Mean Left Ventricular End-diastolic Dimension Research Articles

Phenotype of left ventricular remodeling in heart failure with preserved ejection fraction and its impact on all-cause mortality

Abstract Background/Introduction Heart failure with preserved ejection fraction (HFpEF) refers to a heterogeneous group of patients with unexplored subtypes in terms of a guide to treatment or prognosis. Left ventricular (LV) remodeling is very important as not only an index of structural and functional changes, but also a prognosticator in HF patients. Aims To investigate whether patients with HFpEF can be classified into subgroups by degree of LV remodeling and whether it is related to survival. Methods Patients with HFpEF in the China Heart Failure Center Registry (an ongoing large, nationwide, multicenter registry enrolling the admitted HF patients from secondary and above hospitals since 2017) who had data on the in-hospital LV end-diastolic dimension (LVEDD), ejection fraction (LVEF) by echocardiography, and the 1-year survival were recruited. Patients with major structural heart diseases were excluded. The primary endpoint was all-cause mortality during 1 year after discharge. Kaplan-meier survival curve and Cox regression analysis were adopted to compare among the patients stratified by the LVEDD and LVEF. Results A total of 29727 patients with HFpEF (mean age 73±12 years, 51.3% male) were included, of whom 69.8% was in hypertension, 30.4% in diabetes, 37.3% in atrial fibrillation or flutter, and 14.1% in chronic kidney disease. The mean LVEF of the study population was 60±6%. When the patients were divided into 5 groups as every 5% increase in the LVEF, the risk of all-causemortality was increased in the groups of 50-54% [23.3% patients, age- and gender-adjusted hazard ratio (HR)=1.414, p<0.001] and55-59% (28.8%,1.281, p=0.001), while not different in the groups of 60-64% (26.1%,1.056, p=0.493) and 65-69% (14.3%,0.969,p=0.720) when compared with the group of ≥70% (7.6%) as the reference (Figure 1a). The mean LVEDD was 48±7mm. When the patients were divided into 6 groups as every 5mm increase in the LVEDD, the groups of <40mm (7.7% patients, age-and gender-adjusted HR=1.548, p<0.001) and ≥60mm (5.3%, 1.509, p<0.001) had the highest risk ofmortality, followed by the group of 40-44mm (22.2%,1.214, p=0.001), while the groups of 45-49mm (33.0%,0.991, p=0.863) and 55-59mm (10.0%,1.100, p=0.200) had similar risk when compared with the group of 50-54mm (21.7%) as the reference (Figure 1b). Furthermore, the patients were divided into 8 phenotypes of LV remodeling by using the LVEDD (<40mm, 40-44mm, 45-59mm, ≥60mm) and the LVEF divisions (<60%, ≥60%). When the phenotype of LVEDD of 45-59mm and LVEF of ≥60% taken as the reference, all other phenotypes had an increased risk of death by age and sex adjusted Cox regression analysis (Table1). Conclusion(s) Both the LVEF and LVEDD can provide risk stratification for patients with HFpEF. Those patients with a LVEDD of mid-ranged 45-59mm and a high LVEF ≥60% had the lowest risk of mortality. This concept of phenotyping HFpEF by LV remodeling could be considered in future clinical practice and research.KM survival stratified by EF and EDDRisk of death stratified by EF&EDD

Relationship between enlarged cardiac silhouette on chest X-ray and left ventricular size on transthoracic echocardiography.

The diagnostic accuracy of the cardiothoracic ratio on chest X-ray to detect left ventricular (LV) enlargement has not been well defined despite its traditional association with cardiomegaly. We aimed to determine whether the cardiothoracic ratio can accurately predict LV enlargement based on indexed linear measurements of the LV on transthoracic echocardiography (TTE). We included consecutive patients who had a TTE and a posteroanterior chest X-ray performed within 90days of each other at a tertiary care center. LV size was determined by measuring the LV end-diastolic dimension (LVEDD) and LV end-diastolic dimension indexed (LVEDDI) to body surface area. The cardiothoracic ratio was calculated by dividing the maximum transverse diameter of the cardiac silhouette by the maximum transverse diameter of the right and left lung boundaries. 173 patients were included in the study (mean age 68 ± 15years, 49.1% female). Mean cardiothoracic ratio was 0.56 ± 0.09, and the mean LVEDD and indexed LVEDDI were of 47 ± 8.6mm and dimension of 27 ± 4.5mm/m2 respectively. There was no significant correlation between the cardiothoracic ratio measured on chest X-ray and either the LVEDD or LVEDDI measured on TTE (r = 0.011, p = 0.879; r = 0.122, p = 0.111). The ability of the cardiothoracic ratio to predict LV enlargement (defined as LVEDDI > 30mm/m2) was not statistically significant. The cardiothoracic ratio on chest X-ray is not a predictor of LV enlargement based on indexed linear measurements of the LV by TTE.

