Fractional flow reserve (FFR) measurement was compared to dobutamine stress echocardiography (DSE) instable angina (SA) with stable coronary lesion (s) (SCL (s) ) in a few trials; however, similar comparisons in patients with acute coronary syndrome (ACS) with non-culprit lesion (s) (NCL (s) ) are lacking. Our objectives were to prospectively evaluate the diagnostic performance of FFR with two different cutoff values (< 0.80 and < 0.75) relative to DSE in moderate (30%-70% diameter stenosis) NCLs (ACS group) and to compare these observations with those measured in SCLs (SA group). One hundred seventy-five consecutive patients with SA (n = 86) and ACS (n = 89) with 225 coronary lesions (109 SCLs and 116 NCLs) were enrolled. In contrast to the ACS cohort in SA patients, normal DSE was associated with higher FFR values compared to those with abnormal DSE (P = 0.051 versus P = 0.006). In addition, in the SA group, a significant correlation was observed between DSE (regional wall motion score index at peak stress) and FFR (r = −0.290; P = 0.002), whereas a similar association was absent (r = −0.029; P = 0.760) among ACS patients. In the SA group, decreasing the FFR cutoff value (< 0.80 versus < 0.75) improved the concordance of FFR with DSE (70.6% versus 81.7%) without altering its discriminatory power (area under the curve; 0.68 versus 0.63; P = 0.369), whereas in the ACS group, concordance remained similar (69.0% versus 71.6%) and discriminatory power decreased (0.62 versus 0.51; P = 0.049), respectively. In conclusion, lesion-specific FFR assessment may have different relevance in patients with moderate NCLs than in patients with SCLs.

Fractional flow reserve (FFR) is considered the standard for assessment of the physiological significance of coronary artery stenosis. Intracoronary papaverine (PAP) is the most potent vasodilator used for the achievement of maximal hyperemia. However, its use can provoke ventricular tachycardia (VT) due to excessive QT prolongation. We evaluated the clinical efficacy and safety of the administration of PAP after nicorandil (NIC), a potassium channel opener that prevents VT, for optimal FFR measurement.

A total of 127 patients with 178 stenoses were enrolled. The FFR values were measured using NIC (NIC-FFR) and PAP (PAP-FFR). We administered PAP following NIC (NIC-PAP). Changes in the FFR and electrogram parameters (baseline versus NIC versus PAP) were assessed and the incidence of arrhythmias after PAP was evaluated. In addition, we analyzed another 41 patients with 51 stenoses by assessing the FFR using PAP before NIC (PAP-NIC). After propensity score matching, the electrogram parameters between 2 groups were compared.

The mean PAP-FFR was significantly lower than the mean NIC-FFR (0.82 ± 0.11 versus 0.81 ± 0.11, P < 0.05). The mean baseline-QTc, NIC-QTc, and PAP-QTc values were 425 ± 37 ms^1/2, 424 ± 41 ms^1/2, and 483 ± 54 ms^1/2, respectively. VT occurred in only 1 patient (0.6%). Although PAP induced QTc prolongation (P < 0.05), the PAP-QTc duration was significantly shorter in NIC-PAP compared to PAP-NIC (P < 0.05).

The administration of PAP with NIC may induce sufficient hyperemia and prevent fatal arrhythmia through reductions in the PAP-induced QTc prolongation during FFR measurement.

After a percutaneous coronary intervention (PCI) in patients with coronary artery disease (CAD), in-stent neoatherosclerosis may pose a risk of in-stent restenosis (ISR). To clarify whether non-fasting hypertriglyceridemia contributes to ISR, we examined the relationship between non-fasting hypertriglyceridemia (i.e., triglyceride (TG) level ≥ 200 mg/dL) and ISR after stenting with a bare metal stent (BMS) post-primary PCI in patients with CAD by means of a single-site retrospective analysis. A total of 1,039 patients with CAD were enrolled, and 86 patients (112 lesions) were evaluated for BMS-ISR 3-6 months post-primary PCI. The percentage of patients with non-fasting hypertriglyceridemia was significantly higher in the ISR (+) group than in the ISR (−) group (P < 0.009). The follow-up period and number of patients in the ISR (+) group were significantly smaller than those in the ISR (−) group (P < 0.001). There were no significant between-group differences in the other baseline patient characteristics before the primary PCI or at the time of the follow-up coronary angiography. However, at the follow-up period, the ISR (+) group had significantly lower diastolic blood pressure and high-density lipoprotein cholesterol levels (P = 0.015) and significantly higher TG levels (P = 0.012) than the ISR (−) group. A multiple logistic regression analysis demonstrated that non-fasting hypertriglyceridemia and a follow-up period of ≥ 6 months were independent risk factors for ISR after primary PCI in patients with BMS implantation for stenotic CAD (P = 0.006), with an adjusted odds ratio of 8.232 (1.201-56.410) and 0.006 (95% confidence interval < 0.001-0.045), respectively. Non-fasting hypertriglyceridemia may be an additional independent risk factor for BMS-ISR after primary PCI in patients with CAD.

Angiopoietin-like protein 2 (ANGPTL2) promotes chronic inflammation and plays a key role in the pathogenesis of heart failure. Cardiac rehabilitation (CR) is an integral component of heart failure management and has been shown to have anti-inflammatory effects. However, ANGPTL2 concentration in chronic heart failure patients undergoing CR has not been evaluated. This study aimed to investigate serum ANGPTL2 levels and their associated factors and compare the results with those of N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with chronic heart failure undergoing phase III CR.

