Persistent Left Ventricular Hypertrophy Research Articles

S-50-6: HOW TO ASSESS BENEFICIAL EFFECTS OF ANTIHYPERTENSIVE TREATMENTS

Most hypertensive patients could have hypertension mediated organ damage (HMOD) at the moment of the diagnosis. Even in low 10-year cardiovascular risk patients HMOD is frequent. The presence of HMOD is related to increased cardiovascular risk and mortality, so, at the same time HMOD should be considered as a therapeutic target and a surrogate marker of blood pressure un/controlled. The effects of impaired renal function and left-ventricular hypertrophy could identify patients at a mortality very high risk. Guidelines considered arterial stiffening evaluated as high carotid-femoral pulse wave velocity a factor influencing cardiovascular risk, and a documented carotid artery stenosis > 50 % as a marker of very high cardiovascular risk. The Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA) showed that 50% of the participants at risk category one had a mean of one atherosclerotic plaque, and 80.7 % of individuals at category two had a mean of 2.2 atherosclerotic plaques. The hazard ratio of having a vascular event could increase by 50% in the presence of one HMOD and by 3.8 times when three HMOD are present. In this scenario, to prevent that at least some patients could be misclassified as low risk, screening of HMOD as modifiers of cardiovascular risk estimated by different scores could be recommended in hypertensive patients. The non-significant net reclassification improvement of cardiovascular risk and the lack of evidence suggesting a relationship between vascular images biomarkers regression independently of blood pressure lowering and a reduction in cardiovascular events precludes the routine search of arterial stiffness or carotid atherosclerotic plaques out of research scenarios. A reduction in left ventricular mass during treatment is a favorable prognostic marker that predicts lesser risk for subsequent cardiovascular morbidity and mortality. The association between left ventricular mass regression and cardiovascular outcomes is independent of baseline left ventricular mass, baseline clinic and ambulatory blood pressure, and degree of blood pressure reduction. Suboptimal blood pressure control is a significant covariate of persistent left ventricular hypertrophy, independent of the number and class of antihypertensive drugs. RAS blockade is recommended as the initial treatment of hypertension in patients with reduced glomerular filtration rate or albuminuria since they are the most effective at reducing progression to end stage kidney disease, but a combination with calcium channel blockers or diuretics is recommended due to the difficulties to achieve the targets with monotherapy.

585 Natural history of left ventricular hypertrophy in infants of diabetic mothers

Abstract Aims This study sought to describe the characteristics and the natural course of left ventricular hypertrophy (LVH) in a well-characterized consecutive cohort of infants of diabetic mothers (IDMs). Methods and results Sixty consecutive IDMs with LVH have been retrospectively identified and enrolled in the study. All IDMs were evaluated at baseline and every 6 months until LV wall thickness regression, defined as the decrease of wall thickness measurement into the normal reference range for cardiac parameters (z-score > −2 and <2). A comprehensive assessment was performed in those patients with diagnostic markers suggestive of a different cause and/or without significant reduction of the LVH during follow-up. At 1-year follow-up, all IDMs showed a significant reduction of maximal wall thickness MWT [6.00 mm (IQR: 5.00–712) vs. 5.50 mm (IQR: 5.00–6.00), P-value <0.001; MWT-z-score: 4.86 (IQR: 3.93–7.61) vs. 1.72 (IQR: 1.08–2.85), P-value <0.001] compared to baseline, and all patients showed LV wall thickness regression or residual mild or moderate LVH (57%, 28%, and 12%, respectively), except two patients with persistent severe LVH, that after a comprehensive clinical-genetic assessment were diagnosed as Noonan syndrome with multiple lentigines. At multivariate analysis, MWT was negatively associated with LV wall thickness regression at 1-year follow-up [MWT-mm: OR: 0.48 (0.29–0.79), P-value = 0.004; MWT-z-score: OR: 0.71 (0.56–0.90), P-value = 0.004]. Conclusions LVH in IDMs represents a benign condition with complete regression during the first years of life. In those patients without LV wall thickness regression, combined with clinical markers suggesting a specific disease, a complete work-up is required for a definite diagnosis.

