J Wave and Cardiac Death in Inferior Wall Myocardial Infarction

ORIGINAL ARTICLES Arrhythmia 2015;16(2):67-77

Myung-Jin Cha, MD; Seil Oh, MD, ABSTRACT PhD, FHRS Background and Objectives: The clinical significance of J wave Department of Internal Medicine, Seoul National University presentation in acute myocardial infarction (AMI) patients remains Hospital, Seoul, Korea unclear. We hypothesized that J wave appearance in the inferior leads and/or reversed-J (rJ) wave in leads V1-V3 is associated with poor prognosis in inferior-wall AMI patients. Subject and Methods: We enrolled 302 consecutive patients with inferior-wall AMI who were treated with percutaneous coronary intervention (PCI). Patients were categorized into 2 groups based on electrocardiograms before and after PCI: the J group (J waves in inferior leads and/or rJ waves in leads V1-V3) and the non-J group (no J wave in any of the 12 leads). We compared patients with high amplitude (>2 mV) J or rJ waves (big-J group) with the non-J group. The cardiac and all-cause mortality at 6 months and post-PCI ventricular arrhythmic events ≤48 hours after PCI were analyzed. Results: A total of 29 patients (including 19 cardiac death) had died. Although all-cause mortality was significantly higher in the post-PCI J group than in the non-J group (p=0.001, HR=5.38), there was no difference between the groups in cardiac mortality. When compar- ing the post-PCI big-J group with the non-J group, a significant difference was found in all-cause mortality (n=29, p=0.032, HR=5.4) and cardiac mortality (n=19, p=0.011, HR=32.7). Pre-PCI J waves Received: March 26, 2015 Revision Received: June 3, 2015 were associated with a higher prevalence of post-AMI ventricular Accepted: June 29, 2015 Correspondence: Seil Oh, MD, PhD, FHRS, arrhythmia (p=0.016, HR=31.67). Department of Internal Medicine, Seoul National University College of Medicine and Seoul Conclusion: High-amplitude J waves in inferior leads and/or rJ National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 110-744, Korea waves in leads V1-V3 were possible prognostic factors of all-cause Tel: +82-2-2072-2088, Fax: +82-2-762-9662 E-mail: [email protected] and cardiac mortality in patients with inferior-wall AMI.