A total of 56 patients were enrolled. Clinical characteristics including body composition, grip strength, exercise tolerance, duration of CR, blood counts and biochemistry, and echocardiographic parameters were evaluated for their association with serum ANGPTL2 and NT-proBNP levels.

The median (first and third quartiles) value of ANGPTL2 was 4.05 (2.70-5.57) ng/mL. Clinical parameters that correlated with serum ANGPTL2 levels were body weight, body mass index, body fat mass, body fat percentage, anaerobic threshold (AT), C-reactive protein, and total protein (TP), which were mostly distinct from those that correlated with serum NT-proBNP levels. A multivariate analysis revealed that AT and TP were independent factors related to ANGPTL2 levels, whereas age, left ventricular ejection fraction, and left atrial dimension were independently related to NT-proBNP levels.

These observations suggest that CR increases the exercise tolerance and exhibits anti-inflammatory effects simultaneously, and this situation is reflected by decreased serum ANGPLT2 and TP levels. ANGPTL2 may be a useful marker of inflammation and impaired exercise tolerance in patients with chronic heart failure.

In this study, we aimed to investigate the time course of new-onset complete atrioventricular block (CAVB) and its reversibility after transcatheter aortic valve implantation (TAVI). We analyzed 206 consecutive patients without baseline CAVB who underwent successful TAVI. The incidence of new-onset CAVB was determined to be 12.6% (26/206). Among these patients, 14 recovered from CAVB within 2 weeks (6.8%, 14/206), while the remaining 12 (5.8%, 12/206) underwent permanent pacemaker (PPM) insertion. Among the 12 patients who received the PPM, 4 were able to recover from CAVB within 4 months. Thus, only 8 among 206 patients (3.8%) showed persistent CAVB. Early-onset CAVB on the day of the procedure was the strongest predictor of PPM implantation (OR = 127). The electrocardiographic changes that occurred after TAVI were mostly recovered after 1 month. The most critical procedural factor that predicts CAVB and PPM insertion is the deep implantation (>4 mm) of a big valve (oversizing index >5.9%). In conclusion, the incidence of CAVB after TAVI was estimated to be at 12.6%. Two-thirds of these patients recovered from CAVB within 3 days, resulting in a final rate of persistent CAVB of 4%. To prevent CAVB, we have to implant an appropriate valve type with an optimal size and depth.

Catheter ablation for atrial fibrillation (AF) has been an established and frequently utilized approach in a variety of clinical settings. Nevertheless, real-world data about the clinical course of AF patients after initial catheter ablation remain limited, and these are mainly derived from particular registries or selected high-volume centers.

In this study, we used health check-ups and insurance claims database from a Japanese insurance organization. The study population was comprised of 1777 patients who underwent catheter ablation for AF before June 2016. During the 3-year follow-up period, 396 (22.3%) patients underwent at least one repeated AF ablation, while 74 (4.2%) underwent two or more repeated ablations. In multivariate Cox regression analysis, longer time after AF diagnosis (7-11 months and ≥12 months versus 1-6 months) (HR, 1.05; 95% CI, 1.01-1.08 and HR, 1.04; 95% CI 1.02-1.07) was independently associated with repeated ablation. The discontinuation rates of OACs and AADs after the first ablation were 26.7% and 63.0% at 3 months and 75.2% and 89.1% at 1 year after the initial ablation, respectively. The former was independently associated with shorter time after AF diagnosis and lower diastolic blood pressure, whereas the latter was independently associated with older age, smaller CHADS₂ score, and shorter time after AF diagnosis.

We presented real-world data regarding the clinical course of young Japanese AF patients after initial catheter ablation based on a claims database in Japan.

Esophageal injury is a rare but serious complication of atrial fibrillation (AF) ablation. To minimize esophageal injury, our persistent AF (PerAF) protocol involves complete left atrial posterior wall (LAPW) and pulmonary vein (PV) isolation (box isolation), with a centerline away from the esophagus. However, there has been a concern that extensive LA isolation might deteriorate LA function. There has been a paucity of data on LA remodeling after box isolation. Therefore, we compared LA size pre- and post-box isolation with an LAPW centerline in patients with PerAF.

Patients who underwent catheter ablation (CA) for PerAF between November 2016 and December 2018 were retrospectively evaluated.

The LAPW, including all PVs, was completely isolated in 105 consecutive patients (75 men; mean age: 68 ± 10 years) with PerAF, including 58 patients with long-standing PerAF. During a follow-up of 660 ± 332 days, 76 patients (72%) were arrhythmia-free. The LA dimension (38 ± 6 mm versus 42 ± 7 mm; P < 0.0001) and volume index (38 ± 13 mL/m² versus 47 ± 14 mL/m²; P < 0.0001) at 6 months post-ablation were significantly decreased in patients who maintained sinus rhythm compared to pre-ablation. In patients with recurrent AF/atrial tachycardia (AT), these parameters were also significantly decreased (P < 0.001, respectively).

Box isolation with a posterior centerline has no esophageal complications and a high clinical success rate in patients with PerAF. Reverse remodeling could be achieved even when using extensive isolation of the PV and LAPW in patients with PerAF.

High-degree atrioventricular block (HAVB) or complete heart block (CHB) is a common complication associated with transcatheter aortic valve replacement (TAVR). However, some patients with HAVB/CHB recover with time. The results of electrophysiological studies (EPSs) using permanent pacemaker implantation (PPI) in patients with suspicious HAVB/CHB are considered controversial.

This study aimed to evaluate whether HAVB/CHB induction at the bedside using a temporary pacemaker can predict recurrence in patients who had recovered from HAVB/CHB after TAVR.