Persistent hypertension and left ventricular hypertrophy after repair of native coarctation of aorta in adults

Abstract Background There are limited data about outcomes after repair of native coarctation of aorta (COA) in adulthood. The purpose of this study was to describe the procedural outcomes, hemodynamic improvement, regression of LV hypertrophy and cardiovascular events in adults undergoing repair of native COA. Methods The primary outcomes were procedural complications, re-interventions, and hemodynamic improvement (residual COA gradient <20 mmHg) after COA repair. The secondary outcomes were improvement in the severity of hypertension, regression of left ventricular mass index (LVMI), and incidence of cardiovascular events (atrial fibrillation, heart failure hospitalization, and cardiovascular death) after COA repair. Clinical and imaging indices were assessed pre-intervention, and at 1-year (Y1) and 3-years (Y3) post-intervention. Results A total of 172 patients (age 38 [27–48]) underwent COA repair (surgical 161; transcatheter 11). There were no procedural deaths, and all patients had residual COA gradient <20 mmHg. One patients that received transcatheter stent therapy required re-dilation of stent at 12 months post-intervention. There as a reduction in the prevalence of patients requiring anti-hypertensive therapy from 73% (pre-intervention) to 59% and 64% at Y1 and Y3 respectively. However, 72% and 69% of the patients still had systolic blood pressure >130 mmHg (stage 1 and 2 hypertension) at Y1 and Y3 respectively. As compared to patients without hypertension at Y1, patients with stage 1 and stage 2 hypertension had less robust LVMI regression (% change in LVMI 12±5% vs 9±6% vs 5±3%, p<0.001). Hypertension (HR 1.16, 1.05–1.27) and LVMI regression (HR 0.86, 0.81–0.90) were independently associated with cardiovascular events. Conclusions Persistent hypertension was common after repair of native COA in adults. Hypertension (including stage 1 hypertension) was associated with suboptimal regression of LVMI and cardiovascular events. These results are concerning, and highlight the importance of early COA diagnosis and repair, and optimal medical therapy for hypertension after COA repair. Funding Acknowledgement Type of funding sources: None.

Persistent Hypertension and Left Ventricular Hypertrophy After Repair of Native Coarctation of Aorta in Adults.

[Figure: see text].

LEFT VENTRICULAR HYPERTROPHY REGRESSION DURING ANTIHYPERTENSIVE TREATMENT IN RESISTANT HYPERTENSION PATIENTS

Objective: Objective: to determine the predictors of regression of left ventricular hypertrophy (LVH) in treated resistant hypertensive (RH) patients after 2.1 ± 0.1 years of follow-up. Design and method: We studied 51 patients with RH confirmed by the office and ambulatory blood pressure (BP) monitoring despite the use of 3 antihypertensive medications for at least 3 months. During 2 years-period patients had been treated to 12-week rotations of oral daily treatment with spironolactone, nebivolol, torsemide, eplerenone, moxonidine in addition to their baseline triple-combination. Then participants continued to receive the personal most effective fourth-line agent. Patients were divided into 2 groups: 17 patients had LV mass index (LVMI) which was increased or stayed stable after 2 years (1st group), 34 patients with a reduction of LVMI in 2 years (2nd group). Results: Initially there were no significant differences in sex, duration of hypertension, body mass index, office and average 24-h ambulatory BP between the 2 groups. Compared with the 1st group patients from the 2nd group had a higher prevalence of non-dippers (24.3 vs 65 %, P < 0.001, respectively) and larger baseline LVMI (127.3 ± 4.1 vs 147.8 ± 6.5 g/m2, P < 0.01, respectively). Patients with persistent LVH included more subjects with coronary artery disease, chronic kidney disease and had less baseline active renin concentration (all P < 0.05). After 2 years in both groups office and average 24-h BP levels have been reduced, but goal rates were achieved at 28.6 % patients of the 1st group and 44.1 % patients of the 2nd group (P < 0.05). Reduction in nighttime BP was greater in the 2nd group. Initial higher LVMI (β = 0.655; P < 0.0001), baseline 24-h urinary albumin excretion (β = - 0.475; P < 0.0001), active renin concentration (β = 0.442; P = 0.005) were predictors of δ LVMI in multivariate modeling. Conclusions: Regression of LVH is possible in patients with RH in case of BP control, especially at night. Baseline higher LVMI, an increase of active renin concentration, decline of urinary albumin excretion are factors that determine reversibility LVH.

