2015 Volume 79 Issue 10 Pages 2216-2223
Background: Syncope is a common occurrence. The presence of J-wave, also known as early repolarization, on electrocardiogram is often seen in the general population, but the relationship between syncope and J-wave is unclear.
Methods and Results: After excluding 67 patients with structural heart disease from 326 with syncope, we classified 259 patients according to the presence or absence of J-wave (≥1 mm) in at least 2 inferior or lateral leads. Head-up tilt test (HUT) was performed for 30 min. If no syncope or presyncope occurred, HUT was repeated after drug loading. Before tilt, 97/259 (37%) had J-wave (57 male, 47.6±22.5 years) and 162 patients had no remarkable change (89 male, 51.1±21.2 years). HUT-positive rate was higher in patients with J-wave, compared with patients without (P<0.0001). The combination of J-wave and descending/horizontal ST segment in the inferior leads was more strongly associated with positive HUT than J-wave with ascending ST segment (odds ratio, 3.23).
Conclusions: Prevalence of J-wave in the inferior or lateral leads was high in patients with syncope and was associated with HUT-induced neurally mediated reflex syncope (NMRS). Furthermore, the combination of J-wave and descending/horizontal ST segment in the inferior leads could be associated with a much higher risk of NMRS. (Circ J 2015; 79: 2216–2223)
The presence of J-wave, also known as early repolarization (ER), is a common finding on electrocardiogram (ECG) that is seen in 1–10% of the general population,1,2 especially in young people. J-wave is characterized by a positive deflection at the terminal of the QRS complex or notching/slurring at the terminal of the QRS complex on ECG. Its potential arrhythmogenicity, more recently, has been reported in clinical and experimental studies.3–5 Fatal arrhythmia, however, is not commonly seen in patients with J-wave.6
Editorial p 2110
Syncope is also a common occurrence in 1–5% of the general population.7,8 Neurally mediated reflex syncope (NMRS) is a most frequent cause of syncope. Cardiovascular event and life-threatening arrhythmia are also causes of syncope or cardiac arrest. These are important risk factors for mortality, but clinical diagnosis in some patients with syncope is difficult in the primary care setting. Fatal arrhythmia is not commonly seen in patients with syncope.
In this study we evaluated the clinical significance of syncope and J-wave. Although it has been reported that syncope is a sign of sudden cardiac death (SCD) in patients with J-wave,9 the management of syncope in patients with J-wave remains controversial.
To our knowledge, there are few studies on the prevalence of J-wave in patients with syncope. To evaluate the possibility that syncope in patients with/without J-wave is caused by NMRS, we investigated whether head-up tilt test (HUT), a useful tool for diagnosing NMRS, can provide further insights into the relationship between syncope and J-wave.
We therefore determined the prevalence of J-wave in patients with syncope in order to clarify the association between NMRS and J-wave.
Three hundred and twenty-six consecutive patients with syncope who presented to the Department of Cardiology, Showa University Hospital between January 2011 and June 2014 were enrolled in this study. The following information was collected for every patient: general data (age, gender, height, body weight, and body mass index [BMI]) medical history, comprehensive physical examination, and 12-lead ECG. Patients with findings suggestive of heart disease on 12-lead ECG were excluded from the study. The study was approved by the Ethics Committee of Showa University.
12-Lead ECGResting 12-lead ECG results were independently confirmed by each of 3 cardiologists (Y.C., Y. Minoura, Y.K.). The J-wave pattern was defined according to criteria similar to that of other reports: J-wave (≥1 mm) at the terminal of the QRS complex with/without ST-segment elevation.3,10,11 When ST-segment elevation was present, the J-wave was recognized as a notching or slurring of the terminal of the QRS complex. When ST-segment elevation was absent, the J-wave was recognized as a positive deflection at the terminal of the QRS complex (Figure 1).
Four examples of the J-wave pattern on baseline electrocardiogram. Subject A, notching J-wave with ascending ST-segment pattern. Subject B, slurring J-wave with ascending ST-segment pattern. Subject C, distinct J-wave with descending/horizontal ST-segment pattern (horizontal pattern in lead II and aVF and descending pattern in lead III). Subject D, J-wave with descending/horizontal ST-segment pattern (descending pattern in lead II, lead III, and aVF). Arrows, J-waves.
