Circulation Journal

Circ J 2021; 85: 1093 – 1098

RAPID COMMUNICATION
doi: 10.1253/circj.CJ-21-0354

Regression of Electrocardiographic Left Ventricular

Hypertrophy After Transcatheter Aortic Valve
Implantation for Aortic Stenosis

Akihiro Tobe, MD; Akihito Tanaka, MD, PhD; Yoshiyuki Tokuda, MD, PhD;
Sho Akita, MD; Taro Fujii, MD; Yusuke Miki, MD; Kenji Furusawa, MD;
Hideki Ishii, MD, PhD; Akihiko Usui, MD, PhD; Toyoaki Murohara, MD, PhD

Background:  The changes in electrocardiographic left ventricular hypertrophy (ECG-LVH) after transcatheter aortic valve implanta-
tion (TAVI) are not fully elucidated.

Methods and Results:  The study group included 64 patients who underwent TAVI for aortic stenosis. Their 12-lead ECGs before
and at 2 days and 1, 6 and 12 months after TAVI were analyzed, and ECG-LVH was evaluated using various definitions. Values and
prevalence of each ECG-LVH parameter significantly decreased between 1 and 6 months after TAVI. Values of ECG-LVH param-
eters decreased especially in patients with ECG-LVH at baseline.

Conclusions:  Regression of ECG-LVH was observed between 1 and 6 months after TAVI.

Key Words: Electrocardiogram; Left ventricular hypertrophy; Transcatheter aortic valve implantation (TAVI)

L
eft ventricular hypertrophy (LVH) is commonly Patients with a newly implanted permanent pacemaker
observed in patients with aortic stenosis (AS) due (n=8), with newly recorded bundle branch block at any
to an increase in LV afterload.1 Several studies have time point (n=28), who died within 12 months after TAVI
reported regression of LVH after transcatheter aortic valve (n=10), or whose ECG records at any time point were not
implantation (TAVI), as evaluated by echocardiography,2 available (n=17) were also excluded. Finally, 64 patients
cardiac magnetic resonance imaging (MRI),3 or cardiac were included in the analysis. This study complied with the
computed tomography (CT).4 However, few studies have Declaration of Helsinki and was approved by the institu-
investigated the ECG changes in LVH after TAVI,5 and tional ethics committee.
because previous reports have suggested that electrocar-
diographic LVH (ECG-LVH) is not always equivalent to ECG Analysis
echocardiographic LVH,6,7 it is important to evaluate the We evaluated 12-lead ECGs obtained before TAVI, at 2
ECG changes as well. We used various ECG criteria to days, and 1, 6, and 12 months after TAVI. The ECG
investigate changes in ECG-LVH after TAVI. obtained before TAVI was defined as the baseline. Heart
rate, PR, corrected QT intervals (QTc), QRS duration, and
QRS axis were measured automatically. As an ECG assess-
Methods ment of LVH, the Sokolow-Lyon voltage criteria (sum of
Study Design and Patient Group the amplitude of S in V1 and the amplitude of R in V5 or
This was a retrospective, single-center, observational study V6, with a cutoff ≥3.5 mV; SV1 + RV5 or RV6), Cornell
conducted at Nagoya University Hospital, Aichi, Japan. A voltage criteria (sum of the amplitude of R in aVL and the
total of 156 consecutive patients with severe AS who amplitude of S or QS complex in V3, with a cutoff >2.8 mV
underwent TAVI between April 2016 and December 2019 in men and >2.0 mV in women; RaVL + SV3), Cornell
were included. Patients with an implanted permanent pace- product criteria {[Cornell voltage (+0.8 mV in women)] × 
maker (n=6), complete atrioventricular block (n=1), or QRS duration, with a cut off of 244 mV × ms; [RaVL + SV3
bundle branch block (n=22) before TAVI were excluded. (+0.8 mV in women)] × QRS}, and the Peguero-Lo Presti

Received April 13, 2021; revised manuscript received April 27, 2021; accepted May 2, 2021; J-STAGE Advance Publication released
online May 25, 2021   Time for primary review: 7 days
Department of Cardiology (A. Tobe, A. Tanaka, Y.M., K.F., H.I., T.M.), Department of Cardiac Surgery (Y.T., S.A., T.F., A.U.),
Nagoya University Graduate School of Medicine, Nagoya; Department of Cardiology, Fujita Health University Bantane
Hospital, Nagoya (H.I.), Japan
Mailing address:  Akihiro Tobe, MD, Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai-
cho, Showa-ku, Nagoya 466-8560, Japan.   E-mail: [email protected]
All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: [email protected]
ISSN-1346-9843

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1094 TOBE A et al.