We enrolled a total of 11 patients who had recovered from HAVB/CHB and evaluated their electrophysiology using right ventricular pacing and/or procainamide administration.

HAVB/CHB induction was positive. Three patients tested positive for HAVB/CHB, whereas 8 tested negative. The ejection fraction and the interval between HAVB/CHB onset and EPS were found to be significant. HAVB/CHB positive patients underwent PPI. A patient with a balloon-expandable valve tested positive just before recovery of CHB, but tested negative 5 days later and was included in the negative group. The 4 patients who tested negative received a cardiovascular implantable electric device (CIED). We observed HAVB/CHB in 2 patients who had previously tested positive after 3 months. Among those who tested negative, those with CIED had no HAVB/CHB, and others showed neither HAVB/CHB on electrocardiogram nor experienced syncope or sudden death.

Our EPS revealed that HAVB/CHB induction may predict HAVB/CHB recurrence after TAVR. Valve type and EPS timing may affect the results.

The aortic regurgitation (AR) index, proposed as an objective indicator of postprocedural AR, decreases in proportion to AR severity, besides reportedly providing additional prognostic information. Meanwhile, left ventricular (LV) function has also been considered an essential prognostic factor. This study aimed to clarify whether LV function affected the AR index using cardiac catheterization data.

A retrospective study was performed in patients whose LV function was evaluated using a micromanometer-tipped catheter. Patients with grade 2 or higher AR were excluded to explore non-AR factors affecting the AR index value. The AR index was calculated as a ratio of the gradient between the aortic diastolic blood pressure (DBP) and the LV end-diastolic pressure (EDP) to the aortic systolic blood pressure (SBP): AR Index = [ (DBP − LVEDP) / SBP] × 100.

A total of 64 patients [age, 62 (interquartile range: 48-70) years; LV ejection fraction, 19% (16%-26%) ] were examined. AR index values ranged from 18.3 to 68.6. Despite having no AR, two patients displayed an AR index < 25, indicating significant AR. Multiple-regression analysis revealed that LV diastolic stiffness (β = −0.750, P < 0.001), LV max dP/dt (β = −0.296, P = 0.006), and heart rate (β = 0.284, P = 0.011) were independent determinants of the AR index value.

Patients with impaired LV diastolic function and preserved systolic function had low AR index values. The additional prognostic information of the AR index may be related to LV diastolic function.

Studies conducted in developed nations have shown that increase in life expectancy has brought with it a rise in the incidence and treatment of degenerative aortic and mitral heart valve diseases. Current standards recommend valve replacement among even some asymptomatic patients. In this research, we examine the epidemiology of valvular heart disease and rate of valve replacement in Taiwan, where life expectancy now stands at 80.69 years. Patients were enrolled based on claims from a widely used national database and categorized into cohorts defined by type of valve disease and, further, by valve replacements and type of valve (mechanical, porcine, or bovine). Data, including disease type, age, and gender, were analyzed to determine annual and cumulative incidence rates and prosthetic usage from 2000 to 2017. Results showed that across the cohorts, the cumulative incidence rate in 2017 was 3.59%, and in the aortic valve cohort, the percentage of surgical valve replacement for those ≥60 years was 6.99%. Compared with other developed nations, this demonstrates that incidence rates are slightly higher, yet surgical replacements are less than half that of other developed nations. This under-treatment of patients with valvular heart disease presents an important public health challenge in Taiwan.

Septal reduction therapy (SRT) -i.e. septal myectomy and alcohol septal ablation-has been performed to treat medically refractory hypertrophic cardiomyopathy (HCM) for decades. However, it is largely unknown whether SRT prevents HCM-related cardiovascular events or death. The objective was to examine the effects of SRT on acute cardiovascular events and all-cause mortality in HCM. We performed a propensity score (PS) -matched study using databases that capture all hospitalizations and outpatient visits in New York state. We identified patients with HCM who underwent SRT between 2007 and 2014 (i.e. the SRT group) and those who had never had SRT but had at least one hospitalization for HCM during the same period (i.e. the control group). We performed PS matching at a 1:1 ratio. The primary outcome was a composite of acute cardiovascular events and all-cause mortality during 0-180 days and 181-360 days. The secondary outcome was 180- and 360-day all-cause mortality. We included 846 patients with HCM (423 PS-matched pairs). Patients who underwent SRT had a lower risk of the primary outcome event (0-180 days: odds ratio [OR], 0.54; 95% confidence intervals (CI), 0.37-0.80; P = 0.002 and 181-360 days: OR, 0.33; 95% CI, 0.22-0.51; P < 0.0001). Furthermore, the risk of all-cause mortality was lower at 180 days (OR, 0.37; 95% CI, 0.22-0.63; P = 0.0003) and 360 days post-SRT (OR, 0.32; 95% CI, 0.20-0.51; P < 0.0001). In conclusion, our PS-matched study using population-based datasets demonstrated that SRT was associated with a reduced risk of a composite of acute cardiovascular events and all-cause mortality in HCM during the first post-SRT year.

The obesity paradox states higher body mass index (BMI) is associated with better outcomes than normal weight in patients with heart failure with preserved ejection fraction (HFpEF). However, underweight was defined by BMI < 18.5 kg/m², and results have been inconclusive, in part due to small number of participants. The number of underweight patients with HFpEF is higher in Asian than in Western countries. In this study, we aim to determine the prognostic impact of underweight in patients with HFpEF in Asian population.