Patients with the J-wave pattern in at least 2 inferior (II, III, aVF) or lateral (I, aVL, V4–6) leads were defined as the J group. We also subdivided the patients in the J group according to the type of ST segment in the inferior and lateral leads. The definition for the ST-segment type (ascending or descending/horizontal) was borrowed from a previous report.11–13 Ascending ST-segment pattern was defined as elevation of ST (≥0.1 mV) within 100 ms after the J point. Descending/horizontal ST-segment pattern was defined as ST <0.1 mV within 100 ms after the J point.
HUTThe HUT was performed using Impedance Cardiography (Task Force Monitor®; CNSystems Medizintechnik, Graz, Austria) and 12-lead ECG (Dream Electrocardiogram HRES-1000; Fukuda Denshi, Japan). Blood pressure was monitored continuously in a non-invasive manner by measuring arterial pressure beat to beat with a finger cuff. After resting in the supine position for 15 min, the patients underwent HUT at 80° for 30 min. If no syncope or presyncope occurred over the 30-min test, a second HUT was conducted at 80° for 15 min after drug loading (adenosine triphosphate (ATP) 0.1–0.2 mg/kg or/and isoproterenol (ISP) 0.01 mg·kg–1·min–1 or/and isosorbide dinitrate (ISDN) 5 mg).14,15 If no syncope or presyncope was observed after this drug loading, the patients were defined as HUT negative (Figure 2).
Protocol for the head-up tilt test (HUT). Passive HUT was performed (80°, 30 min) after the patient rested for 15 min in a supine position. If no syncope or presyncope occurred, HUT (80°, 15 min) was repeated after drug loading (adenosine triphosphate [ATP], 0.1–0.2 mg/kg or/and isoproterenol [ISP], 0.01 mg·kg–1·min–1 or/and isosorbide dinitrate [ISDN], 5 mg). If no syncope or presyncope was observed even after loading with these drugs, the patient was defined as HUT negative.
Variables are given as mean±SD, median, and 25th–75th percentile. Data were analyzed using JMP ver.11 (SAS Institute) Fisher’s exact test was used for categorical variables and t-test was used for continuous variables. The model was developed to predict the HUT-positive rate using multivariate logistic regression analysis. P<0.05 was defined as statistically significant.
Of the 326 patients with syncope, 67 were excluded from this study because of suspicion of heart disease on resting ECG (right bundle branch block, n=18; ischemic heart disease, n=10; atrial fibrillation, n=7; atrial flutter, n=3; frequent premature atrial/ventricular contraction, n=13; left ventricular hypertrophy, n=3; hypertrophic cardiomyopathy, n=1; atrial or ventricular pacing after implantation of pacemaker, n=4; left bundle branch block, n=1; sick sinus syndrome, n=1; Brugada syndrome (BrS), n=3; and conduction disturbance, n=3).
Of 259 patients, 97 had the J-wave pattern (J group; 57 male, 47.6±22.5 years old) in at least 2 leads of inferior (II, III, aVF) or lateral (I, V4–6) leads on resting ECG. One hundred and sixty-two patients had no remarkable change, and thus were suspected to have idiopathic ventricular fibrillation (IVF) (non-J group; 89 male, 50.1±21.2 years; Figure 3A). Table 1 lists the patient characteristics of the J group and non-J group. We found no differences between the J group and non-J group in age, gender, BMI, number of syncope episodes, duration from the last syncope episode, history of typical vasovagal reflex syncope, presence of prodromal symptoms, and presence of injuries concomitant with syncope. The prodromal symptoms of 190/205 patients (92.7%) were similar to the symptoms just before syncope in the clinical setting.
(A) Flowchart of patient classification based on electrocardiogram findings. (B,C) Positive head-up tilt test (HUT) in the J group and non-J group (B) without drug loading, and (C) without drug loading and also including drug loading. Inferior, inferior (II, III, aVF) leads; infero-lateral, inferior and lateral leads; J group, patients with the J-wave pattern; lateral, lateral (I, aVL, V4–6) leads; non-J group, patients without the J-wave pattern.
