Impact of left ventricular hypertrophy late after aortic valve replacement for aortic stenosis on cardiovascular morbidity and mortality

AIMS: The goal of this study was to assess the prevalence of left ventricular (LV) hypertrophy in patients with aortic stenosis late (>6 months) after aortic valve replacement and its impact on cardiac-related morbidity and mortality. METHODS AND RESULTS: In a single tertiary centre, echocardiographic data of LV muscle mass were collected. Detailed information of medical history and angiographic data were gathered. Ninety-nine of 213 patients (46%) had LV hypertrophy late (mean 5.8 +/- 5.4 years) after aortic valve replacement. LV hypertrophy was associated with impaired exercise capacity, higher New York Heart Association dyspnoea class, a tendency for more frequent chest pain expressed as higher Canadian Cardiovascular Society class, and more rehospitalizations. 24% of patients with normal LV mass vs. 39% of patients with LV hypertrophy reported cardiac-related morbidity (p = 0.04). In a multivariate logistic regression model, LV hypertrophy was an independent predictor of cardiac-related morbidity (odds ratio 2.31, 95% CI 1.08 to 5.41), after correction for gender, baseline ejection fraction, and coronary artery disease and its risk factors. Thirty seven deaths occurred during a total of 1959 patient years of follow-up (mean follow-up 9.6 years). Age at aortic valve replacement (hazard ratio 1.85, 95% CI 1.39 to 2.47, for every 5 years increase in age), coexisting coronary artery disease at the time of surgery (hazard ratio 3.36, 95% CI 1.31 to 8.62), and smoking (hazard ratio 4.82, 95% CI 1.72 to 13.45) were independent predictors of overall mortality late after surgery, but not LV hypertrophy. CONCLUSIONS: In patients with aortic valve replacement for isolated aortic stenosis, LV hypertrophy late after surgery is associated with increased morbidity.     

Four year follow up of aortic valve replacement for isolated aortic stenosis: a link between reduction in pressure overload, regression of left ventricular hypertrophy, and diastolic function

OBJECTIVE—To evaluate changes in left ventricular function and the impact of ventricular hypertrophy and pressure gradient early and late after aortic valve replacement in patients with isolated aortic stenosis.
DESIGN—41 patients with isolated aortic stenosis and normal systolic function underwent cross sectional and Doppler echocardiography two months before and two weeks and four years after aortic valve replacement.
RESULTS—Early after the operation, left ventricular mass index (mean (SD)) decreased from 187 (44) g/m² to 179 (46) g/m², because of a reduction in end diastolic diameter (p < 0.05). Aortic pressure gradients were reduced, as expected. Isovolumic relaxation time was reduced from 93 (20) ms to 78 (12) ms, and deceleration time from 241 (102) ms to 205 (77) ms (p < 0.05). At four years, left ventricular mass index was further reduced to 135 (30) g/m² (p < 0.01) as a result of wall thickness reduction in the interventricular septum (from 14 (1.6) mm to 12 (1.4) mm, p < 0.01) and the posterior wall (from 14 (1.6) mm to 12 (1.3) mm, p < 0.01). Diastolic function, expressed by a reduction in isovolumic relaxation time from 93 (20) ms to 81 (15) ms (p < 0.01) and deceleration time from 241 (102) ms to 226 (96) ms (p < 0.05), remained improved. Prolonged isovolumic relaxation time was associated with significant septal and posterior wall hypertrophy (wall thickness > 13 mm) (p < 0.05), whereas prolonged deceleration time was related to high residual gradient (peak gradient > 30 mm Hg ) (p < 0.01).
CONCLUSIONS—Left ventricular diastolic function improves early after surgery for aortic stenosis in parallel with the reduction in the aortic gradient. However, prolongation of Doppler indices of myocardial relaxation and ventricular filling is observed in patients with significant left ventricular hypertrophy and a residual pressure gradient early after surgery. At four years postoperatively, diastolic function remains improved.