Persistent Aortic Stiffness and Left Ventricular Hypertrophy in Children of Diabetic Mothers

BackgroundFetuses of diabetic mothers develop left ventricular (LV) hypertrophy and are at increased long-term risk of cardiovascular disease. In our previous longitudinal study from midgestation to late infancy we showed persistence of LV hypertrophy and increased aortic stiffness compared with infants of healthy mothers, the latter of which correlated with third trimester maternal hemoglobin A1c. In the present study, we reexamined the same cohort in early childhood to determine if these cardiovascular abnormalities persisted. MethodsHeight, weight, and right arm blood pressure were recorded. A full functional and structural echocardiogram was performed with offline analysis of LV posterior wall and interventricular septal diastolic thickness (IVSd), systolic and diastolic function, and aortic pulse wave velocity. Vascular reactivity was assessed using digital thermal monitoring. Participants also completed a physical activity questionnaire. ResultsTwenty-five children of diabetic mothers (CDMs) and 20 children from healthy pregnancies (mean age, 5.6 ± 1.7 and 5.3 ± 1.3 years, respectively; P = not significant) were assessed. Compared with controls, IVSd z score was increased in CDMs (1.2 ± 0.6 vs 0.5 ± 0.3, respectively; P = 0.006), with one-fifth having a z score of more than +2.0. Aortic pulse wave velocity was increased in CDMs (3.2 ± 0.6 m/s vs 2.2 ± 0.4 m/s; P = 0.001), and correlated with IVSd z score (R2 = 0.81; P = 0.001) and third trimester maternal A1c (R2 = 0.65; P < 0.0001). Body surface area, height, weight, blood pressure, vascular reactivity, and physical activity scores did not differ between groups. Our longitudinal analysis showed that individuals with greater IVSd, and aortic stiffness in utero, early and late infancy also tended to have greater measures in early childhood (P < 0.001 and P < 0.0001, respectively). ConclusionsCDMs show persistently increased interventricular septal thickness and aortic stiffness in early childhood.

Renin-Angiotensin System Blockade in Aortic Stenosis: Implications Before and After Aortic Valve Replacement.

Aortic stenosis (AS) is a common valvular heart disease in the aging population that is characterized by a variable period of asymptomatic phase before development of symptoms and severe AS. Mortality and morbidity is substantial even after aortic valve replacement, in part related to persistent left ventricular hypertrophy, diastolic dysfunction, and heart failure. Renin‐angiotensin system (RAS) blockade therapy is associated with modulation of adverse left ventricular remodeling, reduction in myocardial hypertrophy, and fibrosis, resulting in clinical improvements in patients with congestive heart failure There are emerging data to suggest benefit of RAS blockade in patients with AS before and after AVR with regard to potentially slower progression of aortic valve calcification, left ventricular mass and survival benefit in favor of RAS blockade group before AVR, and also survival benefit in patients after AVR. We review the available data to understand the role of RAS blockade before AVR and in patients undergoing surgical AVR and transcatheter AVR. There are significant survival advantages of RAS inhibition in patients with AS undergoing surgical AVR or transcatheter AVR. On the basis of existing literature, adequately powered randomized trials are needed to evaluate the role of RAS inhibition in patients with AS.

Effect of persistence of left ventricular hypertrophy and left atrial dilatation after aortic valve replacement on early outcomes and survival: a prospective study

Background: The objective of the study was to evaluate the early outcomes and survival in patients with severe aortic stenosis associated with concentric left ventricular hypertrophy following aortic valve replacement.Methods: This is a prospective study done at SVIMS, Tirupati, from June 2014 to September 2015 evaluating out comes and survival in patients undergoing primary isolated aortic valve replacement (AVR) for severe aortic stenosis, severe aortic stenosis with mild aortic regurgitation and severe aortic stenosis with moderate aortic regurgitation.Results: A total of 40 cases 26 males and 14 females aged 18 to 60 years (mean age, 48.5±13.4 years) underwent elective AVR. Left ventricular end diastolic diameter (p=0.008) at 6 months, a statistically highly significant difference in left ventricular mass preoperatively, at discharge, at 3rd and 6th month follow up. The difference in mean left ventricular mass index (LVMI) had declined from 244.425 to 141.100 at 6 months, showing a statistically highly significant difference in LVMI preop, at discharge, at 3rd month and at 6th month follow up.Conclusions: Patients with preoperative increase in LVMI, with large left atrial diameter carries a strong predictor of postoperative mortality for patients undergoing aortic valve surgery. We also conclude that there will be significant regression of LVMI following successful AVR. But, the decrease in LVMI is maximum during early three months and it is minimal though significant in the later course of follow up.

Donor Left Ventricular Hypertrophy: Over-Rated or Does Donor History of Hypertension Make a Difference for Post-Heart Transplant Outcome?