Clinical impact of pulmonary artery to aorta diameter ratio on left ventricular reverse remodeling in patients with dilated cardiomyopathy

Abstract Background Left ventricular reverse remodeling (LVRR) is an important predictor for a good prognosis in patients with dilated cardiomyopathy (DCM). Previous reports indicated the pulmonary artery diameter (PAD) to ascending aortic diameter (AoD) ratio as a predictor of adverse outcomes in heart failure patients. However, the impact of the PAD/AoD ratio for predicting LVRR in patients with DCM is unknown. Aim The aim of this study is to investigate the association between PAD/AoD ratio and LVRR in patients with DCM. Methods From a prospective study, clinically stable DCM patients who were investigated the LVRR on echocardiography and underwent CT at baseline were enrolled. LVRR is defined as left ventricular (LV) ejection fraction increase of 10% and a decrease in indexed LV end-diastolic diameter of 10% compared to those at baseline. PAD and AoD data was collected with nonenhanced computed tomography images at baseline. Results In sixty-nine patients (mean age 50.0±13.3 years), the mean LV ejection fraction was 29.8%, and mean LV end-diastolic dimension was 64.5mm, and both of which data was no significant difference between patients with or without LVRR. LVRR was observed in 23 (33.3%) patients. The PAD/AoD ratio was significantly lower in patients with LVRR than without LVRR (81.4% vs. 92.4%, p=0.003). By ROC analysis, the best cut-off for the detection of LVRR was found for a PAD/AoD ratio of 0.9. From multivariate analyses, PAD/AoD ratio was identified as a significant predictor of LVRR. After a median follow-up duration of 2.5 years, the DCM patients with PAD/AoD≥0.9 revealed a significant higher cardiac event than those with PAD/AoD<0.9 (log-rank, p=0.007) Conclusions The PAD/AoD ratio is useful for predicting LVRR in patients with DCM. The DCM patients with high PAD/AoD ratio had a poor long-term outcome. Funding Acknowledgement Type of funding sources: None. ROC curve for LVRR predictionKaplan-Meier survival curves

A clinical score for predicting left ventricular reverse remodelling in patients with dilated cardiomyopathy.

AimsLeft ventricular reverse remodelling (LVRR) is a well‐established predictor of a good prognosis in patients with dilated cardiomyopathy (DCM). The prediction of LVRR is important when developing a long‐term treatment strategy. This study aimed to assess the clinical predictors of LVRR and establish a scoring system for predicting LVRR in patients with DCM that can be used at any institution.Methods and resultsWe consecutively enrolled 131 patients with DCM and assessed the clinical predictors of LVRR. LVRR was defined as an absolute increase in left ventricular ejection fraction (LVEF) from ≥10% to a final value of >35%, accompanied by a decrease in left ventricular end‐diastolic dimension (LVEDD) ≥ 10% on echocardiography at 1 ± 0.5 years after a diagnosis of DCM. The mean patient age was 50.1 ± 11.9 years. The mean LVEF was 32.2 ± 9.5%, and the mean LVEDD was 64.1 ± 12.5 mm at diagnosis. LVRR was observed in 45 patients (34%) at 1 ± 0.5 years. In a multivariate analysis, hypertension [odds ratio (OR): 6.86; P = 0.002], no family history of DCM (OR: 10.45; P = 0.037), symptom duration <90 days (OR: 6.72; P < 0.001), LVEF <35% (OR: 13.66; P < 0.0001), and QRS duration <116 ms (OR: 5.94; P = 0.005) were found to be independent predictors of LVRR. We scored the five independent predictors according to the ORs (1 point, 2 points, 1 point, 2 points, and 1 point, respectively), and the total LVRR predicting score was calculated by adding these scores. The LVRR rate was stratified by the LVRR predicting score (0–2 points: 0%; 3 points: 6.7%; 4 points: 17.4%; 5 points: 48.2%; 6 points: 79.2%; and 7 points: 100%). The cut‐off value of the LVRR predicting score was >5 in receiver‐operating characteristic curve analysis (area under the curve: 0.89; P < 0.0001; sensitivity: 87%; specificity: 78%). An LVRR predicting score of >5 was an independent predictor compared with the presence of late gadolinium enhancement on cardiovascular magnetic resonance or the severity of fibrosis on endomyocardial biopsy (OR: 11.79; 95% confidence interval: 2.40–58.00; P = 0.002).ConclusionsThe LVRR predicting score using five predictors including hypertension, no family history of DCM, symptom duration <90 days, LVEF <35%, and QRS duration <116 ms can stratify the LVRR rate in patients with DCM. The LVRR predicting score may be a useful clinical tool that can be used easily at any institution.

Cardiac hypertrophic risk markers of left ventricle and left atrium in chronic heart failure due to aortic and mitral valve disease.

