Prognostic Significance of ST-Segment Elevation in Leads V_1–2 in Patients With Severe Aortic Stenosis

Abstract

Background: ST-segment elevation (STE) in leads V_1–2 is often observed in patients with severe aortic stenosis (AS), but its significance remains unknown.

Methods and Results: We retrospectively evaluated baseline ECGs and 5-year clinical outcomes in 211 consecutive patients with severe AS, defined as peak aortic jet velocity (Aortic V_max) >4.0 m/s, or mean aortic pressure gradient >40 mmHg, or aortic valve area (AVA) <1.0 cm². The primary outcome measure was a composite of death or surgical aortic valve replacement (AVR). Patients with STE in leads V_1–2 (≥0.15 mV) had greater Aortic V_max and smaller AVA than patients without. With a median follow-up of 4.9 years, the cumulative 5-year incidence of death or AVR was significantly higher in patients with STE in leads V_1–2 than in patients without (91.4% vs. 77.1%; P=0.003). After adjusting for confounders, STE in leads V_1–2 was independently associated with higher risk for death or AVR (hazard ratio, 1.53; 95% confidence interval, 1.06–2.22; P=0.02). In 64 asymptomatic patients without any indication for AVR at initial diagnosis of severe AS, the cumulative incidence of AVR was significantly higher in patients with STE in leads V_1–2 than in patients without (57.6% vs. 30.5%; P<0.001).

Conclusions: STE in leads V_1–2 independently predicted poorer prognosis and more frequent need for AVR in patients with severe AS.

Aortic stenosis (AS) is a slowly progressive degenerative aortic valve disease associated with narrowing of the aortic valve orifice. Currently, echocardiographic indices of AS severity, such as peak aortic jet velocity (Aortic V_max), mean aortic pressure gradient (PG), or aortic valve area (AVA), are regarded as the most important factors to predict the long-term outcomes of patients with AS.¹ Left ventricular (LV) pressure overload because of AS is compensated by the hypertrophy of the LV myocardium. A number of studies have demonstrated that LV hypertrophy (LVH) and LV strain on ECG are independently associated with poor outcomes in patients with AS.^2–6 It is well recognized that ST-segment elevation (STE) in the precordial leads is often seen in patients with LVH.^7,8 However, the prevalence and prognostic value of STE in the precordial leads have yet to be investigated in patients with AS. In addition, previous studies assessing the prognostic significance of ECG LVH or LV strain in AS included only patients with mild or moderate AS.^3,4,9,10 The present study examined the prevalence and clinical features of STE in leads V_1–2, and the prognostic impact on long-term clinical outcomes in patients with severe AS from a single center.

Methods

Study Population

We retrospectively evaluated 272 consecutive patients who were diagnosed as having severe AS by transthoracic echocardiography at Kyoto University Hospital from January 2003 to December 2011. We searched the hospital database of transthoracic echocardiography, and selected consecutive patients who met the definitions of severe AS (Aortic V_max >4.0 m/s, mean aortic PG >40 mmHg, or AVA <1.0 cm²).¹ After excluding 37 patients who had bundle branch blocks, 22 patients with previous myocardial infarction, and 2 patients whose ECG was not available, the study population for the current analysis consisted of 211 patients with severe AS (Figure 1). The institutional review board approved this study. Informed consent from each patient was waived because we used routinely obtained clinical information, and no patient refused to participate in the study when contacted for follow-up.

Figure 1.

Study flow chart of patients with severe aortic stenosis.

Electrocardiography

We evaluated the index 12-lead ECG that was recorded when patients were initially diagnosed as having severe AS during this study period. We focused on the presence or absence of STE in leads V_1–2, LV strain, and LVH. Two independent investigators retrospectively interpreted all ECGs in a blinded fashion to the clinical and echocardiographic data. STE in leads V_1–2 was defined according to a previous study evaluating normal ECG.¹¹ In that study, the prevalence of STE >0.1 mV in one or more leads through V_1–4 was 93% in men who were 17–24 years old, and its prevalence declined gradually with increasing age, reaching less than 20% in men who were 76 years of age or older. In contrast, less than 20% of women had STE >0.1 mV, and its prevalence was not affected by age.¹¹ Therefore, in the present study, STE in leads V_1–2 was considered to be present when the J-point deviation was ≥0.15 mV in both V₁ and V₂, because our study population consisted mostly of elderly patients. The inter- and intra-observer variability for the diagnosis of STE in leads V_1–2 in this study was 0.66 and 0.78, respectively.¹² LV strain was defined as ST-segment depression and T-wave inversion in leads V_4–6.¹³ LVH in the current analysis was defined as Sokolow-Lyon voltage (RV_5/6+SV₁) ≥35 mm on the basis of prior studies (Figure 2).^3,4

Figure 2.

