Background: To compare the outcomes of hybrid endovascular and open surgical repair for proximal aortic arch diseases. Methods: A total of 55 consecutive patients with an aortic arch aneurysm or aortic dissection involving any of zone 0 to 1 (39 male, age 63.4±14.3 years) who underwent a hybrid endovascular repair (n=35) or open surgical repair (n=20) from 2006 to 2014 were included in a retrospective analysis. Perioperative and late outcomes were compared. Results: The two groups had similar baseline characteristics, except age and EuroSCORE II, which were higher in the hybrid group. Perioperative mortality or stroke did not differ significantly between the two groups, but tended to be lower in the hybrid repair group than in the open repair group (11.4% vs. 30.0%, p=0.144). Incidences of other morbidities did not differ. During follow-up, similar over-all survival was observed between the hybrid group and the open repair group (87.3% vs. 79.7% at 1 year and 83.8% vs. 72.4% at 3 years; p=0.319). However, significantly lower reintervention-free survival was observed for hybrid repair compared with open repair (83.8% vs. 100% at 1 year and 65.7% vs. 100% at 3 years; p=0.022). Conclusions: Comparable perioperative and late outcomes were observed for hybrid endovascular repair of proximal aortic disease compared with open surgical repair, despite a higher reintervention rate during follow-up. Therefore, hybrid repair may be considered as an acceptable treatment alternative to surgery, particularly in patients at high surgical risk.

Background: Stem cells are known to restore the injured myocardium. This capability may improve if there is enhanced in vivo survival of the transplanted stem cells. The hAMSCs are isolated from amniotic membrane underlying the chorion of a human placenta and are located in the fetal-maternal border, demonstrating unique immunomodulatory properties characterized by CD59 +, HLA-G +, and HLA-DR- to suppress the host immune response. A single polycistronic lentivirus reprograms the hAMSCs robustly to generate MiPSCs. Hypothesis: The MiPSCs retain the immunomodulatory properties of hAMSCs to attenuate immune rejection in an immunocompetent mouse to restore the injured myocardium. Methods and results: 250K MiPSCs were transplanted into the LAD ligated heart of FVB mice. 250K hAMSCs were injected into the hearts of LAD ligated immunodeficient SCID mice as control. In vivo bioluminescence (BLI) demonstrated robust viability signal in the luciferase-transduced MiPSCs for 2 weeks in FVB mice (Figure 1). When comparing the MiPSC-treated vs. the control (hAMSC-treated) mice during the 4-wk follow-up period, cardiac MRI demonstrated significantly improved LVEF (29.75 vs. 22.45%, p<0.05), decreased infarct % (21.47 vs. 31.06%, p<0.05), and increased viable myocardial volume (78.07 vs. 67.9 cm3, p<0.05). Notably, the MiPSCs did not form any teratoma. Conclusion: The MiPSCs exhibit unique immunomodulatory properties, which attenuate rejection by an immunocompetent mouse and significantly restore the injured heart. The MiPSCs may enable allogeneic cardiac stem cell therapy.

Purpose: Myocardial viability may influence the diastolic function of left ventricle (LV) reflecting chamber remodeling in the early phase after acute myocardial infarction (AMI). However, the precise relationship in human has not been determined yet. So we aimed to evaluate whether myocardial viability assessed by strain rate parameters on low-dose dobutamine echocardiography (LD-DSE) may influence on LV diastolic function and remodeling process in AMI. Methods: In this prospective single center study, 134 consecutive patients with AMI and akinetic wall motion in at least two segments were enrolled and underwent LD-DSE on 5~9 days after the event. Myocardial viability was quantitatively evaluated by global peak systolic strain rate (psSR) and global time to peak of psSR. Within 6 hours after LD-DSE, left and right heart catheterization with the recording of LV end diastolic pressure and pulmonary capillary wedge pressure were performed. And then 6 months later, echocardiography and thallium scan with delayed image were followed. Results: Patients (67.9% men, mean age 60.1±1.1years, 54.5% anterior wall, 53.7% ST-segment elevation) were tolerated LD-DSE without significant complications. 71.6% of patients underwent revascularization therapy. After 6 months later, LV ejection fraction was significantly increased from 48.7±1.1% to 52.0±1.1% (p=0.00) and LV end diastolic volume was significantly decreased from 94.6±4.0cc to 89.1±3.8cc (p=0.00). As we expected, global psSR at baseline of LD-DSE showed significant linear correlations with LV end diastolic pressure, E/E’ ratio and left atrial volume index (r=−0.43 and p=0.01, r=0.52 and p=0.00 and r=0.52 and p=0.00, respectively). And also global psSR at 10mcg of LD-DSE correlated with E/E’ ratio and left atrial volume index(r=0.52 and p=0.00 and r=0.36 and p=0.02, respectively). Interestingly, global psSR at 10mcg of LD-DSE correlated significantly with the change of LV end diastolic volume during 6 months follow-up (r=−0.42 and p=0.04). Conclusions: Strain rate data on LD-DSE correlates with LV diastolic function in the early phase and chamber remodeling in 6 months follow-up after AMI. So strain stress echocardiography may provide useful prognostic information for LV remodeling in AMI.

