This study aimed to evaluate the efficacy of percutaneous coronary intervention (PCI) for significant atherosclerosis lesions proximal to myocardial bridge (MB) at left anterior descending coronary artery (LAD).

A total of 330 consecutive patients with LAD significant stenosis, diagnosed as acute coronary syndrome (ACS), were included. Based on whether combined with MB, the patients were divided into the MB group (MB, n = 48) and non-MB group (NMB, n = 282). Drug eluting stents (DES) were successfully implanted in the stenostic segments prior to MB. All patients were followed up during the hospital stay, 30 days and 12 months after PCI, to evaluate the major adverse cardiac events (MACEs).

There was no difference in the incidence of MACEs between the two groups (6.2% versus 2.1%, P = 0.254) when in the hospital. During the follow-up of 30 days and 12 months after PCI, the rate of MACEs was significantly higher in the MB group than in the NMB group (18.2% versus 6.4% and 43.8% versus 17.0%, respectively, P < 0.001). Stent restenosis occurred in four patients in the MB group; whereas, in five patients in the NMB group, the rate of stent restenosis was higher in the MB group than in the NMB group (8.3% versus 1.8%, P = 0.036). Cox proportional hazards regression analysis revealed that the presence of MB was an independent predictor of MACEs (hazard ratio (HR) = 1.781, 95% confidence intervals (95% CI) = 1.108-2.863, P = 0.017).

DES implantation for significant atherosclerosis stenosis in the segments proximal to MB have higher incidence of MACEs. MB appears to be associated with a higher incidence of stent restenosis after PCI and is a significant factor in the occurrence of MACEs.

We have developed off-pump coronary artery bypass approach with lower distal mini-sternotomy (TM-OPCAB) for multivessel coronary revascularization. The aim of this retrospective study is to provide evidence for the feasibility and safety of this technique in the treatment of triple-vessel diseases.

Two hundred eighty-eight patients with triple-vessel coronary artery disease who underwent TM-OPCAB or standard off-pump coronary artery bypass surgery (S-OPCAB) were included in this study after propensity-score matching. We retrospectively reviewed the clinical data of all patients and compared their demographic data, intra- and perioperative details, as well as short-term and long-term outcomes.

TM-OPCAB resulted in significantly shorter periods of time on ventilation (P = 0.0222), shorter postoperative in-hospital stays (P < 0.0001), and lower blood transfusion rates (P = 0.0013) than S-OPCAB. Transit-time flow measurement showed there was no significant difference in postoperative graft patency between both groups. Within the 30-day post-surgical period, no death or occurrence of stroke was observed in patients undergoing TM-OPCAB or S-OPCAB. After an average of 35 months of follow-up, Kaplan-Meier survival analysis indicated that overall survival and the percentage of patients freed from major adverse cardiac and cerebrovascular events were similar between both groups. Additionally, the rate of repeat revascularization was slightly lower in the TM-OPCAB group (1.4%) than in the S-OPCAB group (2.2%), although there was no statistical difference noted.

Our findings suggest that TM-OPCAB is technically feasible and safe for use in revascularization procedures in patients with triple-vessel diseases.

Bleeding complications following percutaneous coronary interventions (PCI) have been closely associated with morbidity and mortality. Although radial arteries have been widely used in current PCI, including primary PCI, transfemoral PCI remains necessary for complex PCI. The purpose of this study was to compare the incidence of complications following elective transfemoral PCI between manual compression with and without protamine. We identified 249 consecutive patients who underwent elective transfemoral PCI from hospital records, and divided them into two groups: patients who used protamine for manual compression (the protamine group; n = 205) and patients who did not (the non-protamine group, n = 44). Complications including acute thrombosis, bleeding requiring blood transfusion, transient hypotension, skin rash, and death within 30 days were compared between groups. The baseline clinical and procedural characteristics were comparable between the protamine and non-protamine groups. The incidences of all complications were not different between the protamine (5.9%) and the non-protamine groups (9.1%) (P = 0.43). While more than 90% of the patients received drug-eluting stent implantation, there was no acute thrombus in either group. The incidence of bleeding requiring blood transfusion was significantly lower in the protamine group (0.5%) than in the non-protamine group (6.8%) (P = 0.002). Multivariate logistic regression analysis revealed the inverse association between protamine use and bleeding requiring blood transfusion (odds ratio 0.08, 95% confidence interval 0.01-0.84, P = 0.04). In conclusion, the use of protamine for manual compression following elective transfemoral PCI was safe and was associated with less bleeding complications.