| All patients (n=259) | J group (n=97) | Non-J group (n=162) | P-value | |
|---|---|---|---|---|
| Age (years) | 49.2±21.7, 51 (29–69) |
47.6±22.5, 49 (26–67) |
50.1±21.2, 51 (30.75–69.25) |
0.37 |
| Male | 146 (56.4) | 57 (58.8) | 89 (54.9) | 0.55 |
| BMI (kg/m2) | 22.1±3.3, 21.8 (19.6–23.9) |
22.5±3.0, 22.3 (20.5–24.5) |
21.8±3.5, 21.6 (19.3–23.7) |
0.12 |
| Syncope episode in the last 6 months | 3.7±26.1, 1 (1–2) |
1.4±1.5, 1 (1–1) |
5.1±32.6, 1 (1–2) |
0.17 |
| Duration from last syncope episode (days) | 91.5±125.7, 54.5 (19.3–103.8) |
79.4±110.0, 46.0 (15.0–88.0) |
97.8±133.5, 56.5 (21.3–107.0) |
0.28 |
| History of typical vasovagal reflex syncope | 147 (56.8) | 60 (61.9) | 87 (53.7) | 0.20 |
| Prodromal symptoms | 205 (79.2) | 82 (84.5) | 123 (75.9) | 0.12 |
| Injuries concomitant with syncope | 95 (36.7) | 42 (43.3) | 53 (32.7) | 0.09 |
| HR (beats/min) | 66.8±11.7, 66.0 (58.3–74.0) |
65.9±10.8, 66.0 (59.0–73.0) |
67.3±12.2, 66.0 (58.0–75.0) |
0.37, 0.33 |
| PQ interval (ms) | 169.8±27.7, 170.0 (152.3–190.0) |
164.4±26.0, 160.0 (148.0–181.0) |
173.0±28.3, 176.0 (160.0–196.0) |
0.016 |
| QRS duration (ms) | 101.7±78.0, 95.0 (80.0–110.0) |
93.3±20.0, 93.0 (80.0–110.0) |
106.8±97.3, 97.0 (80.0–117.0) |
0.11 |
| QTc duration (ms) | 424.9±44.7, 420.0 (99.7–450.5) |
424.2±41.7, 421.3 (400.1–447.2) |
425.3±46.5, 422.0 (399.0–451.0) |
0.86 |
| J-wave elevation (mm) | 1.4±0.6, 1.0 (1.0–1.5) |
Data given as mean±SD, median (IQR) or n (%). BMI, body mass index; ECG, electrocardiogram; HR, heart rate; HUT, head-up tilt test.
Table 1 also lists the ECG parameters in the 2 groups. The PR interval of the non-J group was longer than that of the J group. There were no differences in QRS complex or QTc duration between the 2 groups. The average J point elevation in the J group was 1.4±0.6 mm (Table 1).
Localization of J-Wave Pattern on 12-Lead ECGFigure 3A shows the location of the J-wave pattern in the 2 groups. Of 97 patients, 55 patients had J-wave pattern in the inferior leads (lead II, n=51; lead III, n=51; aVF, n=55), 8 had J-wave pattern in the lateral leads (V4, n=4; V5, n=8; V6, n=8), and 34 had the J-wave pattern in both the inferior and lateral leads (lead II, n=28; lead III, n=33; aVF, n=1; lead I, n=1; aVL, n=15; V4, n=34; V5, n=34; V6, n=34). The J-wave pattern was identified in the inferior leads more frequently than in the lateral leads (J-wave pattern in inferior leads, n=89 vs. J-wave pattern in the lateral leads, n=8; P<0.001).
HUTJ-Wave Pattern and HUT-Positive Rate Figures 3B,C shows the HUT-positive rate according to presence of J-wave. Positive HUT in the passive phase was observed in 18 patients (18.6%) in the J group and in 13 patients (8.0%) in the non-J group (Figure 3B). Positive HUT on drug loading was observed in 41 patients (42.3%) in the J group (ATP, n=13; ISP, n=14; ISDN, n=28) and in 37 patients (22.8%) in the non-J group (ATP, n=12; ISP, n=8; ISDN, n=26). Altogether, positive HUT with/without drug loading was observed in 59 patients (60.8%) in the J group and in 50 patients (30.9%) in the non-J group (P<0.001; Figure 3C). The response was vasodepressor (VD) type in 21 (21.6%), cardioinhibitory type in 3 (3.1%) and mixed type in 35 (36.1%) in the J group, and VD type in 23 (14.2%), cardioinhibitory type in 6 (3.7) and mixed type in 21 (13.0%) in the non-J group.