Representative ECGs of ST-T abnormalities with and without ST-segment elevation in leads V_1–2. (A) An 81-year-old man with ST-segment elevation in leads V_1–2 and LVH. The patient had surgical AVR shortly after initial diagnosis because of heart failure, and (B) ST-segment elevation in leads V_1–2 and LVH resolved 8 months after surgical AVR. (C) A 66-year-old woman with LVH and LV strain, but without ST-segment elevation in leads V_1–2. She had asymptomatic severe AS at initial diagnosis and no subsequent surgical AVR or symptomatic worsening for 8 years. AVR, aortic valve replacement; LVH, left ventricular hypertrophy.

Echocardiography

All patients underwent comprehensive 2D and Doppler echocardiographic evaluation by in-house physicians or ultrasonographers and the echocardiographic data were transferred to the hospital databases. Aortic V_max and mean aortic PG were obtained with the use of the simplified Bernoulli equation. AVA was calculated with the use of the standard continuity equation, and was indexed to body surface area.¹⁴ LV end-diastolic diameter (LVDd), LV end-systolic diameter (LVDs), interventricular septum thickness (IVST) and posterior wall thickness (PWT) were measured on 2D images following the guidelines.¹⁴ LV mass was calculated using the formula: LVM=0.8×{1.04 [(LVDd+IVST+PWT)³–(LVDd)³]}+0.6,¹⁵ and was indexed to body surface area.

Clinical Data and Follow-up

Collection of baseline and follow-up clinical information was conducted through review of the hospital charts, and additional follow-up information was collected through contact with patients, relatives, and referring physicians by mail with questions regarding symptoms and subsequent hospitalizations. We evaluated the patients’ symptomatic status related to AS, and the reasons why surgical aortic valve replacement (AVR) was not initially planned. The follow-up was commenced on the day when the index echocardiography was performed. The primary outcome measure in this analysis was a composite of death or surgical AVR. We also assessed sudden death, hospitalization for heart failure, emerging symptoms related to severe AS, as well as the individual components of the primary outcome measure (death or surgical AVR). The effect of STE in leads V_1–2 on the clinical outcome was also evaluated in conservatively managed patients who were asymptomatic without having any other indications for surgical AVR (LV ejection fraction (LVEF) ≤50%, and/or Aortic V_max ≥5 m/s) at initial diagnosis to assess the future risk during watchful waiting.

Statistical Analysis

Categorical variables are presented as numbers and percentages, and were compared with the chi-square test when appropriate; otherwise, we used the Fisher’s exact test. Continuous variables are expressed as the mean and SD or median and interquartile range (IQR). Based on their distributions, continuous variables were compared using Student’s t-test or the Wilcoxon rank-sum test. A multivariate logistic regression model was used to identify clinical factors associated with STE in leads V_1–2. We used the Kaplan-Meier method to estimate the cumulative incidence and assessed the differences with the log-rank test. The effect of STE in leads V_1–2 on the primary outcome measure was expressed as a hazard ratio (HR) with 95% confidence interval (CI) by a multivariable Cox proportional hazard model adjusting for the baseline differences between patients with and without STE in leads V_1–2. We incorporated 9 clinically relevant factors indicated in Table 1 (age ≥75 years, male, hypertension, history of smoking, atrial fibrillation (AF), an increase in LVM index, AVA <0.6 cm², LVH and LV strain) as the independent variables in the multivariable model. We did not include the variable of symptomatic status in the Cox proportional hazard model because symptoms related to severe AS directly lead to surgical AVR according to the guidelines.¹⁶ We dichotomized the continuous variables such as age or AVA by clinically relevant reference values. All statistical analyses were conducted with the use of JMP 10.0 (SAS Institute Inc, Cary, NC, USA). All reported P values were 2 tailed, and P<0.05 was considered statistically significant.

