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The decrease in QRS amplitude after aortic valve replacement in patients with aortic valve stenosis
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Journal of Electrocardiology 42 (2009) 410 – 413 www.jecgonline.com
The decrease in QRS amplitude after aortic valve replacement in patients with aortic valve stenosis Satoshi Kurisu, MD,⁎ Ichiro Inoue, MD, Takuji Kawagoe, MD, Masaharu Ishihara, MD, Yuji Shimatani, MD, Yasuharu Nakama, MD, Tatsuya Maruhashi, MD, Eisuke Kagawa, MD, Kazuoki Dai, MD, Junichi Matsushita, MD, Hiroki Ikenaga, MD Department of Cardiology, Hiroshima City Hospital, Moto-machi, Naka-ku, Hiroshima, Japan Received 24 August 2008
Abstract
Purpose: The purpose of this study was to evaluate the effect of aortic valve replacement on electrocardiogram (ECG) in patients with aortic valve stenosis. Methods: Serial 12-lead ECGs were obtained in 15 patients with aortic valve stenosis who underwent aortic valve replacement. Three ECG indexes for left ventricular hypertrophy were manually measured in each ECG: Sokolow-Lyon index (sum of S wave in V1 and R wave in V5), Cornell voltage index (sum of R wave in aVL and S wave in V3), and Gubner index (sum of R wave in I and S wave in III). Results: After aortic valve replacement, Sokolow-Lyon index gradually decreased during 2 years (51.1 ± 17.9 to 34.8 ± 12.5 mm, P b .01). Cornell voltage index (25.6 ± 7.0 to 15.0 ± 4.8 mm, P b .01) and Gubner index (15.8 ± 7.6 to 10.3 ± 5.5 mm, P b .01) also gradually decreased during 2 years. ST depression in V6 was found in 14 patients (93%) before aortic valve replacement. It resolved in 9 of 14 patients during 2 years. Conclusions: Electrocardiographic evidence of left ventricular hypertrophy gradually resolved after aortic valve replacement in patients with aortic valve stenosis. © 2009 Elsevier Inc. All rights reserved.
Keywords:
Left ventricular hypertrophy; Valve replacement; ECG indexes
Introduction
Methods
Left ventricular pressure overload in response to aortic valve stenosis leads to a marked hypertrophic response of the myocardium, and electrocardiogram (ECG) often shows the increase in QRS amplitude and the strain pattern of ST-T wave. Previous studies have shown anatomical regression of left ventricular hypertrophy (LVH) after aortic valve replacement with echocardiography,1 computed tomography,2 or magnetic resonance imaging.3 However, there have been few reports assessing whether ECG evidence of LVH resolve or not during follow-up. In this study, we evaluated the effect of aortic valve replacement on ECG in patients with aortic valve stenosis.
Study population
⁎ Corresponding author. Department of Cardiology, Hiroshima City Hospital, 7-33, Moto-machi, Naka-ku, Hiroshima 730-8518, Japan. E-mail address: [email protected] 0022-0736/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2009.03.001
A total of 15 patients with aortic valve stenosis undergoing aortic valve replacement in Hiroshima City Hospital (Hiroshima, Japan) were retrospectively enrolled in this study. All patients underwent both transthoracic echocardiography and coronary angiography. Aortic valve stenosis was diagnosed by transthoracic echocardiography, and patients with a pressure gradient of more than 50 mm Hg were included. Patients with depressed ejection fraction, coronary artery disease, severe aortic valve regurgitation, or bundlebranch block were excluded because these factors might affect ECG or echocardiographic findings. The study protocol was approved by our hospital's committee on ethics. Electrocardiogram Twelve-lead ECGs were obtained immediately before, and then at 2 weeks, 6 months, 1 year, and 2 years after aortic
S. Kurisu et al. / Journal of Electrocardiology 42 (2009) 410–413
in V6 was also manually measured. ST depression was considered present if it was 0.5 mm or greater.