Purpose Donor left ventricular hypertrophy (LVH) defined as either the interventricular septum (IVS) or posterior wall (PW) > 1.2 cm has been a concern for donor heart acceptance for transplantation. Cardio-pulmonary resuscitation (CPR) with chest compressions may also cause edema within the IVS and PW. It is not clear whether LVH due to a history of hypertension (HTN) in the donor or LVH due to edema from CPR have the same outcome after heart transplantation. Methods Between 2014 and 2017, we assessed 54 heart donors with LVH > 1.2 cm. We divided these donor hearts into those with a history of HTN (n=19) and those without (n=35). Post-operatively, we assessed for the presence of primary graft dysfunction (PGD), 1-year freedom from any-treated rejection (ATR), acute cellular rejection (ACR), and antibody-mediated rejection (AMR), 1-year freedom from cardiac allograft vasculopathy (CAV) as defined by stenosis ≥ 30% by angiography, and 1-year survival. We also assessed for the persistence of LVH at 6 and 12 months post-transplantation. Results There was no significant difference between LVH donors with and without a history of HTN in PGD, 1-year survival and 1-year freedom from CAV, ATR, ACR and AMR. LVH donors with HTN were older than those without HTN. LVH in donors with and without a history of HTN resulted in similar rates of LVH persistence at 6 and 12 months after transplantation. The persistence of LVH at 1 year was similar between the groups. (see table) Conclusion Donor heart LVH and history of HTN does not increase the risk of poor outcome after heart transplantation. Acceptable survival and resolution of LVH (occurs in most patients) indicates that LVH is well tolerated and may not be a concern in donor heart selection. Larger studies will be needed to confirm these findings.

THE EFFECT OF CAREER PLAYING POSITION AND DETRAINING TIME ON THE PREVALENCE AND PERSISTANCE OF LEFT VENTRICULAR HYPERTROPHY IN A POPULATION OF FORMER PROFESSIONAL FOOTBALL PLAYERS

Left ventricular hypertrophy (LVH) is recognized as a component of athlete's heart and has been widely reported in elite athletes. However, there are few reports on the prevalence and persistence of LVH in elite athletes following retirement. Former professional football players (n = 1172) were

Left ventricular mass regression after aortic valve replacement: Sex differences or effect of different methods of indexation?

The influence of sex on regression of left ventricular (LV) hypertrophy (LVH) after aortic valve replacement (AVR) for aortic stenosis (AS) remains elusive. The lack of consensus on how to correct LV mass (LVM) for body size, and different normalcy values, contribute to inconclusive results. In 164 consecutive patients (mean age 80±4years, 59% females) with AS, we analyzed LVM (Devereux formula) before and 1year after AVR (St.Jude Trifecta bio-prosthesis). LVM was indexed to BSA (Du Bois and Gehan formulas), to height1.7 and height2.7 . Limits of normalcy were (women and men, respectively): <95 and <115g/m², BSA-indexed LVM; <60 and <81g/m, LVM/height1.7 ; <44 and <48g/m, LVM/height2.7 . Women had smaller BSA, but not body mass index, than men. AS severity and incidence of hypertension did not differ. LVM indexed to height2.7 was greater in women. LVH incidence was similar in males and females. Independently of the indexation method, LVH reduced significantly (P<0.0001). LVM reduction was greater in women (P<0.05 for all methods). At follow-up, nearly half the patients, irrespective of sex, showed residual LVH, and diastolic dysfunction. We tested different methods of LVM indexation in AS patients. LVM was similar between men and women. Indexation to height2.7 gives higher LVM in women because of their shorter stature. LVH prevalence is independent of sex. Irrespective of the indexation method, LVM reduction is greater in females, whereas LVM normalization occurs in equal proportion. Persistent LVH and diastolic dysfunction suggest earlier AVR in elderly.

OP.7B.02] LONG TERM CHANGES IN LEFT VENTRICULAR MASS

Objective We sought to perform a comprehensive assessment of long-term changes in left ventricular (LV) mass, focusing on new onset, persistence, regression and severity of LV hypertrophy (LVH), as well as independent demographic and clinical variables related to this dynamic process in a population-based sample. Design and method A total of 1,113 participants with measurable echocardiographic parameters at baseline evaluation and at the end of a ten-year follow-up period were included in the present analysis. Cut-points for LVH were derived from current echocardiographic guidelines Results LVH prevalence significantly increased from 13% to 33%, as a consequence of new onset LVH in 254 and regression in 31 cases, respectively. Severe LVH increased about 1.8 times as compared to baseline and this trend was mainly related to the transition from mild and moderate to severe LVH in subjects with pre-existing cardiac hypertrophy. A number of baseline variables such as age, female gender, office and out-of-office systolic BP, body mass index, ATP 3 metabolic syndrome, and use of antihypertensive drugs were independently correlated either to new-onset and persistent LVH. Conclusions Long-term LV mass changes in the general population are associated to a marked worsening in cardiovascular risk profile related to increased prevalence and severity of LVH. As BP, metabolic variables and BMI emerged as key correlates of a such dynamic process, our findings suggest that early interventions aimed to modify such risk factors at the community level may have a role in preventing new onset and progression LVH.