Table 1. Baseline Characteristics of Patients With and Without ST-Segment Elevation in Leads V_1–2

Variable	ST-segment elevation in leads V1–2		P value
	Yes (n=97)	No (n=114)
Age (years)	73.1±8.9	74.1±10.2	0.46
≥75 years*	42 (43%)	65 (57%)	0.047
Male	50 (52%)	40 (35%)	0.02
BMI†	22.6±4.3	22.7±4.0	0.92
<25.0	71 (74%)	78 (71%)	0.63
BSA	1.52±0.20	1.49±0.18	0.18
Hypertension*	80 (82%)	76 (67%)	0.009
Dyslipidemia	34 (35%)	52 (47%)	0.12
On statin therapy	24 (25%)	42 (37%)	0.06
Diabetes mellitus	21 (22%)	33 (29%)	0.22
On insulin therapy	9 (9%)	7 (6%)	0.39
History of smoking*	41 (42%)	30 (26%)	0.01
Previous PCI	8 (8%)	13 (11%)	0.45
Previous CABG	1 (1%)	4 (4%)	0.38
Previous heart failure	10 (10%)	19 (17%)	0.18
Previous stroke (symptomatic)	14 (14%)	16 (14%)	0.93
Aortic/peripheral vascular disease	14 (14%)	17 (15%)	0.92
Creatinine level >2 mg/dl	19/94 (20%)	16/113 (14%)	0.25
Hemodialysis	15 (15%)	12 (11%)	0.28
Atrial fibrillation*	17 (18%)	37 (32%)	0.01
Malignancy	17 (18%)	22 (19%)	0.74
Chronic lung disease	26 (27%)	35 (31%)	0.53
Coronary artery disease	27 (29%)	29 (25%)	0.69
Left main trunk	2/83 (2%)	4/81 (5%)	0.44
Left anterior descending artery	14/83 (17%)	12/81 (15%)	0.72
Left circumflex artery	11/83 (13%)	8/81 (10%)	0.50
Right coronary artery	9/83 (11%)	13/81 (16%)	0.33
Anemia‡	50/93 (54%)	70/113 (62%)	0.24
Symptoms related to AS	63 (65%)	55 (48%)	0.01
Chest pain	15 (15%)	25 (22%)	0.23
Syncope	11 (11%)	3 (3%)	0.01
Heart failure	49 (51%)	35 (31%)	0.003
NYHA class 2	35	20
NYHA class 3 or 4	14	15
BNP, median (IQR) (pg/ml)	355 (111–837)	114 (43–294)	0.02
Etiology of aortic stenosis
Degenerative	84 (87%)	90 (79%)	0.03
Congenital	10 (10%)	10 (9%)
Rheumatic	3 (3%)	14 (12%)
ECG variables
Sinus rhythm	93 (96%)	91 (80%)	<0.001
Atrial fibrillation/flutter	4 (4%)	23 (20%)
LV strain*	55 (57%)	28 (25%)	<0.001
LVH*	85 (88%)	50 (44%)	<0.001
Echocardiographic variables
LV end-diastolic diameter (mm)	46.4±6.7	45.0±7.1	0.14
LV end-systolic diameter (mm)	30.0±7.0	28.0±8.3	0.07
LVEF (%)	64.2±12.5	67.2±14.1	0.1
LVEF <50	12 (12%)	13 (11%)	0.83
IVST in diastole (mm)	13.2±2.8	11.1±1.7	<0.001
PWT in diastole (mm)	13.1±1.9	11.0±1.6	<0.001
LV mass index (g/m2)	159±4	122±4	<0.001
Increase in LV mass index§,*	81 (84%)	75 (66%)	0.004
Peak aortic jet velocity (m/s)	4.7±0.8	4.1±0.7	<0.001
Maximum aortic pressure gradient (mmHg)	91±30	69±25	<0.001
Mean aortic pressure gradient (mmHg)	53±19	39±16	<0.001
AVA (equation of continuity) (cm2)	0.73±0.19	0.78±0.14	0.04
AVA <0.6 cm2*	23 (24%)	11 (10%)	0.007
AVA index (cm2/m2)	0.48±0.13	0.52±0.11	0.01
Moderate to severe AR	15 (15%)	11 (10%)	0.2
Moderate to severe MS	1 (1%)	6 (5%)	0.13
Moderate to severe MR	14 (14%)	12 (11%)	0.39
Moderate to severe TR	7 (7%)	19 (17%)	0.04
TR pressure gradient ≥40 mmHg	8 (13%)	17 (20%)	0.3