Table 1 Patient characteristics No. of patients Age (y) Male Hypertension Diabetes Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) Total cholesterol (mg/dL) Creatinine (mg/dL) Use of antihypertensive drug (%) Use of statin (%) Etiology of aortic valve stenosis Degenerative calcification Bicuspid aortic valves Postinflammatory calcification Electrocardiographic index for LVH Sololow-Lyon index N35 mm Cornell voltage index N28 mm Gubner index N25 mm
411
15 69 ± 9 7 (47%) 10 (67%) 3 (20%) 126 ± 23 73 ± 13 203 ± 35 0.85 ± 0.27 6 (40%) 7 (47%) 12 (80%) 3 (20%) 0 (0%) 12 (80%) 6 (40%) 2 (13%)
valve replacement. Three ECG indexes for LVH were manually measured in each ECG4-6: Sokolow-Lyon index (sum of S wave in V1 and R wave in V5), Cornell voltage index (sum of R wave in aVL and S wave in V3), and Gubner index (sum of R wave in I and S wave in III). ST depression
Echocardiography Transthoracic echocardiographic data were obtained immediately before, and then at 2 weeks and 1 year after aortic valve replacement by the 3 experienced echocardiographers using a commercial ultrasound machine. Twodimensional guided M-mode measurements of left ventricular end-diastolic diameter (LVDD), interventricular septum thickness (IVS), and posterior wall thickness (PW) were measured. Left ventricular mass was calculated using the formula of Deverreux and Reichek: left ventricular mass (grams) = 1.04[(LVDD + IVS + PW)3 − (LVDD)3] − 13.6.7,8 Left ventricular mass (LVM) index was calculated by dividing LVM by body surface area. Statistical analysis Continuous variables were presented as means ± SD, and categorical variables were presented as relative frequencies (percentage). Statistical analysis was performed with the paired Student t test for continuous variables. The χ2 test was used for categorical variables. Differences were considered significant if the P value was less than .05.
Fig. 1. Serial ECGs in the patient with a pressure gradient of 112 mm Hg. Three electrocardiographic indexes for left ventricular hypertrophy gradually decreased during 2 years. ST depression in lead V6 also resolved during 2 years. Serial ECGs were shown as 5 mm/mV because of marked high voltage during early phase. Left ventricular mass index assessed by echocardiography decreased from 230 to 133 g/m2 during 1 year.
412
S. Kurisu et al. / Journal of Electrocardiology 42 (2009) 410–413
Results Patient characteristics There were 7 male and 8 female patients (Table 1). Age ranged from 58 to 82 years (69 ± 9 years). Ten patients had systemic hypertension, and 3 patients had diabetes. The etiology of the aortic valve stenosis was degenerative calcification of tricuspid aortic valves in 12 patients and calcification of congenitally bicuspid aortic valves in 3 patients. There was no patient with postinflammatory calcification and fibrosis. Electrocardiogram Serial ECGs of the representative case are shown in Fig. 1, and serial measurements of ECG findings are shown in Table 2. Sokolow-Lyon index, which was 51.1 ± 17.9 mm before aortic valve replacement, significantly decreased at 2 weeks (45.9 ± 18.7 mm, P b .01), and subsequently decreased more and more during 2 years (34.8 ± 12.5 mm, P b .01). Cornell voltage index, which was 25.6 ± 7.0 mm before aortic valve replacement, significantly decreased at 6 months (16.6 ± 5.9 mm, P b .01), and subsequently decreased more and more during 2 years (15.0 ± 4.8 mm, P b .01). Gubner index, which was 15.8 ± 7.6 mm before aortic valve replacement, significantly decreased at 6 months (12.2 ± 4.9 mm, P b .01), and subsequently decreased more and more during 2 years (10.3 ± 5.5 mm, P b .01). ST depression in lead V6 was found in 14 patients (93%) before aortic valve replacement. It resolved in 9 of 14 patients during 2 years. Echocardiography Serial measurements of echocardiographic findings were shown in Table 3. There was no significant correlation between each ECG index and LVM index before aortic valve replacement. Aortic valve replacement significantly decreased pressure gradient from 105 ± 37 to 28 ± 12 mm Hg (P b .01), and this improvement persisted at 1 year (24 ± 10 mm Hg, P b .01). LVM index, which was 173 ± 51 g/m2 before aortic valve replacement, did not significantly change at 2 weeks (162 ± 48 g/m2), but significantly decreased to 121 ± 26 g/m2 at 1 year (P b .01).