Table 1.  Baseline Characteristics

voltage criteria (sum of the amplitude of the deepest S
wave in any lead and the S wave in lead V4; SD + SV4)
n=64
were evaluated.8,9 The PR segment was used as the base-
Age, years 82.6±5.7　　
line. The voltage of R or R’ and S or QS was measured
Male sex, n (%) 22 (34.4) both manually by the same cardiologist and automatically.
Height, cm 149±9　　　　 When the voltages were different in the same lead, the tallest
Body weight, kg 50.6±10.6 R or R’ and the deepest S or QS complex were measured.
Body mass index 22.6±3.7　　 The number of patients with the strain pattern and
Hypertension, n (%) 47 (73.4) inverted T wave were counted. Strain pattern was defined
Diabetes mellitus, n (%) 23 (35.9) as ≥1 mm convex ST-segment depression with asymmetri-
Dyslipidemia, n (%) 38 (59.4) cal T wave inversion.8 The T wave was considered to be
Smoking history, n (%) 20 (31.3)
inverted when it was deeper than 1 mm.10 A beat after
premature beats was not used for measurement.
eGFR <60 mL/min/1.73 m2, n (%) 44 (68.8)
Atrial fibrillation, n (%) 9 (14.1)
Echocardiographic Analysis
Obstructive pulmonary disorder, n (%) 16 (25.0) Echocardiographic data including the LV mass (LVM)
Extracardiac arteriopathy, n (%) 11 (17.2) index at baseline and 12 months were obtained. LVM was
Previous stroke/TIA, n (%) 9 (14.1) calculated by the Devereux formula: LVM (g) = 0.80 × {1.04 × 
 revious cardiovascular surgery,
P 5 (7.8) [(septal thickness + internal diameter + posterior wall thick-
n (%) ness)3 − (internal diameter)3]} + 0.6. LVM was indexed
Previous PCI, n (%) 10 (15.6) according to body surface area.
Previous MI, n (%) 4 (6.3)
NYHA III/IV, n (%) 32 (50.0) Statistical Analysis
Echocardiography Categorical variables are presented as numbers and per-
   Aortic valve area, cm2 0.59 (0.46–0.71) centages, and continuous variables are presented as
   Peak velocity, m/s 4.5±0.7 mean ± standard deviation or median (interquartile range).
   Peak pressure gradient, mmHg 79.5 (65.8–99.5)
The Wilcoxon signed rank test was used to compare con-
tinuous ECG variables between baseline and 2 days and at
   Mean pressure gradient, mmHg 43.4 (36.4–59.5)
1, 6, and 12 months. To compare the prevalence of ECG-
  LVEF, % 67 (61.3–73)
LVH, strain pattern, and inverted T wave between baseline
Computed tomography and 2 days, 1, 6, and 12 months after TAVI, the chi-square
   Annulus area, cm2 412±64　　 test or Fisher’s exact test was used. Intraclass correlation
   Annulus perimeter, mm 72.8±5.7　　 coefficient (ICC) was evaluated to assess the inter- and
STS score 5.8 (3.8–7.28) intra-observer variabilities. An ICC value >0.90 was con-
EuroSCOREII 4.0 (2.5–6.4)　　 sidered as excellent reliability. Differences were considered
Logistic Euro SCORE 12.7 (9.5–19.8)　　 statistically significant at P<0.05. All statistical analyses
Transcatheter heart valve were performed using SPSS version 27.0 (SPSS, Chicago,
  Type IL, USA).
    SAPIEN XT/3, n (%) 43 (67.2)
    Evolut R/Pro, n (%) 21 (32.8) Results
  Size
The baseline characteristics of the enrolled patients are
    20 mm, n (%) 2 (3.1) shown in Table 1: one-third of the patients were male
    23 mm, n (%) 31 (48.4) (35.4%), and the majority of patients had hypertension
    26 mm, n (%) 23 (35.9) (72.3%).
    29 mm, n (%) 8 (12.5) The inter- and intra-observer variabilities for the analy-
  Approach site sis of the voltage of RaVL, RV5, SV1, SV3, SV4 and SD
    Transfemoral, n (%) 60 (93.8) were well correlated [RaVL: inter-, 0.96 (P<0.001), intra-,
    Non-transfemoral, n (%) 4 (6.3) 0.97 (P<0.001); RV5: inter-, 0.96 (P<0.001), intra-,
Procedural complication 1.00 (P<0.001); SV1: inter-, 0.97 (P<0.001), intra-,
  Disabling/ nondisabling stroke, 2 (3.1)
1.00 (P<0.001); SV3: inter-, 0.99 (P<0.001), intra-,
n (%) 0.99 (P<0.001); SV4: inter-, 0.98 (P<0.001), intra-,
  Life-threatening/disabling bleeding, 1 (1.6) 0.98 (P<0.001); SD: inter-, 0.97 (P<0.001), intra-,
n (%) 0.97 (P<0.001)].
   Major vascular complication, n (%) 0 (0.0) Figure 1 and Table 2 show the electrocardiographic and
echocardiographic changes. QRS duration significantly
LVEF, left ventricular ejection fraction; MI, myocardial infarction;
NYHA, New York heart Association; PCI, percutaneous coronary decreased at 6 and 12 months after TAVI. The number of
intervention; STS, Society of Thoracic Surgeons; TIA, transient patients with strain pattern decreased significantly at 1, 6,
ischemic attack. and 12 months when compared with baseline, and the
number of those with an inverted T wave also tended to
decrease over time. The LVM index at 12 months after
TAVI significantly decreased compared with baseline.
The Sokolow-Lyon voltage, Cornell voltage, Cornell
product, and Peguero-Lo Presti voltage at 1, 6, and 12
months decreased significantly compared with baseline.