*Potential independent variables selected for Cox proportional hazard models. ^†Body mass index was calculated as weight in kilograms divided by height in meters squared. ^‡Defined as a hemoglobin level <12 g/dl in women and <13 g/dl in men. ^§Defined as LV mass index >95 g/m² in women and >115 g/m² in men. AR, aortic regurgitation; AS, aortic stenosis; AVA, aortic valve area; BNP, B-type natriuretic peptide; BSA, body surface area; CABG, coronary artery bypass grafting; Hb, hemoglobin; IVST, interventricular septum thickness; LV, left ventricular; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; MR, mitral regurgitation; MS, mitral stenosis; PCI, percutaneous coronary intervention; PWT, posterior wall thickness; TR, tricuspid regurgitation.

Results

Baseline Characteristics

Among 211 patients with severe AS, STE in leads V_1–2 was present in 97 patients (46%). LV strain pattern (39%) and LVH (64%) were also frequently seen. Baseline characteristics were significantly different in several aspects between the 2 groups of patients with and without STE in leads V_1–2 (Table 1). Patients with STE in leads V_1–2 more often had hypertension, but less often had AF. Coronary angiography or coronary computer tomographic angiography was performed in 164 (78%) patients, and the prevalence of coronary artery disease was not different between the 2 groups.

Association of Baseline STE in Leads V_1–2 With Baseline Characteristics

Patients with STE in leads V_1–2 had significantly greater Aortic V_max and mean aortic PG than patients without STE in leads V_1–2 (Figure S1A). AVA was significantly smaller in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (Figure S1B). Patients with STE in leads V_1–2 had increased LVM index compared with patients without STE in leads V_1–2, but there were no significant differences in LVEF, LVDd, and LVDs between the 2 groups (Table 1). Independent clinical factors associated with of STE in leads V_1–2 included age, male, absence of AF, symptoms related to AS, an increase in LVM index, and AVA <0.6 cm² (Table 2).

Table 2. Predictors of ST-Segment Elevation in Leads V_1–2 in Univariate and Multivariable Analyses

Variable	Univariate analysis				Multivariable analysis
	STE in leads V1–2		OR	P value	OR	95% CI	P value
	Yes (n=97)	No (n=114)
Age ≥75 years	42 (43%)	65 (57%)	0.58	0.047	0.51	0.27–0.96	0.04
Male	50 (52%)	40 (35%)	2.13	0.007	2.50	1.20–5.36	0.01
Hypertension	80 (82%)	76 (67%)	2.35	0.008	1.90	0.89–4.14	0.10
History of smoking	41 (42%)	30 (26%)	2.05	0.01	1.46	0.69–3.11	0.32
Atrial fibrillation	17 (18%)	37 (32%)	0.44	0.01	0.49	0.23–0.99	0.049
Symptoms related to AS	63 (65%)	55 (48%)	1.99	0.01	2.04	1.05–4.02	0.03
Increase in LV mass index*	81 (84%)	75 (66%)	2.63	<0.001	2.79	1.29–6.31	0.009
AVA <0.6 cm2	23 (24%)	11 (10%)	2.83	0.007	2.63	1.10–6.56	0.03

*Defined as LV mass index >95 g/m² in women and >115 g/m² in men. CI, confidence interval; OR, odds ratio; STE, ST-segment elevation. Other abbreviations as in Table 1.

Clinical Effect of STE in Leads V_1–2

At baseline, patients with STE in leads V_1–2 more often had symptoms related to AS such as chest pain, syncope and heart failure as compared with patients without STE in leads V_1–2 (65% vs. 48%, P=0.01) (Table 1). Surgical AVR was performed in 105 patients based on their baseline clinical and echocardiographic findings, and 106 patients were managed conservatively. Most of the patients underwent surgical AVR with established indications according to contemporary guidelines,¹⁷ but 9 asymptomatic patients with severe AS were referred to surgical AVR without any formal indications, and surgical AVR was performed in 2 asymptomatic patients before non-cardiac surgery. Surgical AVR was more often performed in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (58% vs. 43%, P=0.03).