Keywords: diastolic function; hypertrophy regression; aortic valve replacement; aortic stenosis     

Changes in left ventricular filling after valve replacement for aortic stenosis

In order to evaluate the short- and long-term effects of aortic valve replacement on the pattern of left ventricular inflow velocity, pulsed wave Doppler analysis was performed in 20 patients with isolated aortic stenosis. Complementary, left ventricular wall thickness was measured, using M-mode echocardiography. One week after operation, left ventricular wall thickness is not changed significantly. The Doppler findings suggest some improvement of left ventricular filling. Six months and 1 year postoperatively, there is a significant, but incomplete regression of left ventricular hypertrophy. Left ventricular filling improved only partially, compared to preoperatively.     

Late chronic hemolysis after valve replacement for aortic stenosis. Relation to residual hypertrophy and impaired left ventricular function

The relationship between intravascular hemolysis induced by aortic valve prosteses and patient status/left ventricular (LV) function (radionuclide cardiography) was examined in 63 patients of 65 who were alive ten to seventeen years after valve replacement (1965-1973) for aortic stenosis. Serum-lactic dehydrogenase (LDH) exceeded upper reference limit in 62 patients and S-haptoglobin (HAPTO) was reduced in 62. One patient with normal LDH had reduced HAPTO and elevated plasma-hemoglobin. Anemia was noted in 4 patients (6%). S-LDH was higher in men than in women (p less than 0.05), in patients with increased ECG hypertrophy score than in those with a normal score (p less than 0.05), in patients with NYHA class II-III than in those with class I (p less than 0.05), in patients with abnormal LV function than in those with a normal radionuclide study (p less than 0.05), in patients with a pathologic Q wave in the ECG than in those without (p less than 0.05), and in patients with a Starr Edwards cloth-covered (SECC) prosthesis than in those with other types (p = 0.07). ECG hypertrophy score correlated directly with LDH (r = 0.33, p = 0.008) and inversely with LV ejection fraction (r = -0.57, p less than 0.0001), peak ejection rate (r = -0.47, p less than 0.0001), and peak filling rate (r = -0.41, p less than 0.001). Multiple linear regression analysis revealed that LDH was accounted for by ECG hypertrophy score (p = 0.001), SECC prosthesis (p = 0.04), and male gender (p = 0.05). Hypertrophic malfunctioning left ventricles may be responsible for higher degrees of turbulent flow characteristics in the vicinity of prosthetic valves in the aortic position and, by inference, explain the increased tendency toward hemolysis in these patients.     

Time course of regression of left ventricular hypertrophy after aortic valve replacement

To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 +/- 0.5 years), and late (8.1 +/- 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 +/- 73 to 105 +/- 35 ml/m2, p less than .01), a fall in left heart filling pressure (19 +/- 9 to 12 +/- 5 mm Hg, p less than .01), and maintenance of the cardiac index (3.3 +/- 0.8 to 3.5 +/- 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 +/- 13% to 64 +/- 10%, NS). By the late study the cardiac index (4.0 +/- 0.6 liters/min/m2, p less than .01) and left ventricular ejection fraction (66 +/- 15%, p less than .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 +/- 38 vs 120 +/- 29 g/m2, p less than .01), and a further 13% from the intermediate to the late study (105 +/- 32 g/m2, p less than .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 +/- 36 g/m2), and greater in those with aortic stenosis (158 +/- 33 g/m2) than in control subjects (85 +/- 9 g/m2, p less than .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 +/- 29 g/m2) and those with stenosis (114 +/- 27 g/m2) than in the control subjects (p less than .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium.     

Left ventricular hypertrophy and remodeling after aortic valve replacement

Left ventricular geometric remodeling and regression of hypertrophy were assessed after aortic valve replacement with a mechanical prosthesis in 37 patients with aortic stenosis and 39 with aortic insufficiency, aged 54.2 +/- 14.3 and 52.6 +/- 16.6 years, respectively. The follow-up period was 2 years. In patients with aortic insufficiency, ejection fraction increased from 54.4 +/- 3.5 preoperatively to 59.6 +/- 3.4 after 6 months and 61.7 +/- 2.7 after 2 years. In patients with aortic stenosis, ejection fraction increased from 56.6 +/- 5.1 preoperatively to 63.9 +/- 4.4 after 6 months and 71.7 +/- 4.1 after 2 years. Geometric remodeling, regression of hypertrophy, and increased ejection fraction of the left ventricle were similar in both groups at 6 months after surgery, but after 2 years of follow-up, greater improvement was found in patients who had undergone valve replacement for aortic stenosis.     