Background : Reciprocal relationships between endothelial dysfunction and insulin resistance imply that improvement in endothelial dysfunction will have beneficial metabolic consequences. We hypothesized that amlodipine therapy will improve endothelial dysfunction and metabolic parameters in hypertensive subjects. Methods : Amlodipine (10 mg daily for 8 weeks) or placebo was given to each 45 patients with mild to moderate hypertension in a randomized, double-blind, placebo-controlled, and paralleled study. Age, sex, and body mass index were matched. Results : Amlodipine therapy significantly reduced systolic and diastolic blood pressure and increased HDL-cholesterol to greater extent than placebo therapy (all P< 0.001). Amlodipine therapy significantly improved flow-mediated dilator response to hyperemia and reduced plasma malondialdehyde levels to greater extent than placebo therapy ( P< 0.001 and P =0.035). Amlodipine therapy significantly increased plasma adiponectin levels ( P =0.009) and decreased plasma leptin and resistin levels ( P< 0.001 and P =0.025, respectively) to greater extent than placebo therapy. Correlations were noted between percent changes in adiponectin levels and percent changes in HDL-cholesterol ( r =0.348, P =0.019) and QUICKI ( r =0.326, P =0.029) following amlodipine therapy. Only changes in HDL-cholesterol (β = 0.469, P = 0.019) and QUICKI (β = 1.786, P = 0.069) were independent predictors of changes in adiponectin levels (multivariate regression analysis). We also observed inverse correlations between percent changes in leptin levels and percent changes in QUICKI ( r = −0.569, P< 0.001) following amlodipine therapy with changes in QUICKI (β = 1.810, P < 0.001) as an independent predictor of changes in leptin levels. Conclusions : Amlodipine therapy improves blood pressure, endothelial function, and metabolic parameters in patients with hypertension.

Background: To compare the outcomes of hybrid endovascular and open surgical repair for proximal aortic arch diseases. Methods: A total of 55 consecutive patients with an aortic arch aneurysm or aortic dissection involving any of zone 0 to 1 (39 male, age 63.4±14.3 years) who underwent a hybrid endovascular repair (n=35) or open surgical repair (n=20) from 2006 to 2014 were included in a retrospective analysis. Perioperative and late outcomes were compared. Results: The two groups had similar baseline characteristics, except age and EuroSCORE II, which were higher in the hybrid group. Perioperative mortality or stroke did not differ significantly between the two groups, but tended to be lower in the hybrid repair group than in the open repair group (11.4% vs. 30.0%, p=0.144). Incidences of other morbidities did not differ. During follow-up, similar over-all survival was observed between the hybrid group and the open repair group (87.3% vs. 79.7% at 1 year and 83.8% vs. 72.4% at 3 years; p=0.319). However, significantly lower reintervention-free survival was observed for hybrid repair compared with open repair (83.8% vs. 100% at 1 year and 65.7% vs. 100% at 3 years; p=0.022). Conclusions: Comparable perioperative and late outcomes were observed for hybrid endovascular repair of proximal aortic disease compared with open surgical repair, despite a higher reintervention rate during follow-up. Therefore, hybrid repair may be considered as an acceptable treatment alternative to surgery, particularly in patients at high surgical risk.

