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Introduction: Functional tricuspid regurgitation (TR) will decrease after atrial septal defect (ASD) closure, but it may persist and require additional tricuspid valve (TV) surgery or intervention. Hypothesis: We aimed to find echocardiographic predictors for persistent TR after successful ASD closure. Methods: Among 348 adults who underwent isolated ASD closure between January 2010 and September 2020, 91 (26.1%) patients with significant TR (at least moderate degree) before ASD closure were included. Persistent TR was defined as a significant TR even after ASD correction on echocardiogram after 6 months to 1 year. To find echocardiographic predictors for persistent TR, conventional and speckle tracking echocardiography performed before ASD closure were analyzed. The right ventricular (RV)-pulmonary arterial coupling was assessed by the ratio of RV global longitudinal strain (RV GLS) and pulmonary arterial systolic pressure (PASP) (RV GLS/PASP). Results: Persistent TR was observed in 22 (24.2%) patients. Patients with persistent TR were significantly older, with larger TR jet area and lower RV GLS/PASP (0.46 ± 0.14 vs. 0.37 ± 0.13, p = 0.013) than those without persistent TR. However, there were no significant differences in RV volumes, RV systolic function, and TV annular diameter between the two groups. On multivariable logistic regression, persistent TR was independently associated with age (HR:2.031, 95% CI, 1.113-2.046; p=0.003) and RV GLS/PASP (HR:0.009, 95% CI, 0.000-0.790; p=0.039). RV GLS/PASP showed a good predictive value for persistent TR after ASD closure (cut off 0.39, the area under the curve 0.702, p=0.003). Conclusions: Persistent TR after successful ASD closure is not uncommon in patients with ASD and significant TR. RV GLS/PASP can predict persistent TR after ASD closure. It can be suggested that concomitant or subsequent TR intervention should be considered in elderly patients and patients with abnormal RV-pulmonary arterial coupling.

Introduction: There is scarce data on whether immune checkpoint inhibitor (ICI) increase the risk of cardiomyopathy, especially when used with cardiotoxic agents. Hypothesis: We evaluated the cardiotoxicity of the ICI in sarcoma patients receiving doxorubicin with or without ICI by echocardiographic parameters and left ventricular global longitudinal strain (LVGLS). Methods: A total of 89 patients were included. Echocardiography and LVGLS were evaluated at baseline and follow-up (after 3 and 6months) and compared between the doxorubicin (n=67) and concomitant ICI with doxorubicin (n=22) groups. Cancer-therapy related cardiac dysfunction (CTRCD) was defined as LVEF drop of >10% and LVEF of 10%, LVEF of > 50% and LVGLS relative reduction of >15% (probable CTRCD) at 6months. Results: There was no significant difference in age, cumulative dose of doxorubicin and cardiovascular risk factors between two groups. At baseline, LVEF was similar between two groups (p=0.493). In doxorubicin group, LVEF decreased to 59±6 % (p Conclusions: ICI increases risk of CTRCD, when concomitantly treated with cardiotoxic agents. Thus, cardiomyopathy should be monitored in patients with ICI by comprehensive echocardiographic assessment including myocardial strain.

Introduction: We aimed to investigate the temporal changes in demographic characteristics, use of multimodal imaging, and treatments in patients with bicuspid aortic valves from a large Korean registry. Methods: A total of 1,514 patients (mean 71.5%, 56 ±14 years old) who were first diagnosed with BAV from Jan 2003 through Dec 2020 in a single tertiary referral center in Korea were investigated. They were divided into 3 groups according to the year of diagnosis: group 1 (2003-2008, n=270), group 2 (2009-2014, n=590), and group 3 (2015-2020, n=654). Significant aortic stenosis (AS) was defined as at least moderate AS and significant aortic regurgitation (AR) was defined as at least moderate AR based on the current guideline. Non-dysfunctional BAV was defined as BAV without significant AR or AR. Presence of aortopathy was defined as any portions of ascending aorta ≥ 45 mm. Use of imaging for diagnosis and the treatment method were comprehensively investigated. Results: Both age at diagnosis [55 (interquartile range [IQR], 44 to 60) in Group 1, 59 (48 to 67) in Group 2, 60 (60 to 68) in Group 3, p for trend Conclusions: In the past 18 years, there were remarkable temporal changes in patients’ demographic characteristics, use of multimodal imaging for diagnosis, complications and treatment in patients with BAV.