Failure of left ventricular hypertrophy to regress after surgery for aortic valve stenosis

BACKGROUND: Regression of left ventricular (LV) hypertrophy usually follows surgery for aortic stenosis (AS); however, a significant number of ventricles remain hypertrophied. The extent of this phenomenon, the reasons for failure to regress, and its significance are unclear. METHODS: We investigated 43 patients before and after aortic valve surgery and divided them into two groups: 30 patients with regression of LV hypertrophy (Group A) and 13 patients without regression (Group B). Preoperative echocardiographic measurements, clinical status, and operative factors were compared between the two groups. The patients were followed up for 42 +/- 22 months for the occurrence of hospitalization for congestive heart failure (CHF) or death. RESULTS: Preoperatively, the two groups were similar except for an excess of patients in New York Heart Association (NYHA) functional Class IV and a greater incidence of old myocardial infarcts in Group B. Postoperatively, Group B patients had larger LVs with decreased systolic function. This was associated with a poor prognosis (23% mortality and 38% CHF vs 0% and 4% for Group A patients, P = 0.0002). Cox regression analysis showed previous myocardial infarction (P < 0.001) and percent mass reduction (P = 0.019) to be independent predictors of CHF or death. CONCLUSIONS: Successful regression of LV mass is difficult to predict before surgery; however, its absence is related strongly to a poor long-term prognosis.     

Clinical value of regression of electrocardiographic left ventricular hypertrophy after aortic valve replacement

Electrocardiographic left ventricular hypertrophy (ECG-LVH) gradually regressed after aortic valve replacement (AVR) in patients with severe aortic stenosis. Sokolow–Lyon voltage (SV₁ + RV_5/6) is possibly the most widely used criterion for ECG-LVH. The aim of this study was to determine whether decrease in Sokolow–Lyon voltage reflects left ventricular reverse remodeling detected by echocardiography after AVR. Of 129 consecutive patients who underwent AVR for severe aortic stenosis, 38 patients with preoperative ECG-LVH, defined by SV₁ + RV_5/6 of ≥3.5 mV, were enrolled in this study. Electrocardiography and echocardiography were performed preoperatively and 1 year postoperatively. The patients were divided into ECG-LVH regression group (n = 19) and non-regression group (n = 19) according to the median value of the absolute regression in SV₁ + RV_5/6. Multivariate logistic regression analysis was performed to assess determinants of ECG-LVH regression among echocardiographic indices. ECG-LVH regression group showed significantly greater decrease in left ventricular mass index and left ventricular dimensions than Non-regression group. ECG-LVH regression was independently determined by decrease in the left ventricular mass index [odds ratio (OR) 1.28, 95 % confidence interval (CI) 1.03–1.69, p = 0.048], left ventricular end-diastolic dimension (OR 1.18, 95 % CI 1.03–1.41, p = 0.014), and left ventricular end-systolic dimension (OR 1.24, 95 % CI 1.06–1.52, p = 0.0047). ECG-LVH regression could be a marker of the effect of AVR on both reducing the left ventricular mass index and left ventricular dimensions. The effect of AVR on reverse remodeling can be estimated, at least in part, by regression of ECG-LVH.     

超声心动图研究单纯主动脉瓣置换术后左心室的可复性

目的:观察单纯主动脉瓣置换术后左心室形态和功能的可恢复性。方法:回顾分析施行单纯主动脉瓣置换术后49例非心房颤动患者的超声心动图资料。结果:患者术前左室舒张末内径(LVEDD)较对照组明显扩大,LVEDD在术后早期(术后3周~6个月)及术后中期(术后1~2年)均有明显减小。收缩期室间隔厚度及收缩期左室后壁厚度在手术前后差异无统计学意义(P>0.05)。术后早期及中期患者的左室射血分数及短轴缩短分数较术前均明显提高,达正常水平。结论:主动脉瓣置换术促进术前扩大受损的左心室恢复,术后左室射血分数及LVEDD明显改善。     

Degree of reversibility of left ventricular systolic dysfunction after aortic valve replacement for isolated aortic valve stenosis