Chronic valvular heart disease leads to systolic dysfunction and left atrial enlargement that ultimately results in heart failure. To investigate prognostic importance of Echocardiography and plasma natriuretic peptide levels that increase as a compensatory response and can be used as predictive markers for cardiac hypertrophy. The patients were divided into three groups: 51 with left ventricle hypertrophy due to aortic valve disease; 126 with left atrial enlargement due to mitral valve dysfunction; and 76 with both conditions. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) plasma levels were measured in all three respective groups showing dilated cardiomyopathy. The mean left ventricular end-diastolic dimension at 64.3 ± 1.6 mm (P < 0.00) and left atrial dimension at 58.3 ± 3.7 mm (P < 0.00) were significantly high. However, patients with both conditions showed significantly high values for left ventricular end-diastolic dimension (63.3 ± 3 mm, P < 0.00) and left atrial dimension (54.9 ± 4 mm, P < 0.00) when compared with controls. A significant positive correlation was found between plasma natriuretic peptides levels and dilated cardiomyopathy. The mean values of ANP were 173 ± 46.6 pg/mL (P < 0.00), 140.4 ± 42.4 pg/mL (P < 0.00), and 295.1 ± 67.5 pg/mL (P < 0.00), significantly high in all three respective disease groups. The levels of BNP were also significantly high at 189 ± 44.5 pg/mL (P < 0.00), 166.6 ± 36.6 pg/mL (P < 0.00), and 323 ± 69.1 pg/mL (P < 0.00) in the disease groups with left ventricular hypertrophy, left atrial enlargement, and the disease group showing both characteristics, respectively. Significant positive associations were found between left ventricle hypertrophy and left atrial enlargement with ANP and BNP.

Retrograde transcatheter closure of perimembranous aneurysmal ventricular septal defects using amplatzer vascular plug II

Introduction Retrograde transcatheter closure of perimembranous aneurysmal ventricular septal defects (pmVSD) can be a better option for transcatheter closure of ventricular septal defect with device placement into ventricular septal aneurysm with fewer complications. Also, a retrograde approach might decrease procedure time and radiation exposure time. Aim The purpose of this study was to report off-label experience using Amplatzer Vascular Plug II (AVPII) for the trans catheter closure of perimembranous aneurysmal VSD. Comparison of haemodynamic effects of ketamine and sevofluorane as in induction of anesthesia. Materials and methods Our series consists of a fifteen child with pmVSD. The mean age was 4.9 years (range: 1.2–10 years), mean left ventricular end-diastolic dimension 38.3 mm. Maximum and minimum defect sizes were 4 and 8 mm by transthoracic echocardiography (mean defect size: 5.2 mm). The procedure was performed under general anesthesia with left heart catheterization for retrograde closure of the defect. The study was done on 15 children from 2016 to 2018 for retrograde transcatheter closure of aneurysmal perimembrance VSDs using an Amplatzer vascular plug II Baseline characteristics of the study patients are set in Table I. All the children who had aneurysmal perimembrance outlet ventricular septal defect with left to right shunt were included for assessment of closure. The children eligiable underwent clinical evaluation that also included electrocardiogram (ECG), and standard echocardiography assessment. Results All participants who met the inclusion criteria were sent to the catheterization laboratory. Following left ventricular angiogram, three patients were excluded as technically nonfeasible. Failure to cannulate the defect in one patient and deficient aneurysmal tissue during left ventricular angiography in two cases. The device was successfully deployed in 12 children with the retrograde technique. In two patients antegrade approach was used using the ADO I device due to deficient aneurysmal tissue. The complete VSD closure rate was 84% immediately, 92% at 24 h, and 92% at the last follow-up. Atrioventricular conduction system was not affected by the procedure in any patients. Arterial complication developed in two patients. There was no device embolization; no aortic regurge developed in any patient. According to children had ketamine in induction of anesthesia HR recorded (122±16) beats /min but the children had sevofuran in indnction of anestherin re corded (108±12) beats/min but not significant different howevere the (MBP) inth children had ketamin had (68±14) mm Hg but the children had sevofluran in induction (60±8) mm Hg but not significant different. Conclusions Retrograde transcatheter closure of pmVSDs using AVPII is a safe and effective alternative method which allow closure of a wider range of VSDs due to availability of wide ranges of AVPII sizes of up to 22 mm in diameter. The retrograde approach can also simply the procedure with less fluoroscopy time and anesthesia time.

Multislice spiral computed tomography of the heart in dilated cardiomyopathy: possibilities in the verification of myocarditis (in comparison with myocardial biopsy) and in the evaluation of prognosis