ST-Segment Type and HUT-Positive Rate The patients in the J group were divided into 2 groups according to ST-segment pattern after the J-wave: ascending pattern (ascending ST-segment pattern; 66/259 patients, 25.5%) and descending/horizontal pattern (descending or horizontal ST-segment pattern; 31/259 patients, 12.0%). Figure 4A shows the location of the ST-segment pattern in both of these groups. Of the 97 patients in the J group, ascending ST-segment pattern was observed in 66 patients (31 in inferior leads, 6 in lateral leads, and 29 in infero-lateral leads: lead II, n=57; lead III, n=55; aVF, n=57), and a descending or horizontal ST-segment pattern was observed in 31 patients (V4, n=3; V5, n=6; V6, n=7).
(A) Flowchart of patient classification according to ST-segment pattern. One patient with the descending/horizontal pattern died suddenly of unexplained causes during follow-up. (B,C) Relationship between J-wave/ST-segment pattern and positive head-up tilt test (HUT) according to (B) ST-segment pattern, and (C) pattern in the inferior leads (inferior or infero-lateral leads). Ascending, J-wave and ascending ST-segment pattern; descending/horizontal, J-wave and descending or horizontal ST-segment pattern; J group, patients with the J-wave pattern; inferior, inferior (II, III, aVF) leads; infero-lateral, inferior and lateral leads; lateral, lateral (I, aVL, V4–6) leads; non-J group, patients without the J-wave pattern.
Both ST-segment patterns were frequently seen in the inferior (inferior or infero-lateral) leads compared with the lateral leads (ascending pattern, 60 vs. 6, P<0.0001; descending/horizontal pattern, 29 vs. 2, P<0.0001; Figure 4A).
Of the 66 patients with J-wave with the ascending ST-segment pattern, 36/66 (54.5%) had positive HUT. Of the patients with J-wave with the descending/horizontal pattern, 23/31 (74.2%) had positive HUT. Patients with J-wave with the descending/horizontal pattern were likely to have positive HUT compared with patients with the ascending pattern (P=0.08; Figure 4B).
Among the patients with a J-wave pattern in the inferior leads (inferior or infero-lateral leads), those who had a descending/horizontal pattern had positive HUT more frequently than those with an ascending pattern (P=0.03; Figure 4C). The presence of a combination of J-wave and descending/horizontal ST segment was associated with an almost 4-fold higher probability (odds ratio [OR], 3.78; 95% confidence interval [CI]: 2.2–6.62). In the J group, descending/horizontal ST segment in the inferior leads was an indicator of high risk of positive HUT compared with the ascending pattern (OR, 3.23; 95% CI: 1.19–9.72; Table 2). One patient with the descending/horizontal pattern had unexplained sudden death during follow-up.
| OR | 95% CI | |
|---|---|---|
| J group vs. non-J group in inferior or lateral leads | 3.78 | 2.20–6.62 |
| BMI | 0.92 | 0.83–1.00 |
| Age | 0.99 | 0.88–1.00 |
| Male sex | 0.78 | 0.45–1.34 |
| Descending/horizontal vs. ascending in inferior or infero-lateral leads | 3.23 | 1.19–9.72 |
| BMI | 0.95 | 0.80–1.11 |
| Age | 0.99 | 0.97–1.01 |
| Male sex | 1.23 | 0.47–3.27 |
Ascending, ascending ST-segment pattern after J-wave; CI, confidence interval; descending/horizontal, descending or horizontal ST-segment pattern after J-wave; J group, patients with the J-wave pattern; non-J group, patients without the J-wave pattern; NMRS, neurally mediated reflex syncope; OR, odds ratio. Other abbreviations as in Table 1.
Table 3 lists patient characteristics according to presence of ascending or descending/horizontal pattern. We found no differences between the patients with ascending pattern and descending/horizontal pattern in age, gender, BMI, number of syncope episodes, duration from the last syncope episode, history of typical vasovagal reflex syncope, presence of prodromal symptoms, and presence of injuries concomitant with syncope.