Background: Stem cells are known to restore the injured myocardium. This capability may improve if there is enhanced in vivo survival of the transplanted stem cells. The hAMSCs are isolated from amniotic membrane underlying the chorion of a human placenta and are located in the fetal-maternal border, demonstrating unique immunomodulatory properties characterized by CD59 +, HLA-G +, and HLA-DR- to suppress the host immune response. A single polycistronic lentivirus reprograms the hAMSCs robustly to generate MiPSCs. Hypothesis: The MiPSCs retain the immunomodulatory properties of hAMSCs to attenuate immune rejection in an immunocompetent mouse to restore the injured myocardium. Methods and results: 250K MiPSCs were transplanted into the LAD ligated heart of FVB mice. 250K hAMSCs were injected into the hearts of LAD ligated immunodeficient SCID mice as control. In vivo bioluminescence (BLI) demonstrated robust viability signal in the luciferase-transduced MiPSCs for 2 weeks in FVB mice (Figure 1). When comparing the MiPSC-treated vs. the control (hAMSC-treated) mice during the 4-wk follow-up period, cardiac MRI demonstrated significantly improved LVEF (29.75 vs. 22.45%, p<0.05), decreased infarct % (21.47 vs. 31.06%, p<0.05), and increased viable myocardial volume (78.07 vs. 67.9 cm3, p<0.05). Notably, the MiPSCs did not form any teratoma. Conclusion: The MiPSCs exhibit unique immunomodulatory properties, which attenuate rejection by an immunocompetent mouse and significantly restore the injured heart. The MiPSCs may enable allogeneic cardiac stem cell therapy.

Purpose: Myocardial viability may influence the diastolic function of left ventricle (LV) reflecting chamber remodeling in the early phase after acute myocardial infarction (AMI). However, the precise relationship in human has not been determined yet. So we aimed to evaluate whether myocardial viability assessed by strain rate parameters on low-dose dobutamine echocardiography (LD-DSE) may influence on LV diastolic function and remodeling process in AMI. Methods: In this prospective single center study, 134 consecutive patients with AMI and akinetic wall motion in at least two segments were enrolled and underwent LD-DSE on 5~9 days after the event. Myocardial viability was quantitatively evaluated by global peak systolic strain rate (psSR) and global time to peak of psSR. Within 6 hours after LD-DSE, left and right heart catheterization with the recording of LV end diastolic pressure and pulmonary capillary wedge pressure were performed. And then 6 months later, echocardiography and thallium scan with delayed image were followed. Results: Patients (67.9% men, mean age 60.1±1.1years, 54.5% anterior wall, 53.7% ST-segment elevation) were tolerated LD-DSE without significant complications. 71.6% of patients underwent revascularization therapy. After 6 months later, LV ejection fraction was significantly increased from 48.7±1.1% to 52.0±1.1% (p=0.00) and LV end diastolic volume was significantly decreased from 94.6±4.0cc to 89.1±3.8cc (p=0.00). As we expected, global psSR at baseline of LD-DSE showed significant linear correlations with LV end diastolic pressure, E/E’ ratio and left atrial volume index (r=−0.43 and p=0.01, r=0.52 and p=0.00 and r=0.52 and p=0.00, respectively). And also global psSR at 10mcg of LD-DSE correlated with E/E’ ratio and left atrial volume index(r=0.52 and p=0.00 and r=0.36 and p=0.02, respectively). Interestingly, global psSR at 10mcg of LD-DSE correlated significantly with the change of LV end diastolic volume during 6 months follow-up (r=−0.42 and p=0.04). Conclusions: Strain rate data on LD-DSE correlates with LV diastolic function in the early phase and chamber remodeling in 6 months follow-up after AMI. So strain stress echocardiography may provide useful prognostic information for LV remodeling in AMI.