67 J Wave and Myocardial Infarction

Introduction in accordance with the Declaration of Helsinki. Patient consent was waived because it was not practical to obtain consent from The J wave is defined as an electrocardiogram (ECG) large numbers of patients for a retrospective review study, and the deflection with a dome or hump morphology, immediately data were analyzed anonymously. following the QRS complex.1 The cellular mechanism of J wave formation consists of transmural differences in the early phases of Patients the action potential.2,3 The augmentation of the J wave or the appearance of ST-segment elevation is caused by an outward shift The study population consisted of 336 consecutive patients in the repolarizing current owing to a decrease in sodium- or without a previous diagnosis of coronary artery disease (CAD). calcium-channel currents, or an increase in Ito, IK-ATP, IK-Ach, or From January 2005 to March 2010, they had received urgent other outward currents.1 percutaneous coronary intervention (PCI) at Seoul National However, the clinical significance of the J wave has not yet been University Hospital to treat inferior-wall AMI. A previous fully evaluated. Although this condition is usually considered diagnosis of CAD was defined as a history of myocardial benign, several studies have revealed a relationship between infarction (MI), coronary revascularization, or significant CAD idiopathic ventricular fibrillation and J point elevation.4,5 confirmed by prior catheterization. PCI was performed ≤90 Moreover, it is not clear whether the J wave represents the genetic minutes of the patient’s visit to the hospital for ST-elevation variant of early repolarization or whether it results from delayed myocardial infarction (STEMI), and ≤48 hours for non-ST- depolarization associated with structural abnormality of the elevation myocardial infarction (NSTEMI). Patients were myocardium.6 included in the study if they were followed up over a 6-month Recently, the appearance of J wave in the inferior leads has been period and received adequate medical support throughout, associated with an elevated risk of fatal arrhythmia or sudden including dual antiplatelet agents (aspirin and clopidogrel). We cardiac death.5,7,8 Some researchers have suggested that J wave excluded patients with bundle-branch block (n=9) and those who appearance is related to the risk of acute myocardial infarction had cardiac pacemakers at baseline (n=1). We also excluded (AMI).9 Based on previous reports, we hypothesized that the patients whose follow-up duration was less than 6 months (n=23) appearance of J waves in inferior leads following inferior-wall AMI and one patient who died during PCI (n=1). A total of 302 might be associated with worse outcomes. To prove our theory, we patients satisfied the inclusion criteria. analyzed the clinical implications of J wave before and after the revascularization of inferior-wall AMI. ECG Analysis We also hypothesized that reversed-J (rJ) waves in leads V1-V3 are the mirror images of J waves in the inferior leads. In AMI Patients’ ECGs, obtained 1 day after PCI, were retrospectively patients, electrocardiographic ST-segment depression is called a analyzed by 2 independent cardiologists using a previously reciprocal change when it occurs simultaneously with ST-segment described method. The J wave was defined as either a slurred or elevation in leads on the opposite side of the heart. In these notched J point elevation in at least 2 consecutive leads.10 The J patients, we hypothesized that a J wave in the inferior leads and its point amplitude was measured at the QRS-ST junction in the reciprocal change, the rJ wave in leads V1-V3, might share a case of slurred J waves, or at the peak J point in the case of notched similar clinical meaning. J waves. J point amplitude was measured relative to QRS onset in order to minimize any baseline wandering effect, as previously Materials and Methods described (Figure 1).11 The J group consisted of patients whose J waves were >0.1 mV Our study protocol was approved by the institutional review in ≥2 leads (among leads II, III, and aVF) and/or who had 2 rJ board of Seoul National University Hospital and was carried out waves that were >0.1 mV in ≥2 leads among leads V1, V2, and V3.

68 Arrhythmia 2015;16(2):67-77

Figure 1. Representative examples of J waves and reversed-J (rJ) waves. (A) J waves in the inferior leads (arrows). (B) rJ waves in leads V1 and V2 (arrows). [scale: 25 mm/s 10 mm/mV 40 Hz]

Patients were grouped into the big-J group (a subgroup of the J The QRS scar score taken 1 day after PCI was used for group) if the amplitude of ≥2 of their J waves or ≥2 of their rJ estimating left ventricular (LV) scar amount in each patient, waves was >2 mV. The non-J group consisted of patients who had calculated according to instructions from previous studies.12,13 This neither J nor rJ waves in any of the 12 leads. score considered Q and R wave duration, R/Q and R/S amplitude Next, pre-PCI ECGs obtained from patients ≤24 hours before ratios, R and S wave amplitudes, and R wave notches. The score PCI were reviewed in order to identify the J wave in the same had 32 total possible points, each of which represented 3% of the manner. LV mass.