5.2, and 5.1 ± 5.0 mm on ECG, respectively. On the other hand, LVM index decreased by 52 ± 45 g/m 2 on echocardiography. There was no significant correlation between the decrease in each ECG index and the decrease in LVM index. Discussion Present findings In this study, we demonstrated that ECG evidence of LVH gradually resolved after aortic valve replacement in patients with aortic valve stenosis. Electrocardiogram and left ventricular hypertrophy Several ECG indexes including Sokolow-Lyon index, Cornell voltage index, or Gubner index have been used to diagnose LVH in the clinical setting.4-6 Left ventricular hypertrophy is associated with increased risk for cardiovascular disease including angina pectoris, myocardial infarction, congestive heart failure, arrhythmia, and sudden death.9-14 The possible mechanism is that LVH increases the oxygen requirement, which imposes a hazard of ischemia in the setting of decreased supply due to atherosclerosis and decreased coronary reserve. However, there is an amount of published evidence that there are discrepancies between the increased QRS amplitude and increased LVM in patients with hypertension 4 or hypertrophic cardiomyopathy. 5 This study also demonstrated that there were no significant correlations between each ECG index and LVM index in patients with aortic valve stenosis. The increased QRS amplitude is seen only in a part of patients with anatomical LVH, and consequently ECG evidence of LVH suffer from a high number of false-negative results and low sensitivity. Bacharova15 formulated a hypothesis that these falsenegative ECG results might reflect changes in electrical properties of myocardium in the LVH development and termed this deviation the relative voltage deficit because the QRS amplitude was lower than expected according to the classic expectations. Despite its limitations, at least the ECG remains a valuable tool to follow the regression of LVH in each one.
Association between decrease in QRS amplitude and decrease in LVM index
Regression of ECG evidence of LVH
During 1 year, Sokolow-Lyon index, Cornell voltage index, and Gubner index decreased by 13.5 ± 9.2, 9.9 ±
Henry et al1 previously showed that the Romhilt-Estes score, a semiquantitative ECG index of severity of LVH,
Table 2 Serial measurements of ECG findings
S wave in V1 + R wave in V5 (mm) R wave in a VL + S wave in V3 (mm) R wave in I + S wave in III (mm) ST depression in V6 (%) AVR indicates aortic valve replacement. ⁎ P b .01 vs before AVR.
Before AVR
2 wk
6 mo
1y
2y
51.1 ± 17.9 25.6 ± 7.0 15.8 ± 7.6 14 (93%)
45.9 ± 18.7⁎ 22.0 ± 9.7 13.9 ± 7.0 12 (80%)
41.0 ± 15.9⁎ 16.6 ± 5.9⁎ 12.2 ± 4.9⁎ 11 (73%)
37.6 ± 13.7⁎ 15.7 ± 5.2⁎ 10.8 ± 5.0⁎ 9 (60%)
34.8 ± 12.5⁎ 15.0 ± 4.8⁎ 10.3 ± 5.5⁎ 6 (40%)⁎
S. Kurisu et al. / Journal of Electrocardiology 42 (2009) 410–413
413
Table 3 Serial measurements of echocardiographic findings
Left ventricular end-diastolic diameter (mm) Left ventricular end-systolic diameter (mm) Interventricular septum thickness (mm) Posterior wall thickness (mm) Left ventricular ejection fraction (%) Pressure gradient (mm Hg) LVM (g) LVM index (g/m2)
Before AVR
2 wk
1y
51.9 ± 6.5 33.3 ± 7.4 12.5 ± 2.6 10.8 ± 2.1 62 ± 11 105 ± 37 281 ± 88 173 ± 51
47.7 ± 5.5⁎⁎ 32.9 ± 5.9 13.3 ± 2.9 10.9 ± 1.8 61 ± 10 28 ± 12⁎⁎ 264 ± 88 162 ± 48
46.9 ± 3.8⁎⁎ 29.5 ± 3.4⁎ 10.6 ± 1.4⁎ 9.0 ± 1.5⁎ 66 ± 8 24 ± 10⁎⁎ 197 ± 45⁎⁎ 121 ± 26⁎⁎
⁎ P b .05 vs before AVR. ⁎⁎ P b .01 vs before AVR.