To investigate whether intravenous contrast-enhanced multislice spiral computed tomography (computed tomography) (MSCT) versus myocardial morphological examination can diagnose myocarditis and the non-inflammatory causes of dilated cardiomyopathy (DCM) and evaluate prognosis in patients with the latter. A study group consisted of 130 patients, including 95 men (46.8±11.9 years), with DCM (mean left ventricular (LV) end-diastolic dimension (EDD), 6.6±0.8 cm; mean LV ejection fraction (EF), 29.8±9.3%; NYHA functional class (FC) III (II; III)). All the patients underwent intravenous contrast-enhanced 320-slice CT of the heart; myocardial morphological examination was made in 48 patients (endomyocardial biopsy in 29 patients, intraoperative biopsy in 7, and autopsy in 9, and study of the explanted heart in 3). In addition, cardiotropic viral DNA in the blood and myocardium and the level of anticardiolipin antibodies were determined; echocardiography (in all the patients), scintigraphy (n = 45), magnetic resonance imaging (MRI) (n = 21), and coronary angiography (CG) (n = 46), and a genetic consultation were performed. A comparison group comprised 20 patients, including 14 men (69.3±9.2 years), with coronary atherosclerosis (40% or more stenoses) according to MSCT findings in the absence of criteria for DCM (mean LV EDD, 4.8±0.5 cm; mean LV EF, 59.4±4.6%). Morphological/comprehensive examination showed that myocarditis as a cause of DCM was diagnosed in 76 (65%) patients; its concurrence with genetic cardiomyopathies was in 17 more patients (17%). MSCT of the heart revealed lower accumulation areas in 2 (1.5%) patients (type 1 based on the proposed rating scale), delayed myocardial contrast agent accumulation (DMCAA) in 81 (62.3%): subendocardial accumulation (type 2) in 8, intramyocardial accumulation in 4 (type 3), subepicardial accumulation in 52 (type 4), and transmural accumulation in 15 (type 5); DMCAA was not noted in 49 patients. DMCAA was not found in the comparison group. As compared with biopsy, the sensitivity, specificity, predictive value of positive and negative results of the tests in detecting active myocarditis for all the types of DMCAA were 77.4, 47.1, 72.7, and 53.3%, respectively; those for types 3-5 of DMCAA were 77.4, 52.9, 75.0, and 56.3%; those in detecting all the morphological types of myocarditis were 68.3, 28.6, 84.8, and 13.3%, and those for types 3-5 were 65.9, 28.6, 84.4, and 12.5%, respectively. Comparison of the data of MSCT and those of comprehensive examination in all the patients with DCM, the diagnostic significance in detecting myocarditis for all the types of DMCAA was 70.6, 67.9, 88.9 and 38.8%, respectively; that for DMCAA types 3-5 was 60.8, 67.9, 87.3, and 32.3%. In the study group, MSCT also identified the non-compacted myocardium (n = 31 (23.8%)), coronary atherosclerosis (n = 31 (23%)), which is confirmed by CG findings in 15 patients. The patients with DMCAA significantly more frequently showed a relationship with previous infection, acute onset, significantly higher NYHA FCs, end-diastolic and end-systolic LV volumes, and insignificantly lower LV EF. During a mean follow-up periods of 12 (6; 37.25) months, the overall mortality rate was 17.7% (23 deaths); the death + transplantation index was 20% (n = 26). All the types of DMCAA were found to be significantly related to prognosis: in the DMCAA group, the mortality rate was 21.5% versus 7.8% in the non-DMCAA group (odds ratio 3.22; 95% confidence interval, 1.02 to 10.21; p < 0.05). MSCT with the assessment of delayed contrast enhancement (and simultaneous CT coronary angiography) can be used for the non-invasive diagnosis of myocarditis in patients with DCM, including that in the presence of contraindications to MRI. DMCAA correlates with the presence of myocarditis, its activity, the degree of functional disorders, and prognosis.

Profile of gestational dyspnoea with focus on peripartum cardiomyopathy

Background: Peripartum cardiomyopathy (PPCM) is even today an incompletely understood and rare disease affecting pregnant women. There have been few studies from south India, especially Kerala on PPCM.Methods: Women who were referred from Department of Obstetrics and Gynecology from May 2010 to April 2016 for evaluation of dyspnoea during pregnancy or within 5 months of delivery were included in the study. They were screened and women with history suggestive of heart failure during peripartum period were evaluated in detail and followed up.Results: 8760 pregnant and peripartum women presented with dyspnoea out of which 20 patients were diagnosed with PPCM. The incidence of PPCM was 1 per 2190 pregnancies. The mean left ventricular end-diastolic dimension was 58±9 mm, the mean end-systolic dimension 45±6 mm and mean left ventricular ejection fraction (LV EF) 31.45±3.73% at diagnosis. Major adverse events (MAE) occurred in 4 patients. Low baseline ejection fraction (LV EF &lt; 30%) significantly correlated with greater incidence of adverse events.Conclusions: The majority of pregnancy related dyspnoea is benign. Echocardiography can reliably diagnose potentially life threatening conditions and should be performed early. Echocardiography aids in both diagnosis and prognostication in PPCM. Low ejection fraction at baseline (LVEF &lt; 30%) significantly correlates with greater incidence of major adverse events in patients with PPCM.

Clinical Characteristics and Outcomes of Patients with Amphetamine-Associated Cardiomyopathy in South Auckland, New Zealand

Amphetamine-associated cardiomyopathy (AAC) is becoming an increasingly recognised entity. The characteristics and outcomes of these patients are poorly understood. Thirty patients admitted with heart failure and echocardiographic evidence of cardiomyopathy between 2005 and 2014 and who had a documented history of amphetamine abuse that was considered an important factor in the causation of their cardiomyopathy were retrospectively identified. Mean age at presentation was 40±10 years with a male predominance (n=25, 83%). The majority were of indigenous Maori ethnicity. At presentation, four patients were in cardiogenic shock. Five patients required intensive care unit (ICU) admission for inotropic support and mechanical ventilation. Fifteen had severe left ventricular (LV) dilation (mean LV end-diastolic dimension 6.8±1.0cm) and all patients had severe LV dysfunction (mean LV ejection fraction 22±8%). Despite optimal heart failure therapy, LV size remained significantly dilated with minimal improvement in LV function. During median follow-up of 18 months, five patients died from end-stage heart failure and 17 had at least one readmission with decompensated heart failure. Amphetamine-associated cardiomyopathy was seen predominantly in young indigenous Maori men. They presented with severe cardiomyopathy, often requiring ICU admission. Severe LV dilation and significant LV dysfunction persisted despite treatment and mortality was high.