Full-root Aortic Valve Replacement by Stentless Aortic Xenografts in Patients with Small Aortic Roots.

In patients with small aortic roots who need an aortic valve replacement with biological valve substitutes, the implantation of the stented pericardial valve might not meet the functional needs. The implantation of a too-small stented pericardial valve, leading to an effective orifice area indexed to a body surface area less than 0.85 cm2/m2, is regarded as prosthesis-patient mismatch (PPM). A PPM negatively affects the regression of left ventricular hypertrophy and thus the normalization of left ventricular function and the alleviation of symptoms. Persistent left ventricular hypertrophy is associated with an increased risk of arrhythmias and sudden cardiac death. In the case of predictable PPM, there are three options: 1) accept the PPM resulting from the implantation of a stented pericardial valve when comorbidities of the patient forbid the more technically demanding operative technique of implanting a larger prosthesis, 2) enlarge the aortic root to accommodate a larger stented valve substitute, or 3) implant a stentless biological valve or a homograft. Compared to classical aortic valve replacement with stented pericardial valves, the full-root implantation of stentless aortic xenografts offers the possibility of implanting a 3-4 mm larger valve in a given patient, thus allowing significant reduction in transvalvular gradients. However, a number of cardiac surgeons are reluctant to transform a classical aortic valve replacement with stented pericardial valves into the more technically challenging full-root implantation of stentless aortic xenografts. Given the potential hemodynamic advantages of stentless aortic xenografts, we have adopted full-root implantation to avoid PPM in patients with small aortic roots necessitating an aortic valve replacement. Here, we describe in detail a technique for the full-root implantation of stentless aortic xenografts, with emphasis on the management of the proximal suture line and coronary anastomoses. Limitations of this technique and alternative options are discussed.

PS 17-32 VARIABLES ASSOCIATED TO LACK OF LEFT VENTRICULAR HYPERTROPHY REGRESSION IN TREATED HYPERTENSIVE PATIENTS

Objective: Left ventricular hypertrophy (LVH) is an independent cardiovascular high risk predictor in hypertension (HBP) and its regression favorably affects the prognosis. The aim of this study is to determine the variables associated to lack of LVH regression in treated HBP patients (p). Design and method: Consecutive HBP p on at least 4 weeks stable treatment with LVH were included. Follow up for at least one year. Left ventricular mass index (LVMI) was measured by Devereux method at baseline and at follow up. LVH was considered > 95 g/m2 in women and > 115 g/m2 in men. Sixty demographic, anthropometric, cardiovascular risk factors, 2-D ultrasonographic, tissue Doppler, central aorta and peripheral hemodynamics, ABPM, laboratory and treatment variables were included in the algorithm. STATISTICAL ANALYSIS: Students t test, odds ratio, multivariate analysis; p < 0.05 considered statistically significant. Results: 188 treated HBP p included, follow up 588+-289 days. Sample mean age was 63.1+-13.8 years, 80 p (42.6%) were males. 144 p showed LVH regression (R) while 44 p (23.4%) persistent (P) LVH. Baseline LVMI was 113.2+-16.1 g/m2 in R LVH p and 118.5+-20.5 g/m2 in P LVH p (p=NS); follow up LVMI was 85.2+-17.6 g/m2 in R LVH p and 115.6+-14.1 g/m2 in P LVH p (p = 0.0005). 140 p (97.2%) decreased 1 SD and 48 p (33.3%) 2 SD LVMI in R LVH p while 4 p (9.1%) decreased 1 SD and 0 p (0%) 2 SD LVMI in P LVH p (p < 0.0005). Framingham score risk > 20% (OR 3.07; 95 % CI 1.55–6.06; p < 0.025), metabolic syndrome (OR 2.14; 95 % CI 1.08–4.25; p < 0.025); and high central aortic pressure (OR 2.80; 95 % CI 1.04–7.51; p < 0.005) were predictors of LVH P. Conclusions: 1) One over four treated HBP LVH p did not show regression; 2) High risk Framingham score, metabolic syndrome and central aortic pressure are LVH P predictors.