decreased after aortic valve replacement. However, time course of ECG index for LVH has not been fully evaluated. In our study, patients had a severe pressure gradient of 105 ± 37 mm Hg. Sokolow-Lyon index significantly decreased at 2 weeks, and Cornell voltage index and Gubner index significantly decreased at 6 months. Thus, our study demonstrated the regression of ECG evidence of LVH after aortic valve replacement. The physicians caring for such patients should be attentive to the improvement in the ECG because this may confer an improvement in risk for cardiovascular disease as shown in the previous study.6 This should be tested in further studies. Although our study showed the regression of ECG indexes for LVH in response to aortic valve replacement, the serial change in each ECG index and the change in LVM index assessed by echocardiography were not correlated. In fact, our results were consistent with those documented in hypertensive patients undergoing antihypertensive treatment.16 These nonlinear regressions of ECG indexes for LVH and anatomical LVH may be explained by the concept of the relative voltage deficit. Further studies are required to evaluate the ability of the ECG to assess myocardial response to aortic valve replacement. Limitations First, in patients with aortic valve stenosis and impaired left ventricular function, LVH may not be reversible after delayed surgery. Because we studied only patients with normal left ventricular function, it remained unclear whether the regression of ECG evidence of LVH occurred or not in patients with impaired left ventricular function. Second, routine follow-up echocardiography was performed only at 2 weeks and at 1 year after aortic valve replacement. The correlation between the decrease in each ECG index and the decrease in LVM index was assessed only at 1 year. It remained unclear whether the discrepancy existed even at 2 years. Conclusion Electrocardiographic evidence of LVH gradually resolved after aortic valve replacement in patients with aortic valve stenosis. The physicians caring for patients undergoing
aortic valve replacement should be attentive to the improvement in the ECG. References 1. Henry WL, Bonow RO, Borer JS, et al. Evaluation of aortic valve replacement in patients with valvular aortic stenosis. Circulation 1980; 61:814. 2. Kurnik PB, Innerfield M, Wachspress JD, et al. Left ventricular mass regression after aortic valve replacement measured by ultrafast computed tomography. Am Heart J 1990;120:919. 3. Lamb HJ, Beyerbacht HP, de Roos A, et al. Left ventricular remodeling early after aortic valve replacement: differential effects on diastolic function in aortic valve stenosis and aortic regurgitation. J Am Coll Cardiol 2002;40:2182. 4. Pewsner D, Juni P, Egger M, et al. Accuracy of electrocardiography in diagnosis of left ventricular hypertrophy in arterial hypertension: systematic review. BMJ 2007;335:711. 5. Montgomery JV, Harris KM, Casey SA, et al. Relation of electrocardiographic patterns to phenotypic expression and clinical outcome in hypertrophic cardiomyopathy. Am J Cardiol 2005;96:270. 6. Levy D, Salomon M, D'Agostino RB, et al. Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy. Circulation 1994;90:1786. 7. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in men. Circulation 1977;55:613. 8. Noda A, Yagi T, Yamada H, Miyahara T, Okada T, Yokota M. Electrocardiographic diagnosis of left ventricular hypertrophy improved by considering both QRS voltage and ST-Tcriteria. Jpn Circ J 1994;58:698. 9. Kannel WB, Gordon T, Castelli WP, Margolis JR. Electrocardiographic left ventricular hypertrophy and risk of coronary heart disease: the Framingham Study. Ann Intern Med 1970;72:813. 