69 J Wave and Myocardial Infarction

expected to accentuate the early repolarization pattern by patients.22,23 However, this system cannot be used as the sole means inhibiting the sodium channel current. The J wave could be the of determining patient disposition.24 genetic variant of early repolarization, or it could be caused by If it were possible to estimate residual injury currents based on J delayed depolarization associated with a myocardial disorder. and rJ waves from the ECGs of AMI patients, then J and rJ waves However, in this study, the distinguishment is still remained could be objective markers of current cardiac status. This system questionable, and this could be one of the important limitations would be useful for evaluating AMI patients after successful of our investigation. Thus, further well-designed prospective revascularization. It is known that precordial ST-segment studies are needed. depression upon admission during inferior-wall AMI predicts To exclude the possibility that MI-related scar was a prognostic higher hospital mortality rate and suggests worse long-term indicator for patient mortality,18 we compared the QRS scar score prognosis after discharge.25 Thus, rJ wave evaluation could better of the J group with that of the non-J group. QRS scar scores help predict AMI patient prognosis as compared to the use of J quantify cardiac scarring in ischemic and non-ischemic waves alone. Hence, combining J wave with rJ wave assessment cardiomyopathy patients,12,19 and their results have been positively might be a more powerful tool for predicting cardiac death. associated with mortality.13,20 In this study, no significant The cutoff value of J waves has not been established. A previous difference was found between the scar scores of the 2 groups (5.53 study suggested that J point elevation >0.2 mV increased the vs. 5.61, respectively, p=0.916). This means that the prognostic relative risk of cardiac death to 2.98.26 In our study, high- power of J waves and rJ waves was not affected by scar size. In fact, amplitude J waves in the inferior leads and/or rJ waves were the relationship between scar size and magnitude of injury possible prognostic factors for all-cause and cardiac mortality in currents is not well defined, and no definitive methods are inferior-wall AMI patients. available for quantifying injury currents. A recent study found that early repolarization before successful Study Limitations reperfusion after AMI increased the risk of VF ≤48 hours after event onset.10 Our study showed similar results-i.e., the pre-PCI J When developing any useful predictive marker, accuracy and wave was associated with post-PCI ventricular arrhythmic events simplified criteria for general clinical use should be considered. (p=0.016, HR=31.671, CI 1.915-523.852), but not with This study showed the power of J waves and rJ waves for mortality. These results imply that pre-PCI J point elevation is a predicting mortality in inferior-wall AMI patients. However, their leading cause of ventricular arrhythmia ≤48 hours after PCI. reverse-predictive value could be low, because J wave or rJ wave In previous studies, many clinical factors, such as old age, prior detection can be confounded by factors such as ST-segment MI, congestive heart failure, and stroke, were associated with poor elevation or bundle-branch block, and only trained ECG outcomes in AMI patients.21 We attempted to control and adjust interpreters can discriminate these waves accurately. Therefore, J for such known predictors during our statistical analyses. waves and rJ waves are limited as sole independent predictors of However, it is impossible to consider all confounding variables mortality after AMI. because many unknown and random factors can affect the Another limitation of this study was the size of our subject prognosis of AMI patients. In our analyses, we adjusted for age, population. The total of 302 patients might be too small to sex, hypertension, diabetes dyslipidemia, LVEF <35%, CKD, definitively establish J waves and rJ waves as predictors of number of involved vessels, STEMI/NSTEMI, and ST-segment mortality after AMI. Therefore, a larger-scale, long-term follow- changes in the precordial leads as confounding factors. None of up study is needed to clarify the prognostic power of J waves and these factors, except for LVEF, directly reflected AMI-induced rJ waves in inferior-wall AMI patients. cardiac conditions. Therefore, clinicians have used simple risk- Lastly, among 29 deceased patients, 10 died of non-cardiac scoring methods, such as the Thrombolysis in Myocardial causes ≤6 months of AMI occurrence. Although they were Infarction (TIMI) system, to discern the prognosis of AMI significantly older than patients who survived or died from cardiac