Aortic valve replacement for severe aortic regurgitation in asymptomatic patients with normal ejection fraction and severe left ventricular dilatation.

According to current guidelines, aortic valve surgery is a Class II indication for asymptomatic patients with severe aortic regurgitation (AR) accompanied by left ventricular (LV) ejection fraction (LVEF) ≥ 50% and left ventricular end-diastolic dimension (LVEDD) >70 mm. This study aims to assess the postoperative outcomes of asymptomatic patients with severe AR accompanied by LVEF ≥ 50% and LVEDD >70 mm after aortic valve replacement (AVR) and to identify prognostic indicators of the surgery, especially in terms of LV ejection fraction and degree of LV dilatation. We retrospectively identified 192 consecutive asymptomatic patients with severe AR accompanied by LVEF ≥ 50% and LVEDD > 70 mm who underwent isolated AVR from January 2003 to December 2013. Postoperative outcomes and prognostic indicators were evaluated and analysed. Patients had a mean age of 52.4 ± 16.1 years, and 69.3% were male. The mean LVEF and the mean LVEDD were 58.6 ± 6.6% and 76.0 ± 6.9 mm, respectively. The in-hospital mortality rate was 2.1% and survival rates at 5 and 10 years were 94.5 and 86.6%, respectively. Multivariable analysis indicated that postoperative mortality was associated with age [hazard ratio (HR) 1.059, 95% confidence interval (CI): 1.010-1.125, P = 0.049], preoperative LVEF (HR 0.860 95% CI: 0.748-0.989, P = 0.035) and LVEDD (HR 1.094 95% CI: 1.008-1.188, P = 0.032). Receiver-operating characteristic analysis showed that preoperative LVEF < 55% and LVEDD ≥ 81 mm were the best cut-off values for predicting postoperative mortality. By subgroup analysis, patients with 50 ≤ LVEF < 55% had poorer 5- and 10-year survival rates of 87.4 and 74.8% compared with 97.3% and 91.7% for patients with LVEF ≥ 55% (P = 0.023). Patients with LVEDD ≥ 81 mm had poorer 5- and 10-year survival rates of 85.6 and 72.6% compared with 98.2% and 85.6% for those with LVEDD < 81 mm (P = 0.027). AVR can be performed with satisfactory outcomes for severe aortic regurgitation in asymptomatic patients with severe AR accompanied by LVEF ≥ 50% and LVEDD > 70 mm. It is observed that 50% ≤ LVEF < 55% or LVEDD ≥ 81 mm are associated with poorer prognosis in patients undergoing AVR.

Therapeutic effects of udenafil on pressure-overload cardiac hypertrophy.

This study was performed to determine whether the newly developed phosphodiesterase type 5 (PDE5) inhibitor udenafil had beneficial effects on pressure-overload cardiac hypertrophy. Pressure overload cardiac hypertrophy was created by using suprarenal aortic constriction (SAC) in male Sprague-Dawley rats. Rats were divided into three groups: sham (n=19), SAC (n=18) and SAC+udenafil (n=14) groups. Three-week periods of SAC provoked significant left ventricular (LV) hypertrophy. Udenafil was administered (20 mg kg(-1) PO, daily) between the 3rd and 20th weeks after SAC in the SAC+udenafil group. Udenafil improved the survival rate (log-rank P=0.012) and exercise capacity (maximal exercise duration at the 20th week after surgery: 448±54 s for the SAC+udenafil group versus 317±73 s for the SAC group, P<0.05) of the rats with SAC. Serial echocardiographic examinations showed that udenafil attenuated LV remodeling processes following SAC (mean LV end-diastolic dimension at the 20th week after surgery: 9.84±0.59 mm for SAC and 9.05±0.58 mm for SAC+udenafil group, P<0.05). Invasive hemodynamic studies showed that udenafil improved the LV performance. Udenafil-attenuated myocardial fibrosis and apoptosis. Udenafil also decreased myocardial matrix metalloproteinase-9 expression and augmented serum interleukin-10 concentration. Long-term udenafil use prevented cardiac remodeling and improved exercise capacity and survival in rats exposed to pressure-overload cardiac hypertrophy.

Outcomes of Anomalous Left Coronary Artery From Pulmonary Artery Repair: Beyond Normal Function