Relevance of residual left ventricular hypertrophy after surgery for isolated aortic stenosis

Persistent left ventricular (LV) hypertrophy after surgery is frequent, but its clinical relevance is controversial. We evaluated if residual LV hypertrophy (LVH) is associated with clinical outcomes after aortic valve replacement (AVR) for severe aortic stenosis (AS). We analysed clinical and echocardiographic parameters before and after AVR, in a prospective cohort of 132 patients with severe AS. The mean follow-up was 6.0 ± 1.5 years. Clinical endpoints were all-cause death and combination of as in all-cause death and non-fatal cardiovascular hospitalization. At AVR, myocardial biopsies for collagen volume fraction (CVF) evaluation were done in 56 random patients. Residual LVH was present in 44% of patients after AVR. Patients with residual LVH were older, more frequently women and had hypertension (HT). Preoperatively, they had higher LV mass indices (LVMI), higher E/e' and left atrial volume indices, as well as lower peak systolic annular velocity. Female gender, HT, LVMI and E/e' were independent predictors of persistent LVH. CVF at the time of surgery was higher in those with residual LVH (20.0 ± 14.6 vs 13.2 ± 11.5%, P = 0.027). The risk of all-cause death and non-fatal cardiovascular hospitalization was higher in patients with residual LVH [OR 2.89 (95% CI 1.12-7.44); P = 0.035], but there were no differences in all-cause mortality. Residual LVH was associated with a worse outcome in women but not in men. Residual LVH after AVR is common and is associated with worse prognosis, particularly in women. In addition, HT, higher baseline LVM and worse diastolic dysfunction can help to identify patients at risk for incomplete normalization of LVM.

Relationship of left ventricular systolic function to persistence or development of electrocardiographic left ventricular hypertrophy in hypertensive patients: implications for the development of new heart failure.

Persistence or development of ECG left ventricular hypertrophy (LVH) by Cornell product criteria is associated with an increased risk of developing heart failure compared with regression or continued absence of LVH. We postulated that this association might be in part mediated via worse left ventricular systolic function in patients with new or persistent ECG LVH. Baseline and year-3 ECG LVH and left ventricular midwall shortening (MWS) were examined in 725 hypertensive patients in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy. Sex-specific criteria were used for abnormal MWS (<14% in men and <16% in women) and abnormal stress-corrected MWS (scMWS; <87% in men and <90% in women). Cornell product LVH greater than 2440 mm ms defined ECG LVH. Between baseline and year-3 follow-up, there was continued absence or regression of ECG LVH in 427 patients and persistence or development of new LVH in 298 patients. At baseline, although there were no significant differences in the mean values of MWS and scMWS, patients with persistence or development of ECG LVH at year 3 had significantly higher baseline prevalences of abnormal MWS (41.9 vs. 30.2%, P = 0.001) and abnormal scMWS (27.4 vs. 20.5%, P = 0.034). At year-3 follow-up, persistence or development of new LVH was associated with significantly lower mean MWS (16.5 ± 2.3 vs. 17.2 ± 1.9%, P < 0.001) and scMWS (104.2 ± 13.1 vs. 106.5 ± 10.9%, P = 0.005), and with higher prevalence and odds of abnormal MWS [23.8 vs. 10.8%, P < 0.001, odds ratio (OR) 2.50, 95% confidence interval (CI) 1.66-3.75, P < 0.001] and abnormal scMWS (11.0 vs. 5.8%, P = 0.011, OR 2.02, 95% CI 1.16-3.51, P = 0.013). After controlling for differences in age, sex, race, treatment group, baseline and change from baseline to year 3 of heart rate, Sokolow-Lyon voltage, systolic and diastolic pressure and baseline severity of LVH by Cornell product, persistent or new ECG LVH remained associated with two-fold increased odds of abnormal MWS (OR 2.20, 95% CI 1.39-3.47, P = 0.001) or scMWS (OR 1.90, 95% CI 1.03-3.50, P = 0.040) at year 3. Persistence or development of new ECG LVH during antihypertensive therapy is associated with an increased risk of left ventricular systolic dysfunction after 3 years' follow-up. These findings provide insight into a possible mechanism by which changes in ECG LVH are associated with the changing risk of developing heart failure. http://clinicaltrials.gov/ct/show/NCT00338260?order=1.

Effect of Kidney Transplantation On Left Ventricular Remodeling and Risk Factors for Posttransplant Left Ventricular Hypertrophy.

