for Medical and Biological Engineering.