We enrolled 846 consecutive patients from the PURSUIT-HFpEF registry. We then divided them into three groups by BMI, namely, underweight (BMI < 18.5 kg/m²), normal weight (18.5 ≤ BMI < 23), and overweight (23 ≤ BMI). The underweight group consisted of 187 patients (22%). Over a mean follow-up of 407 days, 105 deaths were reported as all-cause mortality. On multivariable Cox analysis, the underweight group was determined to be significantly associated with higher risk of all-cause mortality than the normal and overweight groups (Hazard ratios [HR]: 2.33; 95% confidence intervals [CI]: 1.45-3.75, P < 0.001; HR: 3.54; 95% CI: 1.99-6.29, P < 0.001, respectively), after adjustment for age, sex, vital signs, and comorbidities.

Underweight is a useful predictor of poor prognosis in patients with HFpEF in Asian population.

Cardio-renal syndrome is a challenging clinical entity to manage, and is often associated with increased morbidity and mortality. We hypothesized that adaptive servo-ventilation (ASV), non-invasive positive pressure ventilation that ameliorates systemic/pulmonary congestion, may improve renal function in patients with symptomatic heart failure complicated by the cardio-renal syndrome. Patients with symptomatic congestive heart failure who underwent ASV therapy for over 1 month were included in this retrospective study. The trajectory of the estimated glomerular filtration ratio (eGFR) between the pre-1 month period and the post-one-month period (on ASV) were compared. A total of 81 patients (median 65 years old, 65 men) were included. eGFR decreased during the pre-1 month period from 52.7 (41.7, 64.6) down to 49.9 (37.3, 63.5) mL/minute/1.73 m² (P < 0.001) whereas we observed an increase following one-month of ASV therapy up to 53.4 (38.6, 68.6) mL/minute/1.73 m² (P = 0.022). A reduction in furosemide equivalent dose following the initiation of ASV therapy was independently associated with increases in eGFR with an adjusted odds ratio of 13.72 (95% confidence interval 3.40-55.3, P < 0.001). In conclusion, short-term ASV therapy was associated with the preservation of renal function, particularly when the dose of loop diuretics was concomitantly reduced.

Tolvaptan, a vasopressin type-2 receptor antagonist, is utilized to ameliorate fluid retention following cardiac surgery. However, the optimal timing of tolvaptan administration considering novel biomarkers remains unknown. We prospectively included patients who underwent cardiac surgery between 2016 and 2020. We measured perioperative trends of free water reabsorption mediators including plasma arginine vasopressin and urine aquaporin-2. A total of 20 patients (68 [60, 75] years old, 18 men) were included. Urine volume decreased gradually after the initial 3 hours following cardiac surgery. The plasma arginine vasopressin level increased significantly with a peak at postoperative 6 hours, whereas the urine aquaporin-2 level increased later with a delayed peak at postoperative 12 hours. As a result, urine aquaporin-2 relative to the plasma arginine vasopressin level, which represents the activity of the collecting ducts and indicates predicted responses to tolvaptan, was a minimum at postoperative 6 hours. Tolvaptan administration immediately after cardiac surgery might not be recommended given the transient refractoriness to tolvaptan probably due to the stunning of kidney collecting ducts.

This retrospective cohort study aimed to explore the relationship between temporal changes in the cardiac function and peripartum cardiac events in pregnant women with low-risk congenital heart disease.

We performed echocardiography at early and late pregnancy and postpartum in 76 pregnant women with low-risk congenital heart disease, and compared echocardiographic parameters between subjects with and without peripartum cardiac events. Median age at delivery was 27 (range, 24-31) years. The ZAHARA and CARPREG II scores suggested that most women were found to be at low-risk for pregnancy. Fifteen subjects had cardiac events that included heart failure in 10, arrhythmia in 4, and pulmonary hypertension in one subject. The left ventricular and atrial volumes significantly increased from early pregnancy toward late pregnancy, and the E/A ratio and global longitudinal strain significantly decreased from early pregnancy toward late pregnancy. The left atrial volume (67 [53-79] versus 45 [35-55] mL, P = 0.002) and plasma brain natriuretic peptide level (58 [36-123] versus 34 [18-48] pg/mL, P = 0.026) at late pregnancy were significantly higher in subjects with cardiac events than in those without cardiac events.

An increase in the left atrial volume followed by mild left ventricular diastolic dysfunction is related to peripartum cardiac events in women with congenital heart disease who are at low risk for cardiac events during pregnancy.

The surgical strategies for acute type-A aortic dissection (aTAAD) with coronary artery involvement have been controversial, and its prognosis remains unclear. Thus, in this study, we aim to determine the characteristics, surgical strategies, and prognosis of patients with coronary artery involvement due to aTAAD.

Retrospective analysis of 65 consecutive aTAAD patients with coronary artery involvement between September 2005 and January 2012 was performed. The patients were divided into two groups: those treated with aTAAD repair and coronary ostia reimplantation (Neri type-A, group A, n = 37) and those with aTAAD repair and coronary artery bypass grafting (Neri type B and C, group B, n = 28).

Overall in-hospital mortality was determined to be 8.1% for group A and 21.4% for group B (P = 0.124). No significant difference was determined between groups A and B in cardiopulmonary bypass time, cross-clamp time, cerebral perfusion time, and hospitalization time. Intensive care unit (ICU) stay was 5.8 ± 7.4 days for group A, whereas it was 12.4 ± 10.6 days for group B (P = 0.009). The morbidity of postoperative temporary and permanent neurological dysfunction was similar between the two groups, while renal and respiratory dysfunction were 8.1% versus 25.0% and 16.2% versus 39.3%, respectively (P = 0.062, P = 0.036). Average follow-up time was 112.0 ± 44.8 months, and survival curves have not shown statistical significance between two groups (P = 0.386).