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Regression of ECG-LVH After TAVI 1095

Figure 1.   Changes in the values and prevalence

of ECG-LVH according to various criteria: (A)
Sokolow-Lyon voltage criteria; (B) Cornell voltage
criteria; (C) Cornell product criteria; (D) Peguero-
Lo Presti voltage criteria; (E) QRS duration; (F)
strain pattern; (G) inverted T wave. The values and
prevalence at each time point were compared
with those at baseline, and P values are described.
In the box plot, the tops and bottoms of boxes
show the 3rd and 1st quartile, respectively. Hori-
zontal lines in the boxes represent median values.
The tops and bottoms of bars show the maximum
and minimum values without outliers. LVH, left
ventricular hypertrophy.

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1096 TOBE A et al.

Table 2.  Electrocardiographic and Other Parameters

Baseline Day 2 1 month 6 months 12 months
ECG
   Heart rate, beats/min 76 (67~81)　　　 78 (69~88)　　　 73 (68~80)　　　　 75 (67~83)　　　　 73 (66~78)　　　　
  PR interval, # ms 165 (147~187)　 167 (153~187)　 164 (148~183)　　 163 (150~182)　　 168 (152~188)　　
   QRS duration, ms 97 (91~107)　 100 (94~107)　　　 97 (92~102)　　 96 (90~104)•　 95 (90~102)*　
  QTc, ms 435 (416~456)　 435 (423~459)　 434 (416~447)　　 431 (411~450)　　 431 (416~443)　　
   QRS axis, ° 23 (4~54)　　　　　 27(0~58)　　　　 28 (−1~53)　　　　 28(−12~51)　 25 (−3.3~50)•　
  SV1, mV 1.68 (1.10~2.27) 1.73 (1.18~2.50) 1.53 (1.02~1.82)* 1.26 (0.98~1.84)* 1.25 (0.85~1.64)*
  RV5, mV 2.26 (1.76~2.89) 2.31 (1.80~2.76) 2.25 (1.65~2.85)　 1.78 (1.33~2.30)* 1.71 (1.31~2.29)*
  Sokolow-Lyon voltage 4.03 (3.27~4.98) 4.03 (3.33~4.88) 3.84 (2.89~4.69)• 3.19 (2.75~3.79)* 3.05 (2.47~3.71)*
(SV1 + RV5), mV
  RaVL, mV 0.67 (0.36~0.95) 0.69 (0.32~0.97) 0.62 (0.25~0.91)• 0.48 (0.26~0.80)* 0.53 (0.26~0.78)•
  SV3, mV 1.90 (1.26~2.68) 2.04 (1.26~2.57) 1.56 (1.05~2.20)* 1.48 (0.97~2.08)* 1.34 (1.05~1.98)*
  Cornell voltage 2.50 (1.99~3.51) 2.66 (1.91~3.59) 2.12 (1.46~2.87)* 1.98 (1.53~2.69)* 1.91 (1.48~2.59)*
(RaVL + SV3), mV
  Cornell product,ψ mV × ms 312 (240~412)　 326 (224~431)　 268 (201~347)*　 245 (188~306)*　 223 (192~306)*　
  SD,‡ mV 2.32 (1.82~3.21) 2.50 (1.94~3.30) 2.14 (1.60~2.65)* 1.92 (1.45~2.23)* 1.78 (1.49~2.39)*
  SV4, mV 1.21 (0.59~1.74) 1.30 (0.58~1.82) 0.92 (0.45~1.50)* 0.83 (0.40~1.39)* 0.79 (0.42~1.43)*
  Peguero-Lo Presti voltage 3.63 (2.63~4.70) 3.73 (2.71~5.30) 2.88 (2.27~4.18)* 2.63 (2.00~3.62)* 2.74 (1.91~3.64)*
(SD + SV4), mV
   Strain T wave, n (%) 13 (20.3)　　　　　　 18 (28.1)　　　　　　 5 (7.8)•　　　　　　　　 4 (6.3)•　　　　　　　　 2 (3.1)•　　　　　　　　
   Inverted T wave, n (%) 33 (51.6)　　　　　　 42 (65.6)　　　　　　 29 (45.3)　　　　　　　 23 (35.9)　　　　　　　 23 (35.9)　　　　　　　
Echocardiography
   End-diastolic IVS, mm 11.4 (9.8~12.7)　　 10.2 (9.0~12.0)•　　
  End-diastolic posterior wall 10.9 (9.5~12.1)　　 10.0 (9.0~11.9)•　　
thickness, mm
  LVM index,† g/m2 129 (102~162)　 104 (85~126)*　　　
  Moderate to severe AR, 10 (15.6)　　　　　　 3 (4.7)•　　　　　　　　
n (%)
BNP, pg/mL 136 (80~358)　　　 65 (37~121)*　　
#Not ψ
measured in patients with atrial fibrillation. Cornell product = Cornell voltage (+0.8 in women) × QRS duration. ‡SD = amplitude
of the
deepest S wave in any lead. †Calculated by Devereux formula: LVM (g) = 0.80 × {1.04 × [(septal thickness + internal diameter + posterior wall
thickness)3 − (internal diameter)3]} + 0.6. LVM was indexed according to body surface area. •P<0.05 vs. baseline, *P<0.001 vs. baseline. AR,
aortic regurgitation; BNP, B-type natriuretic peptide; IVS, interventricular septum thickness; LVM, left ventricular mass.