Background: The morbidity and mortality of patients with functional mitral regurgitation (MR) remain high, but no pharmacological therapy has been proven effective. The hypothesis of this study was that sacubitril/valsartan would be superior to valsartan alone in improving functional MR via dual inhibition of the renin-angiotensin system and neprilysin. Methods: In this double-blind trial, we randomly assigned 118 patients with heart failure with chronic functional MR secondary to left ventricular (LV) dysfunction to receive either sacubitril/valsartan or valsartan, in addition to standard medical therapy for heart failure. The primary end point was the change in effective regurgitant orifice area of functional MR from baseline to the 12-month follow-up. Secondary end points included changes in regurgitant volume, LV end-systolic volume, LV end-diastolic volume, and incomplete mitral leaflet closure area. Results: The decrease in effective regurgitant orifice area was significantly greater in the sacubitril/valsartan group than in the valsartan group (–0.058±0.095 versus –0.018±0.105 cm 2 ; P =0.032) in an intention-to-treat analysis including 117 (99%) patients. Regurgitant volume was also significantly decreased in the sacubitril/valsartan group in comparison with the valsartan group (mean difference, –7.3 mL; 95% CI, –12.6 to –1.9; P =0.009). There were no significant between-group differences regarding the changes in incomplete mitral leaflet closure area and LV volumes, with the exception of LV end-diastolic volume index ( P =0.044). We noted no significant difference in the change of blood pressure between the treatment groups, and 7 patients (12%) in the sacubitril/valsartan group and 9 (16%) in the valsartan group had ≥1 serious adverse events ( P =0.54). Conclusions: Among patients with secondary functional MR, sacubitril/valsartan reduced MR to a greater extent than did valsartan. Our findings suggest that an angiotensin receptor-neprilysin inhibitor might be considered for optimal medical therapy of patients with heart failure and functional MR. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02687932.

The morbidity and mortality of patients with functional mitral regurgitation (MR) remain high, but no pharmacological therapy has been proven effective. The hypothesis of this study was that sacubitril/valsartan would be superior to valsartan alone in improving functional MR via dual inhibition of the renin-angiotensin system and neprilysin.In this double-blind trial, we randomly assigned 118 patients with heart failure with chronic functional MR secondary to left ventricular (LV) dysfunction to receive either sacubitril/valsartan or valsartan, in addition to standard medical therapy for heart failure. The primary end point was the change in effective regurgitant orifice area of functional MR from baseline to the 12-month follow-up. Secondary end points included changes in regurgitant volume, LV end-systolic volume, LV end-diastolic volume, and incomplete mitral leaflet closure area.The decrease in effective regurgitant orifice area was significantly greater in the sacubitril/valsartan group than in the valsartan group (-0.058±0.095 versus -0.018±0.105 cmAmong patients with secondary functional MR, sacubitril/valsartan reduced MR to a greater extent than did valsartan. Our findings suggest that an angiotensin receptor-neprilysin inhibitor might be considered for optimal medical therapy of patients with heart failure and functional MR.URL: https://www.clinicaltrials.gov . Unique identifier: NCT02687932.