| J-wave group (n=97) |
Ascending (n=66) |
Descending/horizontal (n=31) |
P-value | |
|---|---|---|---|---|
| Age (years) | 47.6±22.5, 49 (26–67) |
45.0±22.2, 47.5 (22.8–64.0) |
53.1±22.5, 60 (28.0–72.0) |
0.10 |
| Male | 57 (58.8) | 43 (65.2) | 14 (45.2) | 0.08 |
| BMI (kg/m2) | 22.5±3.0, 22.3 (20.5–24.5) |
22.6±3.2, 22.6 (20.4–24.6) |
22.3±2.8, 21.3 (20.6–24.3) |
0.57 |
| Syncope episodes in the last 6 months | 1.4±1.5, 1 (1–1) |
1.4±1.8, 1 (1–1) |
1.4±0.9, 1 (1–2) |
0.91 |
| Duration from last syncope episode (days) | 79.4±110.0, 46.0 (15.0–88.0) |
69.4±85.0, 43.5 (15.0–87.5) |
74.1±98.8, 45.0 (15.3–81.8) |
0.82 |
| Typical vasovagal history | 60 (61.9) | 41 (62.1) | 19 (61.3) | 1 |
| Prodromal symptoms | 82 (84.5) | 56 (84.8) | 26 (83.9) | 1 |
| Injuries concomitant with syncope | 42 (43.3) | 24 (36.3) | 18 (58.1) | 0.051 |
| HR (beats/min) | 65.9±10.8, 66.0 (59.0–73.0) |
66.5±10.9, 65.5 (59.0–73.25) |
64.8±10.6, 66.0 (57.0–73.0) |
0.494 |
| PQ interval (ms) | 164.4±26.0, 160.0 (148.0–181.0) |
163.7±26.6, 160.0 (145.5–182.3) |
165.9±24.7, 160.0 (154.0–180.0) |
0.7 |
| QRS duration (ms) | 93.3±20.0, 93.0 (80.0–110.0) |
93.2±18.3, 93.0 (80.0–102.3) |
93.5±23.7, 93.0 (80.0–120.0) |
0.96 |
| QTc duration (ms) | 424.2±41.7, 421.3 (400.1–447.2) |
422.0±39.2, 423.8 (398.0–447.2) |
428.9±47.0, 421.0 (400.3–450.2) |
0.455 |
| J-wave elevation (mm) | 1.35±0.57, 1.0 (1.0–1.5) |
1.37±0.64, 1.0 (1–2) |
1.18±0.48, 1.0 (1–1.5) |
0.11 |
Data given as mean±SD, median (IQR) or n (%). Abbreviations as in Table 1.
Table 3 also lists the ECG parameters in patients with 2 ST-segment patterns. There were no differences in QRS complex, PR interval or QTc duration between the 2 patterns (Table 3).
J-Wave Amplitude and HUT-Positive Rate When the J group patients were divided according to J-wave amplitude (≥2 mm), there was no difference in HUT-positive rate between patients with J-wave amplitude ≥2 mV and those with J-wave amplitude <2 mm (50.0% vs. 64.4%).
In this study, the prevalence of J-wave in the inferior or lateral lead was high in patients with syncope. HUT-positive rate was significantly higher in patients with J-wave pattern in the inferior or lateral leads than in patients without the J-wave pattern in this study. The J-wave pattern was recognized more often in the inferior leads than in the lateral leads. The combination of J-wave and a descending/horizontal ST segment in the inferior leads was more strongly associated with positive HUT than a combination of J-wave and ascending ST segment.
This suggests that J-wave pattern in the inferior or lateral leads is associated with NMRS. Furthermore, a combination of J-wave and descending/horizontal ST segment in the inferior leads is associated with a much higher risk of NMRS.
The presence of J-wave, also known as ER, used to be commonly seen as a benign sign on ECG. More recently, however, the presence of the “J-wave” has been linked with SCD. Its potential arrhythmogenicity has been reported in clinical and experimental studies. Tikkanen et al found that J-point elevation >0.2 mV in the inferior leads was associated with a strongly elevated risk of cardiac death.10 More recent studies on the J-wave pattern have focused on its association with idiopathic VF.3,4 The relationship between J-wave and arrhythmogenicity now seems indisputable.
The issue now will be to discriminate between the small minority of patients with elevated risk of arrhythmogenicity and the much larger group of patients with benign J-wave pattern.16
Syncope is also a common occurrence. The prevalence of syncope was reported at 1–2% in the general population. Syncope, however, mostly is caused by non-arrhythmic events. NMRS is the most frequent cause of syncope. Evaluation of prognosis in patients with syncope is not easy in the primary care setting. Some case reports showed that syncope is a sign of ventricular fibrillation in patients with J-wave,9 but the relationship between syncope and J-wave is unclear.
Autonomic nervous system activity is known to modulate arrhythmia risk. Mizumaki et al found that J-wave elevation at night-time was more strongly increased in IVF patients than in controls.17 In their analysis of heart rate variability (HRV) using ambulatory electrocardiography they found a correlation between J-wave amplitude and high frequency (HF).