Introduction: Cardiovascular disease is a leading cause of mortality in patients with end-stage renal disease, even undergoing transplantation. Left ventricular hypertrophy (LVH) is the most common feature and an independent risk factor for cardiac complications in kidney transplant recipients. The aim of this study was to identify cardiac alteration after kidney transplantation and analyze predictors of the post-transplant LVH. Methods: Among 2957 kidney transplant recipients in a multicenter cohort from 1997 to 2012, a total of 206 patients who conducted echocardiography before and one year after transplantation were enrolled in this study. Echocardiographic findings and clinical parameters were evaluated. Results: Kidney transplantation significantly reduced mean left ventricular mass index (LVMI) from 128.8±47.2g/m<sup style=“font-family: ‘Times New Roman’, serif; line-height: 150%; text-indent: 6pt;”>2[/sup] to 106.4±33.0g/m<sup style=“font-family: ‘Times New Roman’, serif; line-height: 150%; text-indent: 6pt;”>2 [/sup](p<0.001).Figure: No Caption available.The ejection fraction was improved (59.4±8.0% vs. 62.1±6.7%, p<0.001). The prevalence of LVH by echocardiography significantly decreased (62.6% vs. 46.1%, p=0.001). The prevalence of diastolic dysfunction, mitral and tricuspid regurgitation, and pulmonary hypertension also decreased. Pre-transplant lower hemoglobin level (OR 0.74, 95% CI 0.56-0.96, p=0.026) and pre-transplant higher LVMI (OR 1.02, 95% CI 1.01-1.02, p<0.001) were independently associated with persistent LVH after kidney transplantation. On the other hand, ejection fraction, diastolic dysfunction, underlying renal disease, albumin or cholesterol level, blood pressure, rejection, and allograft function were not correlated with post-transplant LVH. Conclusions: Cardiac morphology and function were significantly improved by kidney transplantation. Treatment of anemia might be crucial in regression and prevention of persistent LVH in kidney transplant recipients.

Left Ventricular Hypertrophy and Antiarrhythmic Drugs in Atrial Fibrillation: Impact on Mortality

Despite sparse clinical data, current atrial fibrillation (AF) guidelines favor amiodarone as a drug of choice for patients with left ventricular hypertrophy (LVH). This study tested the hypothesis that patients with persistent AF and LVH on nonamiodarone antiarrhythmics have higher mortality compared to patients on amiodarone. In an observational cohort analysis of patients who underwent cardioversion for AF, patients with LVH, defined as left ventricular wall thickness ≥1.4 cm, by echocardiogram prior to their first cardioversion, were included; clinical data, including antiarrhythmic drugs and ejection fraction (LVEF), were collected. Mortality, determined via the Social Security Death Index, was analyzed using Kaplan-Meier and Cox proportional hazards models to determine whether antiarrhythmic drugs were associated with higher mortality. In 3,926 patients, echocardiographic wall thickness was available in 1,399 (age 66.8 ± 11.8 years, 67% male, LVEF 46 ± 15%, septum 1.3 ± 0.4, posterior wall 1.2 ± 0.2 cm), and 537 (38%) had LVH ≥1.4 cm. Among 537 patients with LVH, mean age was 67.5 ± 11.7 years, 76.4% were males, and mean LVEF was 48.3 ± 13.3%. Amiodarone was associated with lower survival (log rank P = 0.001), including after adjusting for age, LVEF, and coronary artery disease (P = 0.023). In propensity-score matched cohorts with LVH treated with no drugs, nonamiodarone antiarrhythmic drugs (non-AADs), or amiodarone (N = 65 each group), there was early lower survival in patients on amiodarone (P = 0.05). Patients with persistent AF and LVH on non-AADs do not have higher mortality compared to patients on amiodarone. Importantly, these findings do not support amiodarone as a superior choice in patients with LVH.