10. Kannel WB, Dannenberg AL, Levy D. Population implications of electrocardiographic left ventricular hypertrophy. Am J Cardiol 1987; 60:85I. 11. Dunn FG, McLenachan J, Isles CG, et al. Left ventricular hypertrophy and mortality in hypertension: an analysis of data from the Glasgow Blood Pressure Clinic. J Hypertens 1990;8:775. 12. Ghali JK, Kadakia S, Cooper RS, Liao YL. Impact of left ventricular hypertrophy on ventricular arrhythmias in the absence of coronary artery disease. J Am Coll Cardiol 1991;17:1277. 13. McLenachan JM, Henderson E, Morris KI, Dargie HJ. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med 1987;317:787. 14. Lanti M, Puddu PE, Menotti A. Voltage criteria of left ventricular hypertrophy in sudden and nonsudden coronary artery disease mortality: the Italian section of the Seven Countries Study. Am J Cardiol 1990;66:1181. 15. Bacharova L. Electrical and structural remodeling in left ventricular hypertrophy: a substrate for a decrease in QRS voltage? Ann Noninvasive Electrocardiol 2007;12:260. 16. Neaton JD, Grimm Jr RH, Prineas RJ, et al. Treatment of Mild Hypertension Study: final results. JAMA 1993;270:713.
Journal of Electrocardiology 42 (2009) 410 – 413 www.jecgonline.com
The decrease in QRS amplitude after aortic valve replacement in patients with aortic valve stenosis Satoshi Kurisu, MD,⁎ Ichiro Inoue, MD, Takuji Kawagoe, MD, Masaharu Ishihara, MD, Yuji Shimatani, MD, Yasuharu Nakama, MD, Tatsuya Maruhashi, MD, Eisuke Kagawa, MD, Kazuoki Dai, MD, Junichi Matsushita, MD, Hiroki Ikenaga, MD Department of Cardiology, Hiroshima City Hospital, Moto-machi, Naka-ku, Hiroshima, Japan Received 24 August 2008
Abstract
Purpose: The purpose of this study was to evaluate the effect of aortic valve replacement on electrocardiogram (ECG) in patients with aortic valve stenosis. Methods: Serial 12-lead ECGs were obtained in 15 patients with aortic valve stenosis who underwent aortic valve replacement. Three ECG indexes for left ventricular hypertrophy were manually measured in each ECG: Sokolow-Lyon index (sum of S wave in V1 and R wave in V5), Cornell voltage index (sum of R wave in aVL and S wave in V3), and Gubner index (sum of R wave in I and S wave in III). Results: After aortic valve replacement, Sokolow-Lyon index gradually decreased during 2 years (51.1 ± 17.9 to 34.8 ± 12.5 mm, P b .01). Cornell voltage index (25.6 ± 7.0 to 15.0 ± 4.8 mm, P b .01) and Gubner index (15.8 ± 7.6 to 10.3 ± 5.5 mm, P b .01) also gradually decreased during 2 years. ST depression in V6 was found in 14 patients (93%) before aortic valve replacement. It resolved in 9 of 14 patients during 2 years. Conclusions: Electrocardiographic evidence of left ventricular hypertrophy gradually resolved after aortic valve replacement in patients with aortic valve stenosis. © 2009 Elsevier Inc. All rights reserved.
Keywords:
Left ventricular hypertrophy; Valve replacement; ECG indexes
Introduction
Methods
Left ventricular pressure overload in response to aortic valve stenosis leads to a marked hypertrophic response of the myocardium, and electrocardiogram (ECG) often shows the increase in QRS amplitude and the strain pattern of ST-T wave. Previous studies have shown anatomical regression of left ventricular hypertrophy (LVH) after aortic valve replacement with echocardiography,1 computed tomography,2 or magnetic resonance imaging.3 However, there have been few reports assessing whether ECG evidence of LVH resolve or not during follow-up. In this study, we evaluated the effect of aortic valve replacement on ECG in patients with aortic valve stenosis.