To determine whether a low preoperative left ventricular (LV) ejection fraction (EF) returns to normal late after aortic valve replacement for aortic stenosis, 42 patients with critical aortic stenosis (valve area 0.7 cm2 or less), LV systolic dysfunction (EF 0.45 or less), angiographically normal coronary arteries, and no other significant valvular disease were studied at 10 to 84 months (mean 41 +/- 21) postoperatively. All patients survived aortic valve replacement and were discharged clinically improved. There were 4 late deaths; these patients were older (79 +/- 6 vs 64 +/- 13 years, p = 0.007) and had lower preoperative mean valve gradients (51 +/- 6 vs 68 +/- 23 mm Hg, p = 0.003) than late survivors. Of 23 survivors who returned for follow-up radionuclide angiography and Doppler echocardiography, 21 were asymptomatic. EF returned to normal (0.50 or more) in 14 patients (group 1) and remained low in 9 patients (group 2). Doppler peak prosthetic valve gradient was 24 +/- 8 mm Hg in group 1 and 25 +/- 10 mm Hg in group 2 (difference not significant). Six of the 9 patients in group 2 underwent early postoperative radionuclide imaging, and LVEF was normal in 4 (0.65 +/- 0.14 early vs 0.41 +/- 0.06 late, p = 0.02). Of 77 preoperative and intraoperative variables analyzed, only paroxysmal nocturnal dyspnea (0 of 14 vs 4 of 9, p = 0.01) distinguished group 1 from group 2. Thus, LVEF does not always normalize after aortic valve replacement for AS, implying impaired myocardial contractility.(ABSTRACT TRUNCATED AT 250 WORDS)     

Severe aortic stenosis with impaired left ventricular function and clinical heart failure: results of valve replacement

Nineteen patients, aged 58-80 years, with severe isolated aortic valve stenosis, severely reduced ejection fraction and clinical heart failure underwent aortic valve replacement between January 1970 and April 1977. Ten had concomitant coronary artery disease (all underwent additional coronary bypass surgery), 17 had angina pectoris and four had syncope. Aortic valve area index was 0.32 +/- 0.03 cm2/m2 (mean +/- SEM); left ventricular (LV) end-diastolic volume index was 117 +/- 9 ml/m2 and LV ejection fraction was 0.37 +/- 0.02. There were four operative deaths and one late death. The follow-up time ranged from six to 74 months (38 +/- 6 months). Actuarially determined three-year survival is 74 +/- 10%; the expected five-year survival is the same. One patient had a serious cerebrovascular accident. Of the remaining survivors, seven were initially Functional Class IV and six Class III; currently, six are Class I and seven Class II (New York Heart Association classifications). The cardiothoracic ratio has decreased from 0.54 +/- 0.03 to 0.49 +/- 0.03. Repeat hemodynamic evaluation has been performed in 10 patients, 22 +/- 6 months after surgery. In these 10 patients, the aortic valve gradient decreased from 55 +/- 7 11 +/- 1.3 mm Hg; LV end-diastolic pressure from 22 +/- 2.4 to 9 +/- 1.9 mm Hg; LV end-diastolic volume index from 119 +/- 16 ml/m2 to 107 +/- 11 ml/m2. LV ejection fraction has increased dramatically from 0.34 +/- 0.03 to 0.63 +/- 0.05 and mean velocity of circumferential fiber shortening from 0.57 +/- 0.08 to 1.3 +/- 0.18 circ/sec. The encouraging long-term survival, improved functional class and the marked improvement in left ventricular function that occurred in our patients indicate that all patients with severe aortic stenosis in clinical heart failure should be offered aortic valve replacement.     

Longitudinal strain predicts left ventricular mass regression after aortic valve replacement for severe aortic stenosis and preserved left ventricular function