The voltage of RV5 decreased significantly at 6 and 12 with the strain pattern decreased at 1 month after TAVI.
months. The voltage of SV1, RaVl, SV3, SV4 and SD Regression of ECG-LVH after surgical aortic valve
decreased significantly at 1, 6 and 12 months. The rate of replacement (SAVR) has been previously reported,11,12 but
ECG-LVH for each parameter is shown in Figure 1. the same phenomenon after TAVI has not been fully inves-
Regarding the criteria of Sokolow-Lyon voltage, Cornell tigated. Recently, Tanaka et al showed regression of ECG-
voltage and Peguero-Lo Presti voltage, the prevalence of LVH after TAVI, as evaluated using the Sokolow-Lyon
ECG-LVH decreased significantly at 6 and 12 months voltage.5 However, there are various criteria for ECG-
compared with baseline. For the Cornell product criterion, LVH, and it is considered important to validate using the
the rate of LVH decreased significantly at 1, 6, and 12 other criteria.
months compared with baseline. With regard to the time course of ECG-LVH, regression
Figure 2 shows the change in each ECG-LVH parameter has been observed as per several criteria between 2 weeks
when the patients were divided into those with and without and 6 months after SAVR.11 After TAVI, regression of
ECG-LVH at baseline. ECG-LVH parameter values ECG-LVH evaluated by Sokolow-Lyon voltage was
decreased significantly, especially in patients with ECG- observed at 1 month.5 Our results, revealing the time
LVH at baseline. course of various ECG parameters after TAVI, support
those conclusions.
Similar to ECG-LVH, previous studies have shown
Discussion regression of LVH after TAVI, as assessed quantitatively
We have presented the changes in ECG-LVH parameters by echocardiography, MRI, or CT. Regression of LVH
and the prevalence of ECG-LVH according to various was observed by echocardiographic assessment at 1
criteria. Compared with baseline, significant reductions in month,2 and regression of LVM was observed by MRI 4
the values and prevalence of ECG-LVH were observed days after TAVI.3 Therefore, regression of ECG-LVH is
between 1 and 6 months after TAVI, especially in patients thought to indicate regression of anatomic LVH.
with ECG-LVH at baseline. In addition, the QRS duration However, the relationship between ECG- or anatomic
significantly decreased at 6 months, and the ratio of patients LVH and prognosis after TAVI is unclear.5,13–17 Although

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Regression of ECG-LVH After TAVI 1097