Serum indoxyl sulfate (IS; a uremic toxin) levels, which are significantly higher in patients with chronic kidney disease, including those undergoing hemodialysis, than in the robust, are associated with both cardiovascular disease (CVD) and CVD-related mortality. Furthermore, coronary artery calcium (CAC) is an independent predictor of cardiovascular events in patients undergoing hemodialysis. This study aimed to interpret the association between serum IS levels and coronary plaque burden (CPB) or CAC.

A total of 30 consecutive patients on hemodialysis, who underwent 320-row coronary multidetector computed tomography (MDCT) angiography for suspected coronary artery disease, were enrolled in this prospective study. Coronary artery percent atheroma volume (a CPB marker) and percent calcium volume (a CAC marker) assessed using MDCT were evaluated. Furthermore, various oxidative and inflammatory markers typified by serum IS levels at a dialysis-free day were measured. Using these data, we investigated correlation between the inflammatory marker IS and CPB or CAC.

Multivariable analysis indicated that serum IS levels were positively correlated with CAC [partial regression coefficient, 2.89; 95% confidence interval (CI), 0.35-5.43; P = 0.03] but not with CPB, even after adjustment for cofounders. Composite cardiovascular events, namely, as all-cause death, non-fatal myocardial infarction, disabling stroke, and hospital admission for other cardiovascular events, were reported to be 50% in all patients (95% CI, 32.1-67.9).

In patients undergoing hemodialysis, serum IS levels were significantly associated with CAC but not with CPB.

Atrial electrical and structural remodeling is related to the perpetuation of atrial fibrillation (AF) subsequent to sinus node dysfunction. We investigated the relationship between AF recurrence after catheter ablation and sinus node dysfunction in long-standing persistent AF patients using the sinus node recovery time (SNRT) after defibrillation.

Fifty-one consecutive patients who underwent a first ablation for long-standing persistent AF were enrolled. Intracardiac cardioversion was applied before ablation in the absence of any antiarrhythmic drugs, and the power required to defibrillate, number, and SNRT after defibrillation were measured. All patients underwent the same designed radiofrequency catheter ablation procedure.

No patient required permanent pacemaker implantation due to sinus dysfunction after the ablation. During the follow-up period of 28.4 months (3.6-43.7), 35 out of 51 patients (69%) experienced an AF recurrence. The AF recurrence was significantly associated with an older age (60 ± 11 versus 52 ± 12 years in the non-recurrence group, P = 0.0196), longer SNRT after defibrillation (1722 [1410-2656] versus 1295 [676-1651] msec, P = 0.0125), and larger left atrial (LA) volume (59 ± 25 versus 41 ± 15 mL, P = 0.0119). There were no significant differences in the AF duration, AF cycle length, and right and total atrial conduction times between the 2 groups. A longer SNRT after defibrillation (adjusted HR 2.13, 95%CI 1.16-3.71, P = 0.0152) and larger LA volume (adjusted HR 1.03, 95%CI 1.01-1.04, P = 0.0054) were independent predictors of AF recurrence after ablation.

Assessment of the SNRT after defibrillation may help to predict a successful ablation in patients with long-standing persistent AF.

Palliative care might be beneficial to heart failure. However, the results remain controversial. We conducted a systematic review and meta-analysis to explore the effect of palliative care on heart failure.

PubMed, Embase, Web of Science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials (RCTs) assessing the effect of palliative care versus usual care on heart failure were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcome was readmission. Meta-analysis was performed using random-effect model.

Five RCTs involving 545 patients were included in the meta-analysis. Overall, compared with control intervention, palliative care intervention was found to significantly reduce the readmission [Std. mean difference = 0.79; 95% confidence intervals (CI) = 0.23 to 1.35; P = 0.006], Edmonton Symptom Assessment Scale (ESAS) (Std. mean difference = -2.5; 95% CI = -4.39 to -0.62; P = 0.009), and PHQ-9 (Std. mean difference = -1.16; 95% CI = -1.73 to -0.58; P < 0.005), as well as improve heart failure questionnaire (Std. mean difference = 4.46; 95% CI = 3.44 to 5.47; P < 0.005), but had no influence on mortality (RR = 1.54; 95% CI = 0.80 to 2.96; P = 0.19) and quality of life questionnaire (Std. mean difference = 1.81; 95% CI = -0.14 to 3.77; P = 0.07).

Compared with control intervention, palliative care intervention was found to significantly reduce readmission, ESAS, PHQ-9, and improve heart failure questionnaire, but showed no influence on mortality and quality of life questionnaire in patients with heart failure.