Coronary artery dissection with Neri type B and C in acute TAAD has been associated with higher early death, but comparable long-term survival after discharge. However, combined immediate coronary artery bypass grafting and aortic repair remains a safe, effective, and acceptable approach to these challenging group of patients.

The impact of beta2-agonists (B2As) on heart failure (HF) remains controversial. This study aimed to investigate whether inhaled B2As increased in-hospital mortality in ICU patients with HF.

The Multiparameter Intelligent Monitoring in Intensive Care III database was initially searched to identify adult patients (≥ 18 years old) with HF in ICU. Then, patients using or not using inhaled B2As were matched using propensity score matching on a 1:1 basis to control for baseline confounders. In-hospital mortality was compared between the two groups, and logistic regression analysis was performed to assess the association between B2As and in-hospital mortality.

The initial search retrieved 2345 eligible patients with HF from the database. After propensity score matching, 705 pairs of patients were included in the final analysis. Patients using B2As had markedly higher in-hospital mortality than those not using B2As (4.68% versus 2.27%; P = 0.013). In the multivariate logistic regression analysis, B2A use (odd ratios (OR), 2.471; 95% confidence interval (CI), 1.289-4.734; P = 0.006), stroke (OR, 4.581; 95% CI, 1.621-12.948; P = 0.004), and simplified acute physiology score II (SAPS-II) scores (OR, 1.090; 95% CI, 1.064-1.116; P < 0.001) were significantly associated with increased risk of in-hospital mortality, whereas renin angiotensin system inhibitor use (OR, 0.396; 95% CI, 0.202-0.778; P = 0.007) was significantly associated with decreased risk of in-hospital mortality. Subgroup analysis further indicated that the association between B2A use and mortality was significant only in patients with HF without chronic pulmonary disease (OR, 2.427; 95% CI, 1.351-4.362; P = 0.003), but not in those with chronic pulmonary disease (OR, 2.094; 95% CI, 0.582-7.537; P = 0.258).

In ICU patients with HF but without chronic pulmonary disease, the use of inhaled B2As is associated with increased in-hospital mortality.

Cardiovascular diseases can affect the clinical course of coronavirus disease 2019 (COVID-19); however, evaluation of COVID-19 contribution to prognosis for each individual disease, such as heart failure, is lacking in South Korea. Therefore, this study aimed to investigate COVID-19 patients with heart failure by matching them with patients with heart failure only and those with COVID-19 only. We performed a nationwide population-based retrospective study using data from the National Health Insurance System. Based on patients with heart failure and COVID-19, up to 1:3 propensity score matching procedures were performed for patients with heart failure only and those with COVID-19 only. The outcome was the composite of complications. After matching, a multivariable-adjusted conditional logistic regression analysis was performed. The number of patients was 317 for heart failure and COVID-19, 951 for heart failure only, and 884 for COVID-19 only. The adjusted odds ratio (OR) and 95% confidence interval (CI) for the composite of complications of patients with heart failure and COVID-19 compared with those with heart failure only was 3.511 (2.501-4.928), and compared with those with COVID-19 only, they were 1.626 (1.112-2.376). In patients with heart failure and COVID-19, age per 10 years increase and diabetes were significant variables with the adjusted OR (95% CI) [2.206 (1.704-2.856) for age and 2.345 (1.244-4.420) for diabetes] for complications. This study demonstrated that patients with both heart failure and COVID-19 in South Korea are associated with a poor prognosis. Patients with heart failure require more surveillance and precautions for COVID-19, as recommended by the Center for Disease Control and Prevention.

This is the first study to evaluate directly visceral fat area (VFA) using a visceral fat (VF) meter by the abdominal bioelectrical impedance analysis (A-BIA) method in obstructive sleep apnea (OSA) patients diagnosed with polysomnography (PSG). The purpose of this study is to clarify (1) whether VFA measurement using a VF meter by the A-BIA method is possible even in a private clinic without burdening patients and staff and (2) how much VFA affects OSA compared to body mass index (BMI). Even without a computed tomography scan, which is the gold standard for VFA measurement, a VF meter could analyze patients by the A-BIA method and easily measure VFA. Therefore, it could be used safely even in a private sleep clinic, with very little burden on the patients and the medical staff. We investigated the association between OSA and VFA in 133 OSA patients. Multiple regression analysis revealed that VFA (β = 0.28; P = 0.020) was a stronger coexisting factor for OSA than age, male gender, or BMI (β = 0.26; P = 0.032) in all OSA patients. In the OSA patients with VF accumulation, only VFA was a significant component of OSA severity (β = 0.36; P = 0.006). The A-BIA method instrument could become a useful device for the evaluation of VF accumulation in OSA patients in private sleep clinics. VF accumulation should be recognized as an important risk factor as well as a known risk factor for OSA.

While cardiac imaging has improved the diagnosis and risk assessment for cardiac sarcoidosis (CS), treatment regimens have consisted of generalized heart failure therapies and non-specific anti-inflammatory regimens. The overall goal of this study was to perform high-sensitivity plasma profiling of specific inflammatory pathways in patients with sarcoidosis and with CS.

Specific inflammatory/proteolytic cascades were upregulated in sarcoidosis patients, and certain profiles emerged for CS patients.