Anomalous left coronary artery from pulmonary artery (ALCAPA) is associated with high mortality if left uncorrected. We describe long-term outcomes after surgical repair and ventricular function changes on long-term follow-up. A retrospective review of patients who had ALCAPA repair from January 1996 to December 2011 was completed. Ventricular function was assessed by shortening fraction and ejection fraction, left ventricular end-diastolic dimension, and severity of mitral regurgitation. Speckle tracking echocardiography served as a marker of early myocardial dysfunction. In total, 34 patients underwent ALCAPA repair at median age of 5 months (range, 3 days to 39 years). Surgical interventions included coronary translocation in 31 patients (91%), Takeuchi repair in 2 (6%), and coronary ligation in 1 patient (3%). Concomitant mitral valve repair was performed in 5 patients (15%). No patient required mechanical circulatory support postoperatively. There was no early mortality. At median follow-up of 6 years (range, 1 month to 14 years), there were 5 reoperations: 2 heart transplants (6%), 1mitral valve replacement (3%), 1 coronary artery bypass graft (3%), and 1 ventricular septal defect closure (3%); there was 1 death 2 years after surgery. Ejection fraction improved from 21% ± 6% to 60% ± 7% (p= 0.008), mean shortening fraction from 25% ± 14% to 38% ± 5% (p= 0.01), mean left ventricular end-diastolic dimension Z-score from 6.0 ± 3.8 to 0.9 ± 0.7 (p < 0.001), and number of patients with moderate-severe mitral regurgitation from 44% (15 of 34) to 5% (1 of 21). All patients had normal ejection fraction and shortening fraction at last follow-up. Speckle tracking echocardiography showed decreased global longitudinal (p= 0.01) and circumferential strain (p= 0.03) for 11 of 14 patients (79%). Excellent outcomes are achieved with repair of ALCAPA without mechanical circulatory support and with low reintervention rates. Normal ejection fraction and shortening fraction do not accurately convey myocardial dysfunction in these patients.

LV Unloading with Continuous-Flow Left Ventricular Assist Devices: The Association Between Left Ventricular Size and Late Survival

Purpose Left ventricular assist device (LVAD) therapy for the failing ventricle dramatically improves survival, but the nuances of optimal ventricular unloading remain unknown. Ideally, clinicians would titrate LVAD speed using an easily attainable metric that reflects LV unloading and correlates well with an important outcome such as death. We sought to determine if left ventricular end-diastolic dimension (LVEDD) meets these ideal criteria. Methods and Materials A retrospective review of all patients receiving a continuous-flow LVAD at a single center was undertaken. Patients who underwent an echocardiogram at our institution and had LVEDD recorded in the database were included. Simple descriptive statistics were employed, and survival was modeled using Kaplan-Meier analysis. A Cox proportional hazards model with LVEDD as a time-dependent covariate was used to produce hazard ratio estimates. Results Of 247 continuous-flow LVADs implanted from June 2006 to August 2012, echocardiographic data was available for 215 patients. This cohort included 37 females and 178 males, with an average age of 55+/-14 years. Indications for LVAD implantation was 161 patients bridge to transplant, 85 were destination therapy, and one patient was a bridge to recovery. Mean LVEDD at LVAD implant was 6.53+/-1.23 cm. LVEDD was not associated with survival (HR 2.01, 95% CI 0.45 – 9.0, P=0.36), however as depicted in Figure 1 , a trend towards improved survival is seen in those with LVEDD of 5 cm when compared with LVEDD of > 6 cm. Conclusions The current study does not find a correlation between LVEDD and survival, however further investigation with a larger study is required to rule out type II error.

Interpretation of left ventricular dimensions of neonates obtained from echocardiographic examinations during the early neonatal period

In neonates without physiological pulmonary hypertension, left ventricular end-diastolic dimensions (LVDd) are determined with two-dimensional echocardiography and formulated equations. However, there has not been discussed the meanings of dimensions in early neonatal periods, although the short-axis view of the left ventricle is not round at this age. The objective of this study was to assess LVDd in neonates during early neonatal periods. The study group consisted of 460 full-term neonates (230 boys; 230 girls) without congenital heart disease. The iE33 apparatus was employed to examine and measure the LVDds and the longest and shortest dimensions in the short-axis view. A significant difference was observed between the real LVDds and the estimated normal dimensions that were calculated from the formula; LVDd(mm) = 0.352 × Ht(cm)+1.86), (P = 0.020). The mean LVDds were estimated to be 97% of the normal LVDds. The real LVDds were influenced by the angle formed by the real LVDds and the longest dimension. The real LVDds were shorter than normal LVDds. These findings establish normal values for LVDds in the early neonatal period.

37 Optimal Medical Management and Lowering LVAD Speed Prevents Progression of Aortic Insufficiency

Purpose: Development of aortic insufficiency (AI) in patients (pts) during continuous flow LVAD support is a well known phenomenon that can lead to ineffective LVAD output. Current literature reports an average AI progression by 0.7 grade at 6 months (mo). We hypothesized that optimal medical therapy (MT) together with lowering the LVAD speed to allow aortic valve (AV) opening delays development of significant AI. Methods and Materials: Charts and echocardiograms (echos) of 40 LVAD pts were reviewed for demographics and medications. Medications were uptitrated to MAP of 60-80mmHg. VAD speed (RPM) was reduced according to our outpatient VAD protocol and collected at 1 and 6 mo. Echos were reviewed at baseline (pre LVAD), 1 and 6 mo for left ventricular end diastolic dimensions (LVEDD)(cm), AV opening, presence/ absence of AI. AI was graded: O-none, 0.5-trace,1-mild,1.5-mild-moderate, 2-moderate, 2.5-moderate-severe, 3-severe. Results: Forty pts, mean age 58, were included in the study. At 6 mo 38/40 (93%) pts were receiving beta blocker (BB), 30/40 (73%) ACE-I/ARB, 27/40 (66%) aldosterone receptor blocker (ALDOBL). Fifty six percent of pts achieved half of maximal daily dose of ACE-I/ARB, 45% BB and 53% ALDOBL. Twenty nine out of 40 (71%) pts were on furosemide, mean dose 32 mg. At baseline mean LVEDD was 6.8, AI present in 12/40 pts (30%), mean grade 0.3. At 1 mo LVEDD decreased to a mean 5, AI present in 6/22 (27%) pts, mean grade 0.27. At 6 mo LVEDD was the same, mean 5.1, AI present in 8/19 (42%) pts. Mean grade increased from 0.27 to 0.4 (p 0.3). Mean LVAD speed at 1 mo was 9190 and decreased to 8840 at 6 mo (p 0.001). At 1 mo AV opened with every beat in 33% pts, partially opened in 8%, did not open in 54%. At 6 mo AV opened with every beat in 36% pts, partially opened in 21%, did not open in 43%. Conclusions: Our results suggest slower progression in the AI grade at 6 mo in LVAD pts, than reported to date. An early strategy of decreasing VAD speed combined with optimization of MT may account for this difference and possibly improve long term survival.