Abstract 18185: Regression of Severe Left Ventricular Hypertrophy After Transcatheter Valve Replacement for Aortic Stenosis: Impact on Clinical Outcomes in PARTNER Cohort A

Background: Left ventricular (LV) mass regression after aortic valve replacement (AVR) for aortic stenosis (AS) is a favorable effect of LV unloading, but its relationship to improved clinical outcomes is unclear. We examined the effect on clinical outcomes after transcatheter AVR (TAVR) of: 1) amount of LV mass index (LVMi) regression; and 2) persistent severe LV hypertrophy (LVH). Methods: Of 2115 patients with symptomatic AS at high surgical risk receiving TAVR in the PARTNER randomized trial or continued access registry, 462 (55% women) who had severe LVH (LVMi ≥149 g/m 2 men, ≥122 g/m 2 women, by ASE criteria) at baseline (BL) and LVMi measured 6 mo post-TAVR were included in our analysis. The effect of LVMi regression was evaluated by comparing outcomes in patients with greater vs. lesser decrease (dichotomized by median % change) in LVMi between BL and 6 mo, and in those without vs. with persistent severe LVH 6 mo post-TAVR. Cox PH models evaluated rates of all-cause mortality (6-12 mo), rehospitalizations (through 1 yr), and the composite of these two outcomes. Results: LVMi decreased from 173±32 (BL) to 121±25 g/m 2 (6 mo) (p&lt;0.001) in those with greater LVMi regression, and from 164±30 (BL) to 158±34 g/m 2 (6 mo) (p&lt;0.001) in those with lesser LVMi regression. Patients with greater vs. lesser LVMi regression had similar baseline clinical characteristics, a lower rate of rehospitalization (10.5% vs. 19.9%, p=0.006) and lower rate of the composite endpoint of death or rehospitalization (13.2% vs. 21.4%, p=0.02), but a similar rate of death (4.9% vs. 4.8%, p=0.86). Persistent severe LVH at 6 mo post-TAVR was present in 54% (58% of whom were women). Patients without vs. with persistent severe LVH had similar baseline clinical characteristics, a lower rate of rehospitalization (11.9% vs. 18.1%, p=0.053) and lower rate of the composite endpoint of death or rehospitalization (13.3% vs. 20.7%, p=0.03), but a similar rate of death (3.9% vs. 5.7%, p=0.42). Similar results were obtained when including patients with moderate or severe LVH. Conclusions: In high-risk patients with severe AS and severe LVH undergoing TAVR, greater LV mass regression and resolution of initially severe LVH at 6 months are associated with a lower rate of death or repeat hospitalization.

Prevalence and Significance of Late Gadolinium Enhancement in Children and Adolescents With Hypertrophic Cardiomyopathy

s S97 BACKGROUND: We have previously shown that infants of diabetic mothers (IDM) have increased aortic stiffness in the first 6 months of life, and aortic stiffness is related to poor maternal glycemic control in pregnancy. Increased left ventricular (LV) posterior (LVPW) and interventricular septal (IVS) wall thickness is observed in IDM in late gestation and early infancy, predominantly in mothers with worse glycemic control. Although it is generally believed that the LV hypertrophy in IDM regresses after the first 3 months, we have recently shown that hypertrophy persists even in late infancy. In this study we sought to explore the relationship between aortic stiffness and LV hypertrophy in IDM. We hypothesized that LVPW and IVS wall thickness would be greater in infants with greater aortic stiffness. METHODS: Diabetic pregnancies were prospectively recruited in the mid trimester. Their infants were evaluated in infancy by echocardiography. LVPW and IVS wall thickness was measured by m mode and measurements were compared to normative data for the calculation of z scores based on body surface area. Aortic wall stiffness was assessed with echocardiography, using 2D and pulsed Doppler interrogation of the ascending aorta and distal arch. Aortic pulse wave velocity (PWV) was calculated as the distance from the ascending aorta to distal arch, divided by the time interval from the QRS to the onset of flow for the two interrogated sites (m/s). RESULTS: Twenty-one IDM were investigated at a median age of 7 weeks (range 2-48 weeks). Mean aortic PWV was 4.7 1.7m/s, and the mean IVS and LVPW z scores were 1.3 1.2 and LVPW 1.4 1.1, respectively. Although no relationship was observed between PWV and IVS, there was a weak but positive correlation between aortic PWV and LVPW z score (r1⁄40.50, p1⁄40.027). CONCLUSION: Our study suggests that a potential relationship exists between the degree of stiffness of the aorta and LV wall thickness. This could be due to a common prenatal exposure (hyperglycemia) or to a causal relationship (greater aortic stiffness leading to evolution or persistence of LV hypertrophy). Further studies are underway to determine the etiology of increased aortic stiffness and LV hypertrophy and the natural course of these changes. 025 PREVALENCE AND SIGNIFICANCE OF LATE GADOLINIUM ENHANCEMENT IN CHILDREN AND ADOLESCENTS WITH HYPERTROPHIC CARDIOMYOPATHY L Grosse-Wortmann, J Windram, D Andreea, S Yoo, L Mertens, D Wong, L Benson