70 Arrhythmia 2015;16(2):67-77

Definition of Variables of involved vessels, STEMI/NSTEMI, and ST-segment changes in precordial leads. P values <0.05 were considered statistically Hypertension was defined as systolic blood pressure >140 significant. Analyses were performed using IBM SPSS Statistics mmHg, diastolic blood pressure >90 mmHg, and/or the use of software version 19 (IBM Corp., Armonk, NY, USA). antihypertensive medication. Diabetes was defined as either fasting blood sugar level >126 mg/dL, a 2-hour blood sugar level Results >200 mg/dL, or the use of blood glucose-reducing medications. The NCEP ATP-III definition was used to ascertain the presence Demographic features of enrolled patients of dyslipidemia.14 Transthoracic echocardiography for measuring left ventricular ejection fraction (LVEF) was performed ≤1 day The clinical and demographic features of the J group, big-J after PCI and confirmed by 2 expert cardiologists. A stroke was group, and non-J group are shown in Table 1. Among 302 defined as the rapid loss of brain function due to the disturbance analyzed patients, 26 showed post-PCI J waves in the inferior in blood supply; stroke was classified as ischemic if a brain CT or leads, 2 showed rJ waves only in leads V1-V3, and 4 had both MRI confirmed no evidence of hemorrhage. Chronic kidney inferior J and rJ waves in leads V1-V3. These 32 patients were disease (CKD) was defined as the presence of kidney damage or classified into the J group. The big-J subgroup consisted of 14 glomerular filtration rate (MDRD-estimated GFR <60 mL/ patients. The remaining 270 patients were included in the non-J min/1.73 m2) for >3 months. Heart rate was analyzed based on group. pre- and post-PCI recordings. Thirty patients had pre-PCI J waves, and 13 patients (43.3%) had high-amplitude pre-PCI J waves. Among 30 patients, 16 Study Design patients (53.3%) did not show J waves after revascularization. Newly developed post-PCI J waves were found in 18 patients. This retrospective review study obtained mortality data from the National Statistical Office in Korea. Each case was assessed as All-cause Mortality and Cardiac Death either cardiac death or non-cardiac death. The study’s primary endpoint was cardiac death ≤6 months after AMI, and the Among the total 302 patients studied, 29 (9.6%) died ≤6 secondary endpoints were all-cause mortality ≤6 months and fatal months of AMI. The causes of death were as follows: 19 due to and non-fatal ventricular arrhythmic events (including sustained cardiac causes, 2 due to severe pneumonia, 2 due to stomach and ventricular tachycardia [VT] or ventricular fibrillation [VF]) ≤48 bladder cancer, 1 due to cerebral stroke, and 5 due to unknown hours after PCI. Mortality data and QRS scar scores were causes. Of the total 29 deceased patients, 9 (28.1%) were in the J compared among groups, and the power of the rJ wave for group and 20 (7.4%) were in the non-J group. In the big-J group, 5 predicting death was investigated. patients (35.7%) died. Of all the patients studied, 19 (6.3%) died from cardiac causes-5 (15.6%) in the J group and 14 (5.2%) in the Statistical Analysis non-J group. Among the big-J group patients, 4 (28.6%) died from cardiac causes. Continuous variables are expressed as mean ± standard The J group had a significantly higher all-cause mortality than deviation. The Student t-test was used for data comparison. the non-J group (p=0.001, HR=5.376, CI 1.904-15.181, Figure Categorical variables were compared using Fisher’s exact test and 2A). However, no difference was found in cardiac deaths between the χ2 test. A survival analysis that included cardiac death and all- the 2 groups (p=0.101, Figure 2B). The big-J group had cause mortality was conducted among subjects using a Cox significantly higher rates of all-cause mortality (p=0.032, regression analysis. Statistical analyses adjusted for age, sex, HR=5.768, CI 1.165-28.561, Figure 3A) and cardiac mortality hypertension, diabetes, dyslipidemia, LVEF <35%, CKD, number (p=0.011, HR=32.712, CI 2.203-485.723, Figure 3B) than the

71 J Wave and Myocardial Infarction

Table 1. Baseline characteristics of the enrolled patients

Post-PCI Pre-PCI J non-J J J non-J J

Total (n=32) (n=270) vs. non-J (n=30) (n=272) vs. non-J Big-J Big-J Big-J Big-J All All (n=14) vs. non-J (n=13) vs. non-J

Male sex 227 25 9 202 23 10 204 0.435 0.250 0.999 0.980 (75.2%) (78.1%) (64.3%) (74.8%) (76.7%) (76.9%) (75.0%)

Age 65.5 67.9 70.1 65.2 69.5 71.8 65.1

(range) ±11.7 ±13.6 ±12.6 ±11.5 0.293 0.187 ±11.1 ±11.6 ±11.7 0.049 0.069

(38-92) (38-92) (48-92) (38-92) (48-87) (48-85) (38-92)

STEMI 178 19 8 159 13 6 165 0.558 0.549 0.079 0.180 (58.9%) (59.4%) (57.1%) (58.9%) (43.3%) (46.2%) (60.7%)