B-Type Natriuretic Peptide and Heart Failure in Patients with Ventricular Septal Defect: A Pilot Study

In adults without congenital heart disease, B-type natriuretic peptide (BNP) has been shown to be a very sensitive and specific marker of heart failure. The utility of BNP as a marker of clinical heart failure in children with a ventricular septal defect (VSD) has yet to be determined. A prospective, observational study evaluated BNP levels and other measures of heart failure. Eligible patients were <2 years old, scheduled to undergo surgical repair of a VSD, and without other significant structural heart disease. Data collected before and after surgical repair included echocardiographic measurements, electrocardiographic (ECG) findings, Ross score, BNP measurements, and weight gain. A total of 21 patients were enrolled and 14 patients had complete postoperative follow-up data. For patients with complete data, mean BNP decreased by 94 pg/ml (118 pre vs. 24 post; paired t-test, p = 0.041), mean left ventricular end-diastolic dimension z-score decreased by 1.75 (+0.86 vs. -0.89; paired t-test, p = 0.013), mean weight z-score change per month increased by 0.35 (-0.25 vs. +0.10; Wilcoxon test, p = 0.013), and the incidence of biventricular hypertrophy on ECG decreased (46% vs. 0%; McNemar test, p = 0.031). The change in BNP showed a trend toward a negative correlation with weight z-score change per month (r = -0.531, p = 0.075). In conclusion, BNP, along with other measures of heart failure, decreased following VSD repair, and the change in BNP was most closely correlated with improved weight gain.

Indexed Left Ventricular Dimensions Best Predict Survival After Aortic Valve Replacement in Patients With Aortic Valve Regurgitation

Indications for valve replacement in patients with aortic regurgitation include diminished ejection fraction and increased left ventricular dimensions. Our objective was to examine the effect of preoperative ejection fraction and left ventricular dimensions on survival and return of normal systolic function (ejection fraction > or = 0.50) after valve replacement for aortic regurgitation. Between 1996 and 2006, 301 patients had aortic valve replacement for moderate or greater chronic aortic regurgitation, and 29% had concomitant replacement of the ascending aorta. We reviewed clinical and echocardiographic variables as well as late vital status. Patients' mean age was 55.2 +/- 16.5 years, and 78% were male. The mean preoperative ejection fraction was 0.56 +/- 0.12, the mean left ventricular end-systolic dimension was 43 +/- 10 mm, and the mean left ventricular end-diastolic dimension was 63 +/- 9 mm. Operative mortality was 1.7%, and survival at 1, 5, and 10 years was 96%, 90%, and 77%, respectively. This was similar to an age- and sex-matched population (p = 0.214). The level of ejection fraction preoperatively did not predict late survival, nor did absolute values for left ventricular end-systolic dimension and end-diastolic dimension. Indexed left ventricular end-systolic dimension and end-diastolic dimension were predictors (p < 0.01) of late survival. Data from late echocardiography were available for 159 patients (56%) at a mean follow-up of 3.3 +/- 2.6 years. Preoperative ejection fraction, left ventricular end-systolic dimension, indexed end-systolic dimension, end-diastolic dimension, and indexed end-diastolic dimension were univariately predictive of late ejection fraction. In a multivariate model the only predictor of late normal ejection fraction was a higher preoperative ejection fraction (odds ratio, 2.85; p < 0.001). In patients who received a valve replacement for aortic regurgitation, decreased ejection fraction and increased left ventricular dimensions were not associated with late mortality. However, larger indexed left ventricular systolic and diastolic dimensions were associated with late mortality. Preservation of late ejection fraction is best if the operation is performed in patients with near normal preoperative left ventricular function.