Introduction: Unprovoked venous thromboembolism (VTE) is related higher incidence of occult cancer. However, routine screening for cancer in this population is still controversial. D-dimer is a biomarker reflecting the activation of hemostasis and fibrinolysis. D-dimer is clinically used to exclude VTE, also related in patients with malignancy. Hypothesis: We aimed to explore the predictive value of d-dimer level for detecting occult cancer in patients with unprovoked VTE. Methods: We retrospectively analyzed 840 patients who diagnosed deep vein thrombosis or pulmonary thromboembolism. Among them, 175 (20.8%) patients who diagnosed with unprovoked VTE selected to participate in this study. Odds ratios (OR) with 95% confidence intervals (95% CI) were calculated for incidence of occult cancer as well as d-dimer level reference to patient without occult cancer. Results: During follow-up for 5.0±1.9 years, 30 of 840 patients diagnosed cancer in this population. The primary origin of tumor was 6 (20%) of stomach, 6 (20%) of lung, 4 (13%) of colon and others. Number of patients with metastatic cancer was 17 (57%). Log d-dimer was significantly higher in occult cancer group than unprovoked VTE without cancer (3.5 ± 0.5 vs. 3.2 ± 0.5, p=0.009). When the patients with unprovoked VTE were divided by d-dimer according to Youden index, high d-dimer (≥2432) was associated with higher prevalence of occult cancer (26.9% vs. 9.2%, p=0.002). In logistic regression analysis, d-dimer is independently associated with occult cancer (OR: 3.93, 95% CI: 1.46-10.54, p=0.007) after adjusted gender, age, type of VTE (i.e., deep vein thrombosis or pulmonary thromboembolism) and tumor markers. In addition, d-dimer is more significantly associated with patients who diagnosed cancer with distant metastasis (OR: 4.31, 95% CI: 1.16-15.99, p=0.029) Conclusions: High level of d-dimer concentrations are indicator of an increased risk of occult cancer in patients with unprovoked VTE.

Background: We aimed to characterize progression of aortic stenosis (AS) with end stage renal disease (ESRD), and to determine metabolic and hemodynamic factors attributing to AS progression. Method:A total of 73 ESRD (50 males, age 72±11 years) on dialysis with mild (n=56) to moderate AS (n=17) were enrolled. Age, sex and AS severity matched control group with eGFR above 60 mL/min/1.73m2 was selected (n=79). Transthoracic echocardiography was performed at baseline and during follow up (48±23 months). Severity of AS was accessed by aortic valve area (AVA) calculated by continuity equations. Acceleration of AS was assessed by annual AVA reduction rate. Accelerated group in ESRD patients was defined as those with the highest quartile of AVA reduction rate. Clinical outcomes included aortic valve intervention, hospital admission due to heart failure, and death. Results: Annual AVA reduction rate was significantly higher in ESRD compared to control group (0.36±1.9 vs. 0.05±0.14 cm2/yr, p Conclusion: AS in ESRD progress in more accelerated manner compared to those with normal kidney function, even in mild to moderate AS. Therefore, more frequent follow up with proper risk stratification by assessing hemodynamic and metabolic characteristics, such as LAVI and PTH, may benefit ESRD patients to reduce clinical events.

A 37-year-old man was referred to our emergency department after 4 days of a spiking fever of up to 40°C, myalgia, and new development of multiple, small, nontender erythematous macular lesions on his palms and soles compatible with Janeway lesions (Figure 1). He had a history of a large secundum atrial septal defect for which he underwent transcatheter closure with a 24-mm Amplatzer septal occluder (ASO; AGA Medical Corporation, Goden Valley, Minnesota) 4 years prior. The procedure was successful without any residual shunts. One month before his febrile episode, he had received periodontal scaling without antibiotic prophylaxis based on the current guidelines. He adamantly denied a history of intravenous drug abuse, and there was no evidence of immunodeficiency disorders. His blood cultures grew methicillin-sensitive Staphylococcus aureus within 24 hours. Figure 1. Multiple, small, nontender erythematous macular lesions on palms and soles. Transesophageal echocardiography …