The median duration of follow-up was 4.9 (IQR: 3.2–8.5) years. The cumulative 5-year incidence of death or surgical AVR was significantly higher in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (91.4% vs. 77.1%, P=0.003) (Figure 3, Table 3A). The cumulative 5-year mortality was not significantly different between the 2 groups (Figure 3B), but the cumulative 5-year incidence of surgical AVR was significantly higher in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (82.4% vs. 67.1%, P=0.015) (Figure 3C). No patients underwent transcatheter aortic valve implantation (TAVI) during follow-up. After adjusting for confounders, STE in V_1–2 was independently associated with higher risk for death or surgical AVR (HR, 1.53; 95% CI, 1.06–2.22; P=0.02). Neither LVH nor LV strain was associated with the risk for death or surgical AVR (Table 4).

Figure 3.

Cumulative incidence of death or surgical AVR (A), death (B), and surgical AVR (C) in the entire cohort. AVR, aortic valve replacement; STE, ST-segment elevation.

Table 3. Clinical Outcomes at 5 Years in (A) the Entire Cohort, and (B) Conservatively Managed Patients Without Any Indication of AVR

Outcome	ST-segment elevation in leads V1–2		Log-rank P value
	No. of patients with event (cumulative incidence)
(A)	Yes (n=97)	No (n=114)
Death or surgical AVR	85 (91.4%)	86 (77.1%)	0.003
All-cause death	30 (35.6%)	28 (27.4%)	0.37
Surgical AVR	71 (82.4%)	69 (67.1%)	0.015
Sudden cardiac death	7 (9.9%)	3 (3.2%)	0.44
(B)	Yes (n=21)	No (n=43)
Death or surgical AVR	16 (87.5%)	18 (44.6%)	<0.001
All-cause death	9 (53.2%)	8 (19.0%)	0.08
Surgical AVR	9 (57.6%)	10 (30.5%)	<0.001
Sudden cardiac death	1 (8.3%)	3 (8.1%)	0.65
Hospitalization for heart failure	4 (22.7%)	5 (13.3%)	0.71
Emerging symptoms related to severe AS	13 (83.8%)	12 (33.7%)	<0.001
Chest pain	4	2
Syncope	3	1
Heart failure	6	10

Cumulative incidence at 5 years were estimated by Kaplan-Meier method. AS, aortic stenosis; AVR, aortic valve replacement.

Table 4. Univariate and Multivariable Analyses of the Effect of STE in Leads V_1–2 on the Primary Outcome Measure (Death or Surgical AVR)

Variable	Univariate analysis			Multivariable analysis
	HR	95% CI	P value	HR	95% CI	P value
STE in leads V1–2	1.55	1.15–2.09	0.004	1.53	1.06–2.22	0.02
LVH	1.07	0.80–1.46	0.64	0.88	0.60–1.30	0.52
LV strain	1.00	0.74–1.34	1.00	0.74	0.52–1.05	0.09
Age ≥75 years	0.89	0.67–1.20	0.45	0.81	0.59–1.11	0.18
Male	1.39	1.03–1.87	0.03	1.44	0.99–2.08	0.054
Hypertension	1.04	0.76–1.46	0.80	0.84	0.57–1.25	0.39
Atrial fibrillation	0.92	0.65–1.26	0.60	1.01	0.70–1.43	0.95
History of smoking	1.20	0.88–1.62	0.24	1.15	0.79–1.65	0.47
AVA <0.6 cm2	1.82	1.21–2.66	0.005	1.86	1.21–2.78	0.006
Increase of LV mass index	1.45	1.04–2.06	0.03	1.68	1.13–2.52	0.009

HR, hazard ratio. Other abbreviations as in Tables 1–3.

Among 106 patients with initial conservative management, 12 refused surgery and 30 were not considered good candidates for surgical AVR because of their comorbidities. In the remaining 64 conservatively managed patients who were asymptomatic without having any other indications for surgical AVR at initial diagnosis, the cumulative incidence of death or surgical AVR was significantly higher in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (87.5% vs. 44.6%, P <0.001) (Figure 4A, Table 3B). The cumulative incidence of death tended to be higher in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (53.2% vs. 19.0%, P=0.08) (Figure 4B). The cumulative incidence of surgical AVR was significantly higher in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (57.6% vs. 30.5%, P <0.001) (Figure 4C). Emerging symptoms related to severe AS were more often observed in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 (83.8% vs. 33.7%, P<0.001) (Figure 4D, Table 3B).

Figure 4.

Cumulative incidences of death or surgical AVR (A), death (B), surgical AVR (C), and emerging symptoms related to severe AS (D) in 64 patients who had no symptoms and no indication for surgical AVR at initial diagnosis. AVR, aortic valve replacement; STE, ST-segment elevation.