We explored the influence of global longitudinal strain (GLS) measured with two-dimensional speckle-tracking echocardiography on left ventricular mass regression (LVMR) in patients with pure aortic stenosis (AS) and normal left ventricular function undergoing aortic valve replacement (AVR). The study population included 83 patients with severe AS (aortic valve area <1 cm²) treated with AVR. Bioprostheses were implanted in 58 patients (69.8 %), and the 25 remaining patients (30.2 %) received mechanical prostheses. Peak systolic longitudinal strain was measured in four-chamber (PLS_4ch), two-chamber (PLS_2ch), and three-chamber (PLS_3ch) views, and global longitudinal strain was obtained by averaging the peak systolic values of the 18 segments. Median follow-up was 66.6 months (interquartile range 49.7–86.3 months). At follow-up, values of PLS_4ch, PLS_2ch, PLS_3ch, and GLS were significantly lower (less negative) in patients who did not show left ventricular (LV) mass regression (all P < 0.001). Baseline global strain was the strongest predictor of lack of LVMR (odds ratio 3.5 (95 % confidence interval 3.0–4.9), P < 0.001), and GLS value ≥?9.9 % predicted lack of LVMR with 95 % sensitivity and 87 % specificity (P < 0.001). Other multivariable predictors were the preoperative LV mass value (cutoff value ≥147 g/m², P < 0.001), baseline effective orifice area index (cutoff ≤0.35 cm²/m², P = 0.01), and baseline mean gradient (cutoff ≥58 mmHg, P = 0.01). Finally, we failed to find interactions between GLS and other significant parameters (all P < 0.05). Global longitudinal strain accurately predicts LV mass regression in patients with pure AS undergoing AVR. Our findings must be confirmed by further larger studies.     

Regression of left ventricular mass one year after aortic valve replacement for pure severe aortic stenosis

The aim of the study was to quantify a 1-year change in left ventricular (LV) mass index (MI) and systolic LV function in 30 patients with pure severe aortic stenosis by means of serial 3-dimensional (3-D) echocardiography. To assess the completeness of LVMI regression after 1 year, we compared the postoperative mass of patients with mass values of 30 normotensive control subjects without a history of cardiac disease. Ejection fraction increased from 64 +/- 14% before surgery to 69 +/- 8% at follow-up (p = 0.067), and functional class improved from 2.9 +/- 0.5 to 1.4 +/- 0.5 (p <0.05), with improvement in each patient. During the same period, LVMI regressed by 23.4% (p <0.001). Postoperative LVMI was related to preoperative LVMI (r = 0.82; p <0.001) and baseline ejection fraction (r = -0.5; p = 0.009). LVMI regressed into the normal range in 64% of patients at follow-up. Patients achieving normal mass values did not differ with respect to patient gender, valve type, or valve size. Patients with reduced preoperative LV function had larger volumes (p <0.01), larger mass values (p <0.01), and a trend toward more mass regression (p = 0.062) than patients with normal preoperative function. Although ejection fraction improved after 1 year in all of these patients (p <0.03), they were less likely to achieve normal mass values at follow-up (p = 0.01). Regression of LVMI in patients with pure aortic stenosis is a positive event that occurs in each patient and that is associated with improvement in functional status. LVMI regressed into the normal range in most patients with normal preoperative function. Preoperative LV function, but not patient gender, valve type, or size, was related to normalization of LVMI at follow-up in this selected study population.     

Extended follow up after isolated aortic valve replacement in the elderly

The present paper reviews the extended follow up of all patients aged >/=70 who underwent isolated aortic valve replacement at our institution in the 1980s. Patients were identified from the surgical database and clinical information was gathered. Long-term follow up information was obtained from the patient, their family, or doctor. Ninety-three patients aged >/=70 years (median 73, range 70-80) comprised the study population. The indication for surgery was aortic stenosis in 68 patients (73%). Fifty-two patients (56%) received an allograft valve, 17 (18%) a bioprosthetic valve, and 24 (26%) a mechanical prosthesis. The median hospital stay was 12 days (range 0-105 days). Five surgical deaths occurred. Detailed follow up was obtained for the 71 patients who died later, and the 16 living patients (one patient lost). The median length of follow up was 6.8 years (range 0.1-18.9 years). Patients who received an allograft aortic valve had a significantly better long-term survival (median 10.6, 95% confidence intervals (CI) 8.1-13.8 years) compared to those receiving mechanical or bioprosthetic valves (median 6.5, 95% CI 4.7-11.9 years), P = 0.03. For the entire group, survival was similar to the age- and sex-matched population. Of the 16 patients alive at follow up (mean age 87, range 83-92), most were free of angina (12, 75%) and heart failure (10, 63%). The conclusion from the current study is that isolated aortic valve surgery in the elderly, particularly with an allograft valve, is associated with an excellent long-term outcome. A survival benefit was demonstrated comparing allograft aortic valve replacement to other valve types.     

Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile.