The Effect of Gender on Mortality or Appropriate Shock in Patients with Nonischemic Cardiomyopathy Who Have Implantable Cardioverter‐Defibrillators

As heart disease is increasingly recognized in women and as important studies have elucidated the benefit of implantable cardioverter defibrillators (ICDs) in patients with nonischemic cardiomyopathy (NICM), little is known regarding the effect of gender difference on arrhythmic risk in this population. We sought to determine if there are gender differences in arrhythmic risk and potential defibrillator benefit in patients with NICM. The records of 767 consecutive patients who underwent ICD implant at the Stanford Medical Center from 1984 to 2002 were reviewed. Only patients with NICM were considered (n = 201, 26.2%). Of these, 140 patients had clinical follow-up information available. Baseline variables were examined, including age, baseline heart rate, ejection fraction, and medications. We evaluated the time to first shock as well as all-cause mortality in this patient population. Kaplan-Meier survival curves were plotted, a log-rank test was used to evaluate significance, and Cox-proportional hazards test was used for multivariate analysis. There were 88 (62.9%) men and 52 (37.1%) women. Between male and female patients, there were no significant differences in baseline mean age (54.8 +/- 1.9 years vs 53.1 +/- 2.3 years, respectively), ejection fraction (35.2 +/- 2.0% vs 33.3 +/- 2.3%, respectively), and mean left ventricular end-diastolic dimension (6.4 +/- 0.3 cm vs 5.9 +/- 0.2 cm, respectively). Mean follow-up time was 30.8 months. Thirty-two male patients (36.4 +/- 0.05%) received appropriate shocks compared with 20 female patients (38.5 +/- 0.07%). Mean time to the first appropriate shock was 11.9 +/- 3.9 months for male patients and 21.3 +/- 5.8 months for female patients (P = 0.2). Nineteen male patients (21.6 +/- 0.05%) died or received heart transplant during the follow-up period compared with 6 female patients (11.5 +/- 0.04%) (P = 0.11). Male and female patients with NICM who received ICDs had similar rate of appropriate shock and mortality. In this population gender does not appear to be an important risk factor for mortality or arrhythmic events.

Initial clinical experience with intracardiac echocardiography in guiding transcatheter closure of perimembranous ventricular septal defects: Feasibility and comparison with transesophageal echocardiography

Over the last several years, intracardiac echocardiography (ICE) has been employed successfully in guiding transcatheter device closure of a secundum atrial septal defect (ASD) or patent foramen ovale (PFO). Nothing is known regarding the use of ICE to guide catheter device closure of a perimembranous ventricular septal defect (PMVSD). Twelve patients (seven female/five male) who had a PMVSD (among them, three patients with associated atrial communications: two with an ASD and one with a PFO) underwent attempts at transcatheter device closure using the Amplatzer membranous VSD device of their defects, using sequential transesophageal echocardiography (TEE) and ICE guidance with general endotracheal anesthesia (five patients) and using ICE alone with conscious sedation (seven patients). The mean age of patients was 16.9 +/- 3.7, and their mean weight was 42.4 +/- 6.6. Their mean left ventricular end-diastolic dimension preclosure was 45.7 +/- 2.5. The Qp/Qs ratio ranged from 1.0 to 1.8:1. During the procedure, the ICE catheter was positioned in the right atrium (RA) in all 12 patients and the ICE catheter was advanced to the left atrium to obtain a view of the ventricular septum in 3. Both TEE and ICE provided similar anatomical views of the position of the PMVSD. Furthermore, the relationship of the defect to the aortic valve and tricuspid valves, the measured size of defect, and the guidance of various stages of device deployment were comparable by TEE and ICE. There were no complications encountered during or after closure. We conclude that ICE provides unique images of the PMVSD and measurements similar to those obtained by TEE. ICE potentially could replace TEE in most patients as a guiding imaging tool for PMVSD device closure, thus eliminating the need for general endotracheal anesthesia.

Xenon produces minimal haemodynamic effects in rabbits with chronically compromised left ventricular function

Xenon has only minimal haemodynamic side-effects on normal myocardium and might be a preferable anaesthetic agent for patients with heart failure. We studied the haemodynamic changes caused by 70% xenon in rabbits with chronically compromised left ventricular (LV) function. Anaesthetized rabbits were thoracotomized and a major coronary artery was ligated to induce ischaemic heart disease. Nine weeks later, rabbits were again anaesthetized (ketamine/propofol), and haemodynamics were measured during inhalation of 70% xenon using echocardiography [LV end-diastolic dimension (LVedD), fractional shortening (FS), velocity of circumferential fibre shortening (VcF), ejection fraction (EF)] in closed-chest animals. Subsequently, rabbits were thoracotomized and instrumented for measurement of LV pressure (tip manometer), LV dP/dtmax and cardiac output (ultrasonic flow probe). Haemodynamics were recorded again during inhalation of 70% xenon. All rabbits had compromised LV function 9 weeks after coronary artery ligation. Mean LVedD increased from 12.9 (SD 0.9) mm to 17.1 (0.4) mm; EF decreased from 73 (9) to 64 (8)%; FS decreased from 36 (7) to 29 (5)%; VcF decreased from 28.9 (6.8) to 17.6 (4.7) mm s(-1); all P<0.05. Inhalation of 70% xenon had no effect on haemodynamics in closed-chest rabbits, as measured by echocardiography. After invasive instrumentation, small decreases in LV pressure from 78 (20) to 72 (19) mm Hg, LV dP/dtmax from 3081 (592) to 2633 (503) mm Hg s(-1) and cardiac output from 239 (69) to 225 (71) ml min(-1) were observed during xenon inhalation (all P<0.05). These data show that xenon has only minimal negative inotropic effects in rabbits with LV dysfunction after coronary artery ligation.