Background : Reciprocal relationships between endothelial dysfunction and insulin resistance imply that improvement in endothelial dysfunction will have beneficial metabolic consequences. We hypothesized that amlodipine therapy will improve endothelial dysfunction and metabolic parameters in hypertensive subjects. Methods : Amlodipine (10 mg daily for 8 weeks) or placebo was given to each 45 patients with mild to moderate hypertension in a randomized, double-blind, placebo-controlled, and paralleled study. Age, sex, and body mass index were matched. Results : Amlodipine therapy significantly reduced systolic and diastolic blood pressure and increased HDL-cholesterol to greater extent than placebo therapy (all P< 0.001). Amlodipine therapy significantly improved flow-mediated dilator response to hyperemia and reduced plasma malondialdehyde levels to greater extent than placebo therapy ( P< 0.001 and P =0.035). Amlodipine therapy significantly increased plasma adiponectin levels ( P =0.009) and decreased plasma leptin and resistin levels ( P< 0.001 and P =0.025, respectively) to greater extent than placebo therapy. Correlations were noted between percent changes in adiponectin levels and percent changes in HDL-cholesterol ( r =0.348, P =0.019) and QUICKI ( r =0.326, P =0.029) following amlodipine therapy. Only changes in HDL-cholesterol (β = 0.469, P = 0.019) and QUICKI (β = 1.786, P = 0.069) were independent predictors of changes in adiponectin levels (multivariate regression analysis). We also observed inverse correlations between percent changes in leptin levels and percent changes in QUICKI ( r = −0.569, P< 0.001) following amlodipine therapy with changes in QUICKI (β = 1.810, P < 0.001) as an independent predictor of changes in leptin levels. Conclusions : Amlodipine therapy improves blood pressure, endothelial function, and metabolic parameters in patients with hypertension.

Frailty in heart failure (HF) patients contributes to poor outcomes, emphasizing the need for effective management. In many previous studies, frailty interventions have mainly targeted physical frailty or focused community-dwelling patients, neglecting the multidimensional needs of hospitalized individuals. As a frailty for HF patients need to include clinical, functional, psycho-cognitive, and social domains, nurses must assess it holistically and provide personalized support, especially during care transitions. This study aims to evaluate the effectiveness of a nurse-led, personalized health coaching program for hospitalized HF patients with frailty through a randomized controlled trial. This 12-week intervention program targets hospitalized HF patients with frailty. After screening frailty HF patients using validated tools such as Fried's phenotype, Tilburg Frailty Indicator, participants will be randomly assigned to either an intervention or control group. The intervention group will receive personalized health services, including pre-discharge education and weekly telephone coaching, addressing clinical, functional, psycho-cognitive, and social frailty domains. Psychiatric support and community integration program will be provided as needed. The control group will receive standard care. Frailty, quality of life (QoL), and clinical outcomes will be measured at baseline, 12 weeks, and 24 weeks. The primary outcomes will be improvements in frailty and QoL. Frailty will be measured both multidimensional and each of the 4 domains of frailty for HF patients. This study will clarify the role of multidimensional personalized interventions in addressing adverse outcomes related to frailty in patients with HF, thereby providing evidence of their necessity in its management.

The HFFS is a new multidimensional tool for the identification of frailty in patients with HF. It should also enables healthcare providers to identify potential 'red flags' for frailty in order to develop personalized care plans. The next step will be to validate the new score in patients with HF.

Heart failure (HF) is a major cause of mortality and morbidity in South Korea, imposing substantial physical, emotional, and financial burdens on patients and society. Despite the high burden of symptom and complex care needs of HF patients, palliative care and hospice services remain underutilized in South Korea due to cultural, institutional, and knowledge-related barriers. This position statement from the Korean Society of Heart Failure emphasizes the need for integrating palliative and hospice care into HF management to improve quality of life and support holistic care for patients and their families. By clarifying the role of palliative care in HF and proposing practical referral criteria, this position statement aims to bridge the gap between HF and palliative care services in South Korea, ultimately improving patient-centered outcomes and aligning treatment with the goals and values of HF patients.

This study showed that 3 of 5 patients (60.0%) with high-risk PAH reached PVR ≤ 4 WU and/or mPAP ≤ 40 mmHg by receiving intensive parenteral treprostinil therapy with significant improvements in 6MWD and NT-proBNP levels, and successfully transitioned to oral selexipag. We proposed that transition strategies from parenteral treprostinil to selexipag aiming at hemodynamic targets.