Plasma samples were collected from patients with biopsy-confirmed sarcoidosis undergoing F-18 fluorodeoxyglucose positron emission tomography (n = 47) and compared to those of referent control subjects (n = 6). Using a high-sensitivity, automated multiplex array, cytokines, soluble cytokine receptor profiles (an index of cytokine activation), as well as matrix metalloproteinase (MMP), and endogenous MMP inhibitors (TIMPs) were examined.

The plasma tumor necrosis factor (TNF) and soluble TNF receptors sCD30 and sTNFRI were increased using sarcoidosis, and sTNFRII increased in CS patients (n = 18). The soluble interleukin sIL-2R and vascular endothelial growth factor receptors (sVEGFR2 and sVEGFR3) increased to the greatest degree in CS patients. When computed as a function of referent control values, the majority of soluble cytokine receptors increased in both sarcoidosis and CS groups. Plasma MMP-9 levels increased in sarcoidosis but not in the CS subset. Plasma TIMP levels declined in both groups.

The findings from this study were the identification of increased activation of a cluster of soluble cytokine receptors, which augment not only inflammatory cell maturation but also transmigration in patients with sarcoidosis and patients with cardiac involvement.

The proximal optimizing technique (POT) -proximal balloon edge dilation (PBED) sequence for side branch (SB) dilatation with cross-over single-stent implantation decreases both strut obstruction at the SB ostium and stent deformation at the main branch (MB).

The purpose of this experimental bench test was to assess the impact of stent design on stent deformation, obstruction by stent struts at a jailed SB ostium, and stent strut malapposition in the POT-PBED sequence.

Fractal coronary bifurcation bench models (60- and 80-degree angles) were used, and crossover single-stent implantation (3-link stent: XIENCE Sierra, Abbott Vascular, Santa Clara, CA, n = 10; 2-link stent: Synergy, Boston Scientific, Marlborough, MA, n = 10) was performed from the MB using the POT-PBED sequence. Jailing rates at the SB ostium, stent deformation, and stent strut malapposition of the bifurcation segment were assessed using videoscopy and optical coherence tomography.

After SB dilatation using the PBED technique, jailing rates at the SB ostium and stent deformation did not differ significantly between the two types of stents. Conversely, the rate of malapposed struts of the bifurcation segment after the PBED procedure was significantly lower with 3-link stents than with 2-link stents for both 60- and 80-degree angles (60-degree angle: 4.3% ± 4.4% versus 22.0% ± 11.1%, P = 0.044; 80-degree angle: 20.8% ± 15.1% versus 57.2% ± 17.0%, P < 0.001, respectively).

In the POT-PBED sequence, 3-link stents might be a preferable coronary bifurcation stent, maintaining a jailed SB ostium while significantly reducing stent strut malapposition of the bifurcation segment when compared with 2-link stents.

Doxorubicin (DOX) is a widely used anticancer drug, but its cardiotoxicity largely limits its clinical utilization. Circular RNA spindle and kinetochore-associated protein 3 (circ-SKA3) were found to be differentially expressed in heart failure patients. In this study, we investigated the role and mechanism of circ-SKA3 in DOX-induced cardiotoxicity.

The quantitative real-time polymerase chain reaction and western blot assays were applied to measure the expression of circ-SKA3, microRNA (miR) -1303, and toll-like receptor 4 (TLR4). The viability and apoptosis of AC16 cells were analyzed using cell counting kit-8, flow cytometry, and western blot assays. The interaction between miR-1303 and circ-SKA3 or TLR4 was verified using dual-luciferase reporter and RNA immunoprecipitation assays. Exosomes were collected from culture media by the use of commercial kits and then qualified by transmission electron microscopy.

The expression of circ-SKA3 and TLR4 was increased, whereas miR-1303 expression was decreased in DOX-treated AC16 cells. DOX treatment promoted cell apoptosis and inhibited cell viability in AC16 cells in vitro, which was partially reversed by circ-SKA3 knockdown, TLR4 silencing, or miR-1303 overexpression. Mechanistically, circ-SKA3 served as a sponge for miR-1303 to upregulate TLR4, which was confirmed to be a target of miR-1303. Additionally, circ-SKA3 contributed to DOX-induced cardiotoxicity through the miR-1303/TLR4 axis. Further studies suggested that circ-SKA3 was overexpressed in exosomes extracted from DOX-mediated AC16 cells, which could be internalized by surrounding untreated AC16 cells.

Circ-SKA3 enhanced DOX-induced toxicity in AC16 cells through the miR-1303/TLR4 axis. Extracellular circ-SKA3 was packaged into exosomes, and exosomal circ-SKA3 could function as a mediator in intercellular communication between AC16 cells.

Our study was aimed at exploring the roles of lncRNA RP11-400K9.4 (RP11-400K9.4) on hypoxia/reoxygenation (H/R) -induced cardiomyocytes apoptosis. H/R model was constructed in rat primary cardiomyocytes (PC) and H9c2 cells. In this study, the results showed that H/R significantly induced the apoptosis of PC and H9c2 cells. The expression of RP11-400K9.4 was upregulated in H/R-induced PC and H9c2 cells, but miR-423 expression was downregulated. Silencing RP11-400K9.4 could attenuate H/R-induced apoptosis in PC and H9c2 cells. We also found that miR-423 was a potential target of RP11-400K9.4. The effect of silencing RP11-400K9.4 on H/R-induced apoptosis of PC and H9c2 cells was significantly reversed by miR-423 inhibitor transfection. Furthermore, our data confirmed that silencing RP11-400K9.4 promoted the activation of phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) /extracellular signal-regulated kinase (ERK) pathways and these phenomena can be reversed by miR-423 inhibitor transfection. In conclusion, our study demonstrated that silencing RP11-400K9.4 could alleviate H/R-induced cardiomyocytes damages via suppressing apoptosis by targeting miR-423 with the activation of PI3K/AKT and MEK/ERK signaling pathways.