Hypertension 111 15 8 96 12 6 99 0.144 0.093 0.694 0.769 (36.8%) (46.9%) (57.1%) (35.6%) (40.0%) (46.2%) (36.4%)

Diabetes 185 18 8 167 12 5 173 0.333 0.475 0.017 0.041 (61.3%) (56.3%) (57.1%) (61.9%) (40.0%) (38.5%) (63.6%)

Dyslipidemia 109 15 8 94 12 97 7 0.126 0.084 0.690 0.345 (36.1%) (46.9%) (57.1%) (34.8%) (40.0%) (35.7%) (53.8%) Depressed 20 1 1 19 4 1 16 LVEF 0.349 0.625 0.124 0.165 (<35%) (6.6%) (3.1%) (7.1%) (7.0%) (13.3%) (7.7%) (5.9%) Ischemic stroke 20 4 2 16 4 1 16 history 0.154 0.240 0.128 0.174 (n=298) (6.7%) (12.5%) (14.3%) (6.0%) (13.3%) (7.7%) (6.0%) Chronic kidney 115 9 5 106 8 3 107 disease 0.148 0.618 0.159 0.323 (n=275) (41.8%) (31.0%) (41.7%) (43.1%) (28.6%) (27.3%) (43.3%) ST depression in anterior 31 1 0 30 2 0 29 precordial 0.142 0.211 0.752 0.454 leads (10.3%) (3.2%) (0%) (11.1%) (6.7%) (0.0%) (10.7%) Agiographic 120 13 5 107 11 4 109 finding 0.529 0.493 0.931 0.619 (>2 vessels (39.8%) (40.6%) (35.7%) (39.6%) (36.7%) (30.8%) (40.1%) diseased)

LVEF, left ventricular ejection fraction; PCI, percutaneous coronary intervention; STEMI, ST-elevation myocardial infarction.

72 Arrhythmia 2015;16(2):67-77

A B All-cause mortality Cardiac death non-J group 1.00 1.00 p=0.101 J group

0.97 non-J group 0.97

0.94 0.94 p=0.001

0.91 0.91 Cumulative survival rate J group Cumulative survival rate 0.88 0.88

0.85 0.85

0 50 100 150 200 0 50 100 150 200 Days Days

Figure 2. Survival rate of the J group compared with the non-J group. The solid and dotted lines indicate the J group and the non-J group, respectively. The J group showed significantly higher all-cause mortality than the non-J group (p=0.001; HR=5.376; CI 1.904-15.181). However, there was no difference in cardiac death rates between the two groups (p=0.101).

A B All-cause mortality Cardiac death

1.00 1.00 non-J group p=0.011 non-J group big-J group 0.97 0.97 big-J group p=0.032

0.94 0.94

0.91 0.91 Cumulative survival rate Cumulative survival rate 0.88 0.88

0.85 0.85

0 50 100 150 200 0 50 100 150 200 Days Days

Figure 3. Survival rate of the big-J group compared with the non-J group. The solid and dotted lines indicate the big-J group and the non-J group, respectively. The big-J group showed both significantly higher rates of all-cause mortality (p=0.032; HR=5.768; CI 1.165-28.561)) and cardiac mortality (p=0.011; HR=32.712; CI 2.203-485.723).

non-J group. All-cause or cardiac mortality did not differ between demonstrated no significant relationship with post-PCI patients with or without pre-PCI J waves, regardless of their ventricular tachyarrhythmia, pre-PCI J waves (p=0.016, amplitude. HR=31.671, CI 1.915-523.852) were significantly associated with post-PCI ventricular arrhythmia. Ventricular Arrhythmic Events Prognostic Power of rJ Waves in Leads V1-V3 Among the total 302 patients, 9 ventricular arrhythmic events (4 VT, 2 VT/VF, and 3 VF) occurred, including 5 fatal and 4 All-cause mortality was significantly higher in patients with non-fatal events of VF/VT ≤48 hours after PCI. Although the post-PCI rJ waves (n=6) in leads V1-V3 than in the non-J group post-PCI J wave group (p=0.314) and the big-J group (p=0.361) (p=0.047, HR=13.874, CI 1.035-186.021, Figure 4A). However,