Background: Apical hypertrophic cardiomyopathy (ApHCM) might have different morphological and clinical features according to the age of disease onset, probably result from the distinct mechanism of pathogenesis. The aim of this study was to evaluated the morphological and clinical differences according to the age of disease onset in patients with ApHCM. Methods: This was a retrospective, observational study of 56 ApHCM patients (31 males, mean 65±9 years). Among 426 patients with diagnosed ApHCM from 2000 until 2013, we selected 56 patients who met the inclusion criteria: [[Unable to Display Character: ⑴]] patiens who diagnosed with ApHCM before 60 years old and current age >60 years old, (group A, early onset, n=16); and [[Unable to Display Character: ⑵]] who diagnosed with ApHCM after 60 years old who had no evidence of apical hypertrophy confirmed by previous echocardiography (group B, late onset, n=40). Morphological LV feature was assessed by transthoracic echocardiography, which were divided into pure and mixed type. Furthermore, hemodynamic parameters and clinical events were also evaluated. Results: There were no differences in the presence of hypertension, LV systolic function and left atrial volume index between group A and B. However, early onset group A had more increased maximal wall thickness of LV apex (17.08±2.02 vs 15.43±1.68mm, p=0.005), and more incidence of pure type (100% (16/16) vs 56.8% (21/40), p=0.001) compare than late onset group B. Group B had older age (65±5 vs 72±4 years, p=0.001), increased LV end-diastolic dimension (51.25±2.32 vs 48.58±3.37mm, p=0.006), increased E/E’ (11.24±2.94 vs 14.60±6.37, p=0.049) with decreased E’ (5.61±1.34 vs 4.66±1.38cm/s, p=0.024) respectively.There were no significant differences in the risk of cardiovascular complication such as atrial fibrillation and stoke between group A and B. Conclusions: There was obvious different clinical characteristics according to the age of disease onset. Early onset ApHCM has typical morphological feature and relatively preserved LV diastolic function, compared with late onset ApHCM. Our result supports that late onset ApHCM was related to decreased LV diastolic function and increased LV wall thickness, which reflects the potential myocardial remodeling with aging.

An 86-year-old woman without any history of heart disease or trauma to the chest experienced an acute onset of dyspnea associated with a productive cough for 2 hours. Her medical history revealed that she was hypertensive for the past 20 years. Her blood pressure was 90 mmHg in systole and 50 mmHg in diastole. Immediately after admission, mechanical ventilation was initiated because there was progressive respiratory depression. A chest x-ray showed marked pulmonary congestion (Figure 1A). On physical examination, a grade III systolic murmur was noted at the apex, and a coarse breathing sound was detected within the whole lung field. ECG showed sinus tachycardia without any evidence of myocardial infarction (Figure 1B). Creatine kinase and its MB isoenzyme were not elevated, but high-sensitivity troponin T was 0.035 ng/mL (normal, 0–0.014 ng/mL). Transthoracic echocardiography revealed left ventricular hypertrophy without regional wall motion abnormalities. The left ventricular ejection fraction was >70%, and E/E′ was 34, suggesting …

Accurate anatomical and functional assessment of AV and aortic root is crucial to understand the pathophysiology of abnormalities and management decision-making in patient with aortic valve diease and aortic aneurysm. The aim of this study was to evaluate the feasibility of novel semi-automatic assessment of AV and aortic root from volumetric 3-D Echo compared to CT. Volume-rendered 3-D TEE data were obtained using V5M transducer(Sequoia, Siemens). 6 points(commisures and valve tips) at ED and ES were identified on the 3-D TEE data. Volumetric CT images were acquired using 64-Slice CT(Avanto, Siemens). A dynamic 3-D model of the AV and root were obtained by standard mathematical modeling approach (non-uniform rational B-splines). This enabled automatic visualization and quantification of AV and root. We measured phasic change of the AVA(cm2), diameter of sinotubular junction(d-STJ, mm), sinus of Valsalva(d-SV, mm) and basal ring(d-BR, mm). 364 CT volumes from 41 patients and 23, 3-D TEE volumes from 15 patients with normal to mild AR were acquired. 3-D TEE data about AV and root showed strong correlation with CT data(table ). Figure showed representative examples of 3-D Echo and CT modeling. This novel automated 3-D Echo approach provides accurate dimensions of the AV and the aortic root and may aid in valve and root repair procedures. Comparison of AVA and aortic diameter between 3-D TEE and CT Figure 1. Top; Aortic root model, Bottom; Aortic valve model Figure 2. Automatic calculation from 3D TEE data (left; AVA, right; Aortic root diameter) Figure 3. Aortic root model segmentation (left two; 3D TEE, right two; CT)