BACKGROUND: Previous studies have suggested that regression of hypertrophy may be the underlying determinant of longevity and left ventricular function after valve replacement (AVR) for aortic stenosis (AS). The potential for hypertrophy regression could therefore be related to the preoperative risk profile. METHODS: Ninety-one consecutive patients with AS had a "project" Doppler-echo and radionuclide ventriculography in addition to the standard investigation programme prior to AVR with a disc valve (19-29mm, n=82), a caged ball valve (26-29mm, n=8), or a stented porcine valve (26mm, n=1); 49 (group A) were selected for a serial follow-up study while 42 served as controls (group B). Forty-two group A patients took part in a 1.5-year examination while 47 (26 group A, 21 group B) patients were studied at 10 years. RESULTS: Groups A and B were comparable as regards all pre- and intra-operative data including left ventricular mass index (LVMi). A previously developed preoperative prognostic index (PI) separated the patients into groups with low (n=23), intermediary (n=19) and high risk (n=49) with 10-year survivals of 87%, 58% and 43% (P<0.01). LVMi dropped from 202+/-58g/m(2)preoperatively to 152+/-45g/m(2)(P<0.0001) at 1.5 years, and 139+/-40g/m(2)(P<0.0001) at 10 years (three and six patients, respectively, with paravalvular leak or mitral regurgitation excluded). PI correlated with preoperative (r=0.51, P<0.001), 1.5-year (r=0.46, P<0.01), and 10-year LVMi (r=0.41, P<0.01). Also preoperative left ventricular ejection fraction correlated with the three LVMi measurements. Patients with systemic hypertension had higher LVMi at 1.5 years (193+/-42, n=6 vs 144+/-42, n=33, P<0.05) and 10 years (175+/-39, n=12 vs 124+/-31g/m(2), n=29, P<0.001). Patients with low, intermediary or high PI, excluding those with hypertension, had 1.5-year LVMi of 110+/-35 (n=8), 134+/-43 (n=9) and 164+/-33g/m(2)(n=16; P<0.01), respectively, and 10-year LVMi of 116+/-25 (n=17), 126+/-27 (n=6), and 146+/-41g/m(2)(n=6; P<0.05), respectively. There was no relation between LVMi at 1.5 or 10 years and peak or mean Doppler gradient, prosthetic valve size, or valve size index. CONCLUSIONS: Left ventricular hypertrophy regression for patients who survived up to 10 years after AVR for AS is dependent on the preoperative risk profile indicating that irreversible myocardial disease is the underlying factor. Systemic hypertension is an important factor in its own right.     

Prognostic impact of electrocardiographic left ventricular hypertrophy following transcatheter aortic valve replacement

BackgroundLeft ventricular hypertrophy (LVH) develops with both structural and electrical remodeling in response to elevated afterload due to aortic stenosis (AS). This study evaluated the prognostic value of electrocardiographic LVH (ECG LVH) after transcatheter aortic valve replacement (TAVR).MethodsA retrospective study including 157 consecutive patients who underwent TAVR was conducted. ECG LVH was defined as Sokolow–Lyon voltage (S in V₁ + R in V_5/6) before TAVR was ≥3.5mV. We investigated the association between ECG LVH and the 1-year composite outcome comprising all-cause death and rehospitalization related to heart failure. ECG and echocardiographic measurements at 1, 6, and 12 months after TAVR were assessed.ResultsThe baseline characteristics were comparable between the ECG LVH (n = 74) and non-ECG LVH groups (n = 83). The ECG LVH was associated with a significantly greater reduction of Sokolow–Lyon voltage and LV mass index than the non-ECG LVH after TAVR. The absence of ECG LVH was an independent predictor of the 1-year composite outcome [adjusted hazard ratio (HR), 2.27; 95% confidence interval (CI), 1.01 – 5.60; p = 0.04]. Furthermore, a reduction of Sokolow–Lyon voltage from baseline to 1-month follow-up, but not a reduction of LV mass index, was associated with a lower cumulative composite outcome from 1 month to 1 year (adjusted HR, 0.36; 95% CI, 0.15 – 0.86; p = 0.02).ConclusionsECG LVH was associated with a low incidence of adverse clinical outcomes and greater reverse LV remodeling after TAVR. Preprocedural and serial LVH assessment by ECG might be useful in AS patients undergoing TAVR.