Myocardial fibrosis is an important pathological phenomenon of cardiac remodeling that is induced by hypertension, myocardial ischemia, valvular heart disease, hypertrophic cardiomyopathy, and other heart diseases and can progress to heart failure. Urotensin II (UII) is regarded as a cardiovascular autacoid/hormone that is not only the most potent vasoconstrictor in mammals but also involved in cardiac remodeling. However, the molecular mechanisms responsible for UII-induced cardiac fibrosis have not yet been fully elucidated. Therefore, we aimed to investigate the effect of UII on myocardial fibrosis in cardiac hypertrophy and the mechanism of UII-induced cardiac fibrosis. Cardiac tissue from mice subjected to Transverse aortic constriction (TAC) was collected. Cardiac hypertrophy, myocardial fibrosis, and the expression of UII protein were assessed using echocardiography and pathological and molecular biological analyses. The effect of UII on fibrosis was evaluated in UII-treated mice and isolated rat primary cardiac fibroblasts, and the results indicated that UII induced significant myocardial fibrosis and increases in the proliferation and fibrotic responses both in mice and cultured fibroblasts. Mechanistically, UII treatment induced activation of the TGF-β/Smad signaling pathway, which was suppressed by the UII receptor antagonist. In conclusion, UII plays critical roles in cardiac fibrosis by modulating the TGF-β/Smads signaling pathway, which may be a promising therapeutic target in hypertrophic cardiomyopathy and related problems, such as cardiac remodeling and heart failure.

This study aimed to investigate the effect and mechanism of miR-26a-5p on cardiomyocyte injury induced by hypoxia/reoxygenation (H/R).

After construction of an H/R model in rat cardiomyocyte H9c2 cells, miR-26a-5p in the cells was interfered with (cells transfected with miR-26a-5p inhibitor) or overexpressed (cells transfected with a miR-26a-5p mimics). The viability and the apoptosis rate of cells in each group were detected using CCK-8 and flow cytometry; the relationship between miR-26a-5p and WNT5A was verified by a dual-luciferase reporter assay; the expression of miR-26a-5p, WNT5A, cleavedcaspase3 and Wnt/β-catenin signaling pathway-related proteins in each group was detected using qRT-PCR or Western blot; LDH release, SOD, and GSH-PX activities in each group were detected by kit.

In the H/R group, the expression level of miR-26a-5p was significantly decreased, whereas the expression level of WNT5A was significantly increased. The activity of the Wnt/β-catenin signaling pathway was up-regulated; the level of LDH released was significantly increased; and activities of SOD and GSH-PX were significantly decreased. The aforementioned changes resulted in decreased cell activity and increased apoptosis rate. The overexpression of miR-26a-5p could reduce the expression level of WNT5A, the activity of the Wnt/β-catenin signaling pathway, and the apoptosis rate and restore the cell viability.

These results suggest that miR-26a-5p can target WNT5A and thus, inhibit the Wnt/β-catenin signaling pathway activity, inhibiting H/R-induced cardiomyocyte injury and apoptosis.

A 60-year old male with paroxysmal atrial fibrillation underwent a combined procedure of left atrial appendage occlusion and pulmonary vein isolation. However, an acute intraprocedural 24-mm Watchman device dislodgement occurred, and thus a decision for urgent surgery was made. However, it was noted during the surgery that the device had migrated further to the descending aorta, just distal to the left subclavian artery. Since a right sternotomy access for retrieval was not feasible, a percutaneous approach was justified. A homemade snare was created using a combination of a long sheath, J-wire, and a regular snare, and the device was successfully retrieved without significant difficulty.

A rare complication about "Twiddler syndrome" is reported, and an interesting image about "double twist" is presented. A 78-year-old woman received a single-chamber implantable cardioverter defibrillator (ICD) for secondary prevention of ventricular arrhythmia. After she played mahjong (a traditional Chinese board game) overnight, her ICD lead sense amplitude decreased suddenly and did not recover. The intracardiac electrogram of ICD also found ventricular lead noise before this episode. Chest radiography revealed a twisted lead at the ICD pocket and a twisted and retracted ICD lead in the right atrium. An old ICD lead could not be straightened and removed, and a new ICD lead was implanted at the right ventricle. Anti-coagulation was used to prevent thrombosis for the old ICD lead.

The aortic chordae tendineae strands are suggested to be embryonic remnants of the cusp formation process. We herein describe a 70-year-old male who was admitted to our hospital for shortness of breath and chest tightness. During echocardiographic examination, severe aortic regurgitation with a ruptured fibrous strand was detected. Moreover, another fibrous strand was found by three-dimensional transesophageal echocardiography (TEE). To our knowledge, this is the first literature review of aortic chordae tendineae strands, including diagnosis, management, and mechanisms of aortic regurgitation due to such informal strands.