Based on findings from an ER experimental model, Koncz et al suggested that vagal nervous system activity plays a potential role in arrhythmogenesis via the action of potential notch-related increased dispersion of repolarization and phase 2 re-entry.5 They suggested that vagal activity contributes to the arrhythmogenicity in ER and J-wave syndrome patients.
Other investigators have studied autonomic function during HUT in NMRS patients. An HRV analysis by Kouakam et al indicated that the vagal response was already increased from immediately after tilt in NMRS patients.18 An analysis of the epinephrine blood concentration during HUT by Kikushima et al identified the epinephrine surge leading to vagal nerve hyperactivity as a factor of NMRS.19 In the present study, the prodromal symptoms during HUT in patients with J-wave were similar to that of syncope in the clinical setting.
These reports support an association between J-wave and high vagal nervous system activity leading to the dysfunction of autonomic regulation during HUT.18,19
Furthermore, the manifestation of BrS is caused by the autonomic nervous system modulations, particularly with increased vagal tone.20–22 Early repolarization syndrome (ERS) and BrS share a number of clinical features in the onset of VF. ST-segment elevation in patients with BrS is accentuated by bradycardia at night-time with hypervagal tone. J-wave was also augmented during bradycardia and associated with an increase in vagal activity. The vagal nervous system activity could be related to the arrhythmogenicity of J-wave syndrome and BrS.
Early studies clarified the morphology and amplitude of the J-wave in order to establish risk stratification for patients with ER and J-wave syndrome. More recently, however, the type of ST segment (ascending or descending/horizontal) after the J-point has been identified as a factor of malignant ERS. Rosso et al found that a history of IVF was more frequent in patients with the combination of J-wave and descending/horizontal ST segment than in age- and gender-matched controls.11
Rollin et al produced similar results to that of Rosso et al.11,12 Specifically, they found that a combination of J-wave and descending/horizontal ST segment helps to stratify risk for patients with the J-wave pattern.12
In the present study, the combination of J-wave and descending/horizontal ST segment in inferior leads was more strongly associated with NMRS induced by HUT, but we were not able to determine an association between arrhythmogenicity and HUT-induced NMRS in patients with J-wave. Further studies are needed to explore these associations. We can, however, speculate on the pathophysiology involved in the association of NMRS and the combination of J-wave and descending/horizontal ST segment in the inferior leads. J-wave has been causally linked to augmented transient outward potassium current (Ito) in experimental models. The regional difference in Ito, that is, the far greater abundance of Ito in the inferior regions compared with the other regions,23 supports this causal link. The greater prevalence of J-wave patterns in the inferior leads in the present study was consistent with these reports. Ghosh et al showed that J-wave is associated with short activation-recovery intervals, leading to the dispersion of repolarization in the inferior and lateral leads.24 The mechanistic link between NMRS and the descending/horizontal ST segment is not fully understood, but a pathological condition such as hypervagal tone may underlie on onset of NMRS and arrhythmogenicity in patients with J-wave.
In this study, descending/horizontal ST segment after J-wave very often appeared in the inferior leads, whereas the ascending ST segment appeared in the inferior and infero-lateral leads at approximately equal frequency. The ascending type ST segment in the inferior leads after J-wave is unlikely to produce a positive HUT. Bartczak and Lelonek reported that the elevation of the J point was associated with a high prevalence of positive HUT in middle-aged subjects.25 In their study, the presence of J-wave and the type of ST segment were not noted, hence the majority in their study had J-wave in the lateral leads.
J-wave is also encountered in other conditions such as acute coronary disease myocardial infarction and vasospastic angina.
Physicians must consider all of these many factors in order to identify malignant J-wave syndrome on clinical assessment.
In the present study we used several drugs to induce NMRS (drug-loading HUT). It was important to use drug loading to induce HUT response because HUT cannot be relied upon to unmask NMRS in all cases. The International Study on Syncope of Uncertain Etiology did not find a high rate of HUT-positive response.26
In this study, we investigated the pathology underlying HUT-induced NMRS in patients with J-wave and descending/horizontal ST segment, but further studies on the dysfunction of autonomic regulation and J-wave pattern are needed.
In patients with syncope, the prevalence of J-wave in the inferior or lateral leads was high and was associated with HUT-induced NMRS. Furthermore, the combination of J-wave and descending/horizontal ST segment in the inferior leads could be associated with a much higher risk of NMRS.