Discussion

The main findings of this study were as follows: (1) STE in leads V_1–2 was found in 46% of patients with severe AS, and significantly correlated with the echocardiographic severity of AS; (2) the cumulative 5-year incidence of death or surgical AVR was significantly higher in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 in the entire cohort of patients as well as in patients who had no symptoms and no indication for surgical AVR at initial diagnosis; (3) after adjusting for the echocardiographic index of AS severity and other confounders, STE in leads V_1–2 was independently associated with higher risk for death or AVR, and LVH and LV strain pattern were not associated.

To the best of our knowledge, this is the first report to describe the prognostic significance of STE in leads V_1–2 in patients with severe AS in real-world clinical practice. STE in leads V_1–2 could be regarded as a novel and clinically pertinent risk marker in patients with severe AS, considering that the ECG is an appealing examination because of its availability and measurement reproducibility. The prognostic importance of LVH and LV strain in patients with AS was shown in the previous studies,^3,4,18–20 but not in the present study. The exact reasons for the inconsistencies between our results and those of previous studies are unclear, but might be related to differences in the study populations. In the present study, which included patients with severe AS, 64% of the patients had LVH and 39% had LV strain. However, in the previous studies including asymptomatic patients who had mild to moderate AS,^4,18 the prevalence of LVH was 17–50% and that of LV strain was only approximately 20%. The severity of AS might influence the prevalence of LVH and LV strain and their prognostic effect.

It is well known that STE in the precordial leads is often seen in patients with LVH. The mechanism responsible for STE in precordial leads is not completely understood, but may involve changes in the QRS vector loop or the depolarization and repolarization of the heart secondary to LVH.^7,8 In the present study, STE in leads V_1–2 was closely correlated with the echocardiographic severity of AS and increased LVM index. We speculate that STE in leads V_1–2 might reflect some LV hypertrophic responses that were not represented by other abnormal ECG patterns such as LVH and LV strain.

Furthermore, it was noteworthy that the cumulative incidences of surgical AVR as well as of emerging symptoms related to AS were significantly higher in patients with STE in leads V_1–2 than in patients without STE in leads V_1–2 among patients who had no symptoms and no indication for surgical AVR at initial diagnosis. STE in leads V_1–2 might be useful to stratify the future risk for symptomatic deterioration in apparently asymptomatic patients with severe AS. ECG predictors for the long-term outcomes of patients with AS are clinically appealing because the ECG is a readily available examination with adequate reproducibility. Among 64 asymptomatic patients without any indication for AVR at initial diagnosis, some underwent AVR during follow-up. Considering that the level of STE in leads V_1–2 and the symptoms related to AS change over time, periodic clinical follow-up, ECG and echocardiography should be performed to evaluate symptoms and changes in ECG or AS severity. With the introduction of TAVI in inoperable or high surgical risk patients with severe AS,^21–24 treatment of severe AS has dramatically changed during the past decade. Some patients with severe AS who could potentially benefit from TAVI may not complain of any symptom because of their sedentary life style. Exercise stress test is recommended in asymptomatic patients with severe AS in the ACC/AHA guidelines to confirm both their asymptomatic status and hemodynamic response to exercise.^16,25 However, exercise testing cannot be performed by many potential candidates for TAVI because of their advanced age, limited exercise capacity, and comorbidities.²⁶ In this regard, ECG is very appealing because it is an easily available examination even for patients who are unable to perform exercise.

Study Limitations

First, this was a retrospective study performed at a single center. However, the retrospective design might have little effect on the clinical outcomes of patients with severe AS because ECG and echocardiography have been routinely recorded in Japan, and the indication of AVR has not been determined according to the results of ECG in real-world clinical practice. Second, we were unable to exclude the influence of ascertainment bias for symptoms related to severe AS. Finally, the measured and unmeasured differences in baseline characteristics between patients with and without STE in leads V_1–2 might limit comparability between groups. We intended to make statistical adjustments as extensively as possible to minimize the influence of unmeasured confounders. However, further prospective studies are warranted to confirm the current study’s results in a larger number of patients with severe AS.

Funding / Disclosures / Grant Support

None.

Supplementary Files

Supplementary File 1

Figure S1. (A) Peak aortic jet velocity and (B) aortic valve area according to ST-segment elevation (STE) in leads V_1–2.

Please find supplementary file(s);

http://dx.doi.org/10.1253/circj.CJ-15-0641

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