There is emerging evidence of prolonged recovery in survivors of coronavirus disease 2019 (COVID-19), even in those with mild COVID-19. In this paper, we report a case of a 39-year-old male with excessive body weight and a history of borderline values of arterial hypertension without therapy, who was mainly complaining of progressive dyspnea after being diagnosed with mild COVID-19. According to the recent guidelines on the holistic assessment and management of patients who had COVID-19, all preferred diagnostic procedures, including multidetector computed tomography (CT), CT pulmonary angiogram, and echocardiography, should be conducted. However, in our patient, no underlying cardiopulmonary disorder has been established. Therefore, considering all additional symptoms our patient had beyond dyspnea, our initial differential diagnosis included anxiety-related dysfunctional breathing. However, psychiatric evaluation revealed that our patient had only a mild anxiety level, which was unlikely to provoke somatic complaints. We decided to perform further investigations considering that cardiopulmonary exercise test (CPET) represents a reliable diagnostic tool for patients with unexplained dyspnea. Finally, the CPET elucidated the diastolic dysfunction of the left ventricle, which was the most probable cause of progressive dyspnea in our patient. We suggested that, based on uncontrolled cardiovascular risk factors our patient had, COVID-19 triggered a subclinical form of heart failure (HF) with preserved ejection fraction (HFpEF) to become clinically manifest. Recently, the new onset, exacerbation, or transition from subclinical to clinical HFpEF has been associated with COVID-19. Therefore, in addition to the present literature, our case should warn physicians on HFpEF among survivors of COVID-19.

Erlotinib, an epidermal growth factor receptor tyrosine kinase inhibitor, is a targeted drug used for the treatment of non-small cell lung cancer (NSCLC). Erlotinib is considered relatively safe and generally well-tolerated, with rarely reported cardiac side effects. Herein, we report a case of cardiomyopathy that developed during erlotinib treatment for NSCLC. Two months after erlotinib initiation, our 70 year-old female patient complained of progressive dyspnea, and a diagnostic endomyocardial biopsy confirmed non-specific cardiomyopathy, indicating erlotinib-induced cardiomyopathy. We believed that continued administration of erlotinib would exacerbate her heart failure, while treatment of the heart failure with intensive monitoring would allow the administration of erlotinib to be continued. This case report highlights the potential cardiotoxic effects of erlotinib and suggests the need for close clinical and echocardiographic follow-up of patients receiving erlotinib.

Sarcoidosis is a systemic inflammatory disease characterized by the formation of noncaseating epithelioid granulomas. Multiple organs, including the lung, eyes, and skin, are involved in this disorder, and cardiac involvement is a major cause of morbidity and mortality in patients with this disorder. We present the case history of a 22-year-old man with neurosarcoidosis complicated by abrupt onset of cardiac tamponade. Cardiac tamponade is a rare but potentially fatal manifestation of sarcoidosis, which is treatable with glucocorticoid therapy. Including the present case, previously reported cases of sarcoidosis with cardiac tamponade are reviewed to delineate its clinical characteristics.

A 20-year-old man with arrhythmogenic right ventricular cardiomyopathy (ARVC) was resuscitated from ventricular fibrillation. He was transferred to our hospital because of progressive multiorgan dysfunction despite mechanical circulatory support with peripheral venoarterial extracorporeal membrane oxygenation (VA-ECMO) and intra-aortic balloon pump (IABP). At admission to our hospital, chest X-ray showed bilateral complete lung opacification, and echocardiography revealed a massive thrombus occupying the left atrium (LA) and left ventricle (LV). Conversion to central ECMO with transapical LV venting and thrombectomy were performed. The huge LA thrombus occluded all pulmonary veins (PVs). Despite the surgery and intensive care, complete lung opacity remained, and he died of multiorgan failure associated with sepsis. Autopsy demonstrated bilateral pulmonary multiple red infarctions, and histopathology showed alveolar wall necrosis with extensive hemorrhage, confirming a diagnosis of pulmonary hemorrhagic infarction. Extensive pulmonary infarction was attributable to PV occlusion due to massive LA thrombus. PV thrombosis should be considered when refractory lung opacities are encountered during VA-ECMO and necessitates early intervention.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease with obstructed airflow and frequently causes secondary mild-moderate pulmonary hypertension (PH). However, a low proportion (1%-5%) of COPD patients develop severe therapy-resistant PH, and it is crucial to determine whether the patient has another disease capable of causing severe PH, including pulmonary arterial hypertension.

Here, we describe a case of a 71-year-old male with COPD complicated by severe PH and right heart failure. He had a history of heavy smoking and developed progressive hypoxemia on exertion. He had severe airflow limitation (forced expiratory volume % in one second, FEV 1.0% = 42.8%) with a markedly reduced diffusing capacity of the lung (predicted diffusion capacity of carbon monoxide, %DLCO = 29%), and high-resolution computed tomography (CT) demonstrated significant lung parenchymal abnormalities such as diffuse interlobular septal thickening, ground-glass opacities, and enlarged mediastinal lymph nodes. He was diagnosed with group 3 PH caused by COPD but resistant to the treatment of COPD, diuretics, and oxygen therapy. Pathohistological analysis of autopsy specimens revealed the coexistence of interstitial fibrosis and partial occlusion of the small intrapulmonary veins, which led to a conclusive diagnosis of pulmonary veno-occlusive disease (PVOD).

Because of its rarity and similarity with idiopathic pulmonary arterial hypertension, PVOD is difficult to diagnose antemortem and has a poor prognosis. High-resolution CT findings (septal thickening, ground glass, and enlarged lymph nodes) and severely reduced DLCO should be carefully evaluated for the early detection and treatment of PVOD in COPD patients with severe PH.

The errors in the following list appeared in the article entitled "The Usefulness and Limitations of Impedance Cardiography for cardiac Resynchronization Therapy Device Optimization" by Kojiro Ogawa, Miyako Igarashi, Akihiko Nogami, Masayoshi Yamamoto, Akinori Sugano, Yukio Sekiguchi, Kazutaka Aonuma, and Masaki Ieda (Vol. 61, 896-904, 2020).