Background: We have previously shown that the morphology and location of LV flow vortex is a critical determinant of directed blood flow during ejection. We evaluated whether quantitative LV flow vortex analysis by contrast echocardiography (CE) was superior to conventional echo-Doppler parameters to predict hemodynamics and symptomatic status in patients with systolic heart failure (HF). Methods: 27 patients had 2-D CE with iv Definity in the apical views. Velocity vector and vorticity of LV flow was measured by Particle Image Velocitimetry (PIV) combined with a Feature Tracking Algorithm (Siemens, CA). Relative and vortex relative strength (RS, VRS), and vortex pulsation correlation (VPC) were measured. LVEDP was measured invasively , and LA volume index (LAVI), E/E’ were measured by echo-Doppler. Results: RS, VRS, and VPC showed strong correlation with LVEDP (r=-0.927, psymptomatic versus asymptomatic HF, respectively. LAVI and E/E’ did not differentiate between symptomatic and asymtomatic HF. Figures A and B show LV flow vortex in asymptomatic and symptomatic HF respectively: pulsatility is stronger in asymptomatic HF although steady streaming flow is comparable. Conclusion : The data from this study shows that quantitative LV flow vortex parameters are superior to echo-Doppler measures to predict hemodymics and symptomatic status in patients with systolic HF.

Background : Diastolic dysfunction (DD) is common in patients with Type 2 DM even in the absence of HTN and LVH. We tested whether apical rotational mechanics offered any additional insights into DD in DM over conventional echo-Doppler measures. Methods: We studied 4 groups : 12 normals (wall thickness-WT 0.9±0.1cm); 17 patients with DM (WT 1.0±0.1cm, HbA1c 7±1%, BP 128±4/68±5 mmHg); 16 patients with DM +HTN (WT 0.9±0.1cm, HbA1c 7±1%, BP 134±23/72±18 mmHg); and 20 patients with DM+HTN+LVH (WT 1.4±0.2cm, HbA1c 7±4%, BP 135±13/76±9mmHg). All patients had normal LVEF and mitral E/A ratio. SAX of the LV apex and base were obtained. Velocity Vector Imaging (Siemens, CA) was used to measure: Longitudinal myocardial velocity (LMV, cm/sec) and strain (LS,%); Apical rotation velocity (ARV, cm/sec)and reverse rotation velocity(ARRV, cm/sec); Apical rotation (AR, degree) and LV torsion-LVTOR (degree/cm, and Circumferential (CS,%) and Radial strains (RS,%). Results: Figure shows LVTOR and % reduction in ARRV data. All other data will be presented. Thus, LV torsion is increased in DM alone or DM+HTN (-LVH) groups. But ARRV is reduced by ~ 20% in these groups even with relatively normal E/E’ ratio and LAVI. In the DM+HTN+LVH group, E/E’ and LAVI are increased and apical rotational mechanics resemble the same spectrum as the above groups but are more severe (~25% reduction in ARRV). Thus, reduction in ARRV is a marker of early DD in DM even in the absence of LVH . Conclusions: Apical rotational mechanics is more sensitive than conventional echo-Doppler measures to identify myocardial DD in type 2 DM even in the presence of normal E/A ratio, LAVI and LVEF, and in the absence of HTN and/or LVH.