73 J Wave and Myocardial Infarction

A B All-cause mortality Cardiac death

1.00 1.00 non-J group non-J group

0.97 0.97 p=0.051 p=0.047 0.94 0.94

rJ group 0.91 0.91

Cumulative survival rate rJ group Cumulative survival rate 0.88 0.88

0.85 0.85

0 50 100 150 200 0 50 100 150 200 Days Days

Figure 4. Survival rate of patients with the rJ wave in the right precordial leads (V1-V3) compared with the non-J group. The solid and dotted lines indicate patients in the rJ group and the non-J group, respectively. All-cause mortality was significantly increased in the patients with the rJ wave in V1-V3 compared with the non-J group (p=0.047; HR=13.874; CI 1.035-186.021), but there was weak significance in cardiac death in the rJ group versus the non-J group (p=0.051; HR=16.636; CI 0.992-279.075). cardiac deaths had only marginal significance in the post-PCI rJ increased all-cause and cardiac mortality, and that rJ wave (as a group compared with the non-J group (p=0.051, HR=16.636, CI reciprocal change of the J wave in the inferior leads) could be a 0.992-279.075, Figure 4B). All-cause or cardiac mortality did not prognostic factor of all-cause and cardiac mortality in patients differ between patients with or without pre-PCI rJ waves. with inferior-wall AMI. The pre-PCI J wave was associated with ventricular tachyarrhythmias after PCI. QRS Scar Score Because J waves can appear in ischemic conditions, researchers in previous studies hypothesized that J waves would occur in The QRS scar score of the J group was 5.53±4.03, and the patients with MI.9 Moreover, some researchers thought that the J range was 0-15. The score of the non-J group was 5.61±4.02, and point could be elevated as a result of injury currents during AMI the range was 0-18. No significant difference was seen between and pericarditis.15 Yan et al.16 reported that acute regional these 2 groups (p=0.916). The QRS scar score of the big-J group infarction resulted in heterogeneous loss of Ito-mediated epicardial was 6.64±4.57, and the range was 0-18. The QRS scar score in the action-potential domes across the ischemic border; this would big-J group also did not significantly differ from that in the non-J lead to phase 2 reentry and cause R-on-T extrasystole that could group (p=0.395). The QRS scar score distribution for each group result in VF. However, no previous studies have examined the is shown in Figure 5. The presence of pre-PCI J waves was not power of J point elevation for predicting mortality after MI. In associated with the QRS scar score (4.67±4.26 with pre-PCI J this study, the J wave and its reciprocal change (rJ wave), observed waves vs. 5.71±4.26 without pre-PCI J waves, p=0.211). In 1 day after revascularization therapy in inferior-wall AMI patients, addition, the QRS scar scores did not differ between deceased and were considered to have resulted from ischemia-induced injury living patients, regardless of the cause of death (all-cause deaths, currents. Thus, these events could be considered markers of poor 6.31±4.65; deaths from cardiac causes, 7.47±4.74; living patients, cardiac condition and increased mortality. 5.53±3.95; all-cause deaths vs. living patients, p=0.389; deaths It is unresolved whether J point elevation 1 day after PCI is in from cardiac causes vs. living patients, p=0.096). fact an Ito-mediated J wave or whether it represents delayed activation. The morphological definition of the terminal QRS Discussion abnormality following AMI is sometimes confusing.15 Antzelevitch et al.17 recommended that if the potential is delayed In this study, we found that patients in the J group had activation, heart rate acceleration or quinidine use would be 74 Arrhythmia 2015;16(2):67-77

A 6 J group 5

Frequency 2

0 0 3 6 9 12 15 18 QRS scar score

B 40 non-J group

30 Figure 5. QRS scar score distribution of the J 20 group (A), non-J group (B), and big-J group (C). Frequency 10

0 0 3 6 9 12 15 18 QRS scar score

C 6 big-J group 5

Frequency 2

0 0 3 6 9 12 15 18 QRS scar score

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