Figure 2.   Changes in the ECG-LVH parameters when patients were divided into two groups: with and without baseline ECG-LVH.
(A) Sokolow-Lyon voltage criteria; (B) Cornell voltage criteria; (C) Cornell product criteria; (D) Peguero-Lo Presti voltage criteria.
Tops and bottoms of boxes show the 3rd and 1st quartile, respectively. Horizontal lines in the boxes represent median values.
Tops and bottoms of bars show the maximum and minimum values without outliers. The values and the prevalence at each time
point were compared with baseline. •P<0.05; *P<0.001. LVH, left ventricular hypertrophy.

the existence of echocardiographic LVH before TAVI was TAVI was not evaluated in this study because of the lim-
not associated with 1-year clinical outcomes,13 severe echo- ited number of patients and clinical events.
cardiographic LVH before TAVI was reported to be
related to poor outcomes at 5-year follow-up.14 Conversely,
for ECG assessment, studies have reported that the pres- Conclusions
ence of ECG-LVH at baseline was associated with better Regression of ECG-LVH after TAVI was demonstrated as
clinical outcome.5,15 Regarding the change in LVH, regres- per various criteria. The voltages and prevalence of ECG-
sion of echocardiographic-, CT- and ECG-LVH after LVH decreased significantly between 1 and 6 months after
TAVI has been associated with favorable clinical out- TAVI.
comes.4,5,16,17 The difference in the method of evaluating
LVH might be the main reason for these conflicting out- Funding
comes, and anatomic LVH is thought to be not always None.
equal to ECG-LVH. A relative voltage deficit caused by
reduced intercellular coupling in hypertrophic hearts has Disclosures
been proposed.6 Furthermore, myocardial injury, fibrosis H.I. received lecture fees from Astellas Pharma Inc., Astrazeneca Inc.,
or amyloid deposition decreases the voltage of the QRS Daiichi-Sankyo Pharma Inc., and MSD K. K. A.U. received lecture
wave.18–20 It is important to understand the difference fees from Terumo, Japan Blood Products Organization. A.U. received
between ECG- and anatomic LVH and to evaluate both an unrestricted research grant for the Department of Cardiac Surgery,
Nagoya University Graduate School of Medicine from Edwards
when evaluating patients with AS before and after treat- Lifesciences Corporation, Senko Medical Instrument Mfg., Co., Ltd.,
ment. Further investigations are required to fully elucidate Medtronic, Terumo, and Lifeline. T.M. received lecture fees from
the relationship between LVH and TAVI. Bayer Pharmaceutical Co., Ltd., Daiichi-Sankyo Co., Ltd., Dainippon
Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD K. K., Mitsubishi
Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., Novartis
Study Limitations Pharma K. K., Pfizer Japan Inc., Sanofi-Aventis K. K., and Takeda
First, this was a retrospective, single-center observational Pharmaceutical Co., Ltd. T.M. received an unrestricted research grant
study with a limited number of patients. Second, patients for the Department of Cardiology, Nagoya University Graduate
with bundle branch block or permanent pacemaker and School of Medicine from Astellas Pharma Inc., Daiichi-Sankyo Co.,
Ltd., Dainippon Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD
those whose data were unavailable were excluded, which K. K., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim
might have caused selection bias. Third, the relationship Co., Ltd., Novartis Pharma K. K., Otsuka Pharma Ltd., Pfizer Japan
between LVH/LVH regression and clinical outcomes after Inc., Sanofi-Aventis K. K., Takeda Pharmaceutical Co., Ltd., and

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1098 TOBE A et al.

Teijin Pharma Ltd. Association Electrocardiography and Arrhythmias Committee,

H.I., A.U., and T.M. are members of Circulation Journal’s Editorial Council on Clinical Cardiology; the American College of Cardi-
Team. All other authors have reported that they have no relationships ology Foundation; and the Heart Rhythm Society. Endorsed by
relevant to the contents of this paper to disclose. the International Society for Computerized Electrocardiology. J
Am Coll Cardiol 2009; 53: 992 – 1002.
  9. Peguero JG, Lo Presti S, Perez J, Issa O, Brenes JC, Tolentino A.
IRB Information Electrocardiographic criteria for the diagnosis of left ventricular
This study was approved by the Ethics Committee of Nagoya hypertrophy. J Am Coll Cardiol 2017; 69: 1694 – 1703.
University Hospital (approval no. 2019-0179). 10. Hanna EB, Glancy DL. ST-segment depression and T-wave
inversion: Classification, differential diagnosis, and caveats.
Cleve Clin J Med 2011; 78: 404 – 414.
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