Study population
⁎ Corresponding author. Department of Cardiology, Hiroshima City Hospital, 7-33, Moto-machi, Naka-ku, Hiroshima 730-8518, Japan. E-mail address: [email protected] 0022-0736/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2009.03.001
A total of 15 patients with aortic valve stenosis undergoing aortic valve replacement in Hiroshima City Hospital (Hiroshima, Japan) were retrospectively enrolled in this study. All patients underwent both transthoracic echocardiography and coronary angiography. Aortic valve stenosis was diagnosed by transthoracic echocardiography, and patients with a pressure gradient of more than 50 mm Hg were included. Patients with depressed ejection fraction, coronary artery disease, severe aortic valve regurgitation, or bundlebranch block were excluded because these factors might affect ECG or echocardiographic findings. The study protocol was approved by our hospital's committee on ethics. Electrocardiogram Twelve-lead ECGs were obtained immediately before, and then at 2 weeks, 6 months, 1 year, and 2 years after aortic
S. Kurisu et al. / Journal of Electrocardiology 42 (2009) 410–413
in V6 was also manually measured. ST depression was considered present if it was 0.5 mm or greater.
Table 1 Patient characteristics No. of patients Age (y) Male Hypertension Diabetes Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) Total cholesterol (mg/dL) Creatinine (mg/dL) Use of antihypertensive drug (%) Use of statin (%) Etiology of aortic valve stenosis Degenerative calcification Bicuspid aortic valves Postinflammatory calcification Electrocardiographic index for LVH Sololow-Lyon index N35 mm Cornell voltage index N28 mm Gubner index N25 mm
411
15 69 ± 9 7 (47%) 10 (67%) 3 (20%) 126 ± 23 73 ± 13 203 ± 35 0.85 ± 0.27 6 (40%) 7 (47%) 12 (80%) 3 (20%) 0 (0%) 12 (80%) 6 (40%) 2 (13%)
valve replacement. Three ECG indexes for LVH were manually measured in each ECG4-6: Sokolow-Lyon index (sum of S wave in V1 and R wave in V5), Cornell voltage index (sum of R wave in aVL and S wave in V3), and Gubner index (sum of R wave in I and S wave in III). ST depression
Echocardiography Transthoracic echocardiographic data were obtained immediately before, and then at 2 weeks and 1 year after aortic valve replacement by the 3 experienced echocardiographers using a commercial ultrasound machine. Twodimensional guided M-mode measurements of left ventricular end-diastolic diameter (LVDD), interventricular septum thickness (IVS), and posterior wall thickness (PW) were measured. Left ventricular mass was calculated using the formula of Deverreux and Reichek: left ventricular mass (grams) = 1.04[(LVDD + IVS + PW)3 − (LVDD)3] − 13.6.7,8 Left ventricular mass (LVM) index was calculated by dividing LVM by body surface area. Statistical analysis Continuous variables were presented as means ± SD, and categorical variables were presented as relative frequencies (percentage). Statistical analysis was performed with the paired Student t test for continuous variables. The χ2 test was used for categorical variables. Differences were considered significant if the P value was less than .05.
Fig. 1. Serial ECGs in the patient with a pressure gradient of 112 mm Hg. Three electrocardiographic indexes for left ventricular hypertrophy gradually decreased during 2 years. ST depression in lead V6 also resolved during 2 years. Serial ECGs were shown as 5 mm/mV because of marked high voltage during early phase. Left ventricular mass index assessed by echocardiography decreased from 230 to 133 g/m2 during 1 year.
412
S. Kurisu et al. / Journal of Electrocardiology 42 (2009) 410–413
Results Patient characteristics There were 7 male and 8 female patients (Table 1). Age ranged from 58 to 82 years (69 ± 9 years). Ten patients had systemic hypertension, and 3 patients had diabetes. The etiology of the aortic valve stenosis was degenerative calcification of tricuspid aortic valves in 12 patients and calcification of congenitally bicuspid aortic valves in 3 patients. There was no patient with postinflammatory calcification and fibrosis. Electrocardiogram Serial ECGs of the representative case are shown in Fig. 1, and serial measurements of ECG findings are shown in Table 2. Sokolow-Lyon index, which was 51.1 ± 17.9 mm before aortic valve replacement, significantly decreased at 2 weeks (45.9 ± 18.7 mm, P b .01), and subsequently decreased more and more during 2 years (34.8 ± 12.5 mm, P b .01). Cornell voltage index, which was 25.6 ± 7.0 mm before aortic valve replacement, significantly decreased at 6 months (16.6 ± 5.9 mm, P b .01), and subsequently decreased more and more during 2 years (15.0 ± 4.8 mm, P b .01). Gubner index, which was 15.8 ± 7.6 mm before aortic valve replacement, significantly decreased at 6 months (12.2 ± 4.9 mm, P b .01), and subsequently decreased more and more during 2 years (10.3 ± 5.5 mm, P b .01). ST depression in lead V6 was found in 14 patients (93%) before aortic valve replacement. It resolved in 9 of 14 patients during 2 years. Echocardiography Serial measurements of echocardiographic findings were shown in Table 3. There was no significant correlation between each ECG index and LVM index before aortic valve replacement. Aortic valve replacement significantly decreased pressure gradient from 105 ± 37 to 28 ± 12 mm Hg (P b .01), and this improvement persisted at 1 year (24 ± 10 mm Hg, P b .01). LVM index, which was 173 ± 51 g/m2 before aortic valve replacement, did not significantly change at 2 weeks (162 ± 48 g/m2), but significantly decreased to 121 ± 26 g/m2 at 1 year (P b .01).
5.2, and 5.1 ± 5.0 mm on ECG, respectively. On the other hand, LVM index decreased by 52 ± 45 g/m 2 on echocardiography. There was no significant correlation between the decrease in each ECG index and the decrease in LVM index. Discussion Present findings In this study, we demonstrated that ECG evidence of LVH gradually resolved after aortic valve replacement in patients with aortic valve stenosis. Electrocardiogram and left ventricular hypertrophy Several ECG indexes including Sokolow-Lyon index, Cornell voltage index, or Gubner index have been used to diagnose LVH in the clinical setting.4-6 Left ventricular hypertrophy is associated with increased risk for cardiovascular disease including angina pectoris, myocardial infarction, congestive heart failure, arrhythmia, and sudden death.9-14 The possible mechanism is that LVH increases the oxygen requirement, which imposes a hazard of ischemia in the setting of decreased supply due to atherosclerosis and decreased coronary reserve. However, there is an amount of published evidence that there are discrepancies between the increased QRS amplitude and increased LVM in patients with hypertension 4 or hypertrophic cardiomyopathy. 5 This study also demonstrated that there were no significant correlations between each ECG index and LVM index in patients with aortic valve stenosis. The increased QRS amplitude is seen only in a part of patients with anatomical LVH, and consequently ECG evidence of LVH suffer from a high number of false-negative results and low sensitivity. Bacharova15 formulated a hypothesis that these falsenegative ECG results might reflect changes in electrical properties of myocardium in the LVH development and termed this deviation the relative voltage deficit because the QRS amplitude was lower than expected according to the classic expectations. Despite its limitations, at least the ECG remains a valuable tool to follow the regression of LVH in each one.
Association between decrease in QRS amplitude and decrease in LVM index
Regression of ECG evidence of LVH
During 1 year, Sokolow-Lyon index, Cornell voltage index, and Gubner index decreased by 13.5 ± 9.2, 9.9 ±
Henry et al1 previously showed that the Romhilt-Estes score, a semiquantitative ECG index of severity of LVH,
Table 2 Serial measurements of ECG findings
S wave in V1 + R wave in V5 (mm) R wave in a VL + S wave in V3 (mm) R wave in I + S wave in III (mm) ST depression in V6 (%) AVR indicates aortic valve replacement. ⁎ P b .01 vs before AVR.
Before AVR
2 wk
6 mo
1y
2y
51.1 ± 17.9 25.6 ± 7.0 15.8 ± 7.6 14 (93%)
45.9 ± 18.7⁎ 22.0 ± 9.7 13.9 ± 7.0 12 (80%)
41.0 ± 15.9⁎ 16.6 ± 5.9⁎ 12.2 ± 4.9⁎ 11 (73%)
37.6 ± 13.7⁎ 15.7 ± 5.2⁎ 10.8 ± 5.0⁎ 9 (60%)
34.8 ± 12.5⁎ 15.0 ± 4.8⁎ 10.3 ± 5.5⁎ 6 (40%)⁎
S. Kurisu et al. / Journal of Electrocardiology 42 (2009) 410–413
413
Table 3 Serial measurements of echocardiographic findings
Left ventricular end-diastolic diameter (mm) Left ventricular end-systolic diameter (mm) Interventricular septum thickness (mm) Posterior wall thickness (mm) Left ventricular ejection fraction (%) Pressure gradient (mm Hg) LVM (g) LVM index (g/m2)
Before AVR
2 wk
1y
51.9 ± 6.5 33.3 ± 7.4 12.5 ± 2.6 10.8 ± 2.1 62 ± 11 105 ± 37 281 ± 88 173 ± 51
47.7 ± 5.5⁎⁎ 32.9 ± 5.9 13.3 ± 2.9 10.9 ± 1.8 61 ± 10 28 ± 12⁎⁎ 264 ± 88 162 ± 48
46.9 ± 3.8⁎⁎ 29.5 ± 3.4⁎ 10.6 ± 1.4⁎ 9.0 ± 1.5⁎ 66 ± 8 24 ± 10⁎⁎ 197 ± 45⁎⁎ 121 ± 26⁎⁎
⁎ P b .05 vs before AVR. ⁎⁎ P b .01 vs before AVR.
decreased after aortic valve replacement. However, time course of ECG index for LVH has not been fully evaluated. In our study, patients had a severe pressure gradient of 105 ± 37 mm Hg. Sokolow-Lyon index significantly decreased at 2 weeks, and Cornell voltage index and Gubner index significantly decreased at 6 months. Thus, our study demonstrated the regression of ECG evidence of LVH after aortic valve replacement. The physicians caring for such patients should be attentive to the improvement in the ECG because this may confer an improvement in risk for cardiovascular disease as shown in the previous study.6 This should be tested in further studies. Although our study showed the regression of ECG indexes for LVH in response to aortic valve replacement, the serial change in each ECG index and the change in LVM index assessed by echocardiography were not correlated. In fact, our results were consistent with those documented in hypertensive patients undergoing antihypertensive treatment.16 These nonlinear regressions of ECG indexes for LVH and anatomical LVH may be explained by the concept of the relative voltage deficit. Further studies are required to evaluate the ability of the ECG to assess myocardial response to aortic valve replacement. Limitations First, in patients with aortic valve stenosis and impaired left ventricular function, LVH may not be reversible after delayed surgery. Because we studied only patients with normal left ventricular function, it remained unclear whether the regression of ECG evidence of LVH occurred or not in patients with impaired left ventricular function. Second, routine follow-up echocardiography was performed only at 2 weeks and at 1 year after aortic valve replacement. The correlation between the decrease in each ECG index and the decrease in LVM index was assessed only at 1 year. It remained unclear whether the discrepancy existed even at 2 years. Conclusion Electrocardiographic evidence of LVH gradually resolved after aortic valve replacement in patients with aortic valve stenosis. The physicians caring for patients undergoing
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