We sought to present our institutional protocol to manage incomplete initial repair of degenerative mitral regurgitation and to evaluate its mid-term outcomes. Eight hundred and fifteen patients with degenerative mitral insufficiency undergoing mitral valve repair were investigated in this study. The initial repair attempt was incomplete in 48 patients, leaving a degree of residual regurgitation > mild, and an elevated transmitral gradient or systolic anterior motion (SAM). These patients were further treated with medication or mitral valve re-repair or replacement under reinstituted cardiopulmonary bypass. Transesophageal echocardiographic reports and operational records were reviewed to identify morphological causes and establish management of incomplete initial repair. Mid-term outcomes of patients with re-repair and complete initial repair were evaluated and compared. Residual mitral regurgitation > mild was detected in 25 patients, an elevated transmitral gradient was detected in seven patients, and SAM was detected in 16 patients. The condition of eight patients with SAM was resolved with medication only. Mitral valve re-repair was performed in 23 patients and replacement was performed in 17, with comparable early mortality and morbidity. At 60.3 ± 25.5 months after surgery, late mitral stenosis and reoperation rate were significantly higher in re-repair patients than in patients with complete initial repair, despite comparable survival, left chamber reverse remodeling, and degree of residual regurgitation. Based on our institutional protocol, acceptable outcomes can be achieved for patients with incomplete initial mitral valve repair. Management should be tailored based on the characteristics of the mitral valve complex, expected repair durability, and operative risk.

To assess the potential advantages of minimally invasive surgery using a single femoral venous drainage method versus femoral venous and superior vena cava or jugular venous drainage method during repeat tricuspid valve surgery.

From January 2010 to December 2016, 50 repeat tricuspid valve procedures were performed using a minimally invasive approach without aortic cross-clamping at our institution. The arterial cannula was inserted into the femoral artery, and at the same time, the venous cannula was placed in the femoral vein in 28 patients (FV group) during cardiopulmonary bypass (CPB). The venous cannula was inserted into the femoral vein and the superior vena cava or jugular vein in 22 patients (FSV group).

Overall, 36 patients underwent tricuspid valve replacement (TVR) and 14 patients underwent tricuspid valvuloplasty (TVP). The CPB time and operation time, respectively, were 72.96 ± 25.90 minutes versus 78.59 ± 31.95 minutes (P = 0.495) and 170.75 ± 73.31 minutes versus 228.87 ± 61.45 minutes (P = 0.004) in the FV group versus the FVS group. There were no significant differences in the ventilator-assisted time, the first-day LVEF, and the intensive care unit (ICU) stay between the FV group and the FSV group.

Both types of drainage were effective and could ensure safety during the operative procedure. The vacuum-assisted single femoral venous drainage method simplified the minimally invasive isolated repeat tricuspid valve surgical process more significantly and is the more appropriate choice.

To achieve further risk stratification in hypertrophic cardiomyopathy (HCM) patients, we localized and quantified layer-specific LVM fibrosis on MRI in HCM patients using regional layer-specific peak longitudinal strain (PLS) and peak circumferential strain (PCS) in LV myocardium (LVM) on speckle tracking transthoracic echocardiography (TTE). A total of 18 HCM patients (14 males; 58 ± 17 years) underwent 1.5T-MRI and TTE. PLS and PCS in each layer of the LVM (endocardium, epicardium, and whole-layer myocardium) were calculated for 17 AHA-defined lesions. MRI assessment showed that fibrosis was classified as endocardial, epicardial, or whole-layer (= either or both of these). Regional PLS was smaller in fibrotic endocardial lesions than in non-fibrotic endocardial lesions (P = 0.004). To detect LV endocardial lesions with fibrosis, ROC curves of regional PLS revealed an area under the curve (AUC) of 0.609 and a best cut-off point of 13.5%, with sensitivity of 65.3% and specificity of 54.3%. Regional PLS was also smaller in fibrotic epicardial lesions than in non-fibrotic epicardial lesions (P < 0.001). To detect LV epicardial lesions with fibrosis, ROC curves of PLS revealed an AUC of 0.684 and a best cut-off point of 9.5%, with sensitivity of 73.5% and specificity of 55.5%. Using whole-layer myocardium analysis, PLS was smaller in fibrotic lesions than in non-fibrotic lesions (P < 0.001). To detect whole-layer LV lesions with fibrosis, ROC curves of regional PLS revealed an AUC of 0.674 and a best cut-off point of 12.5%, with sensitivity of 79.0% and specificity of 50.7%. There were no significant differences in PCS of LV myocardium (endocardium, epicardium, and whole-layer) between fibrotic and non-fibrotic lesions. Quantitative regional PLS but not PCS in LV endocardium, epicardium, and whole-layer myocardium provides useful non-invasive information for layer-specific localization of fibrosis in HCM patients.

The cardiac phenotype of laminopathies is characterized by cardiac conduction disorders (CCDs) and dilated cardiomyopathy (DCM). Although laminopathies have been considered monogenic, they exhibit a remarkable degree of clinical variability. This case series aimed to detect the causal mutation and to investigate the causes of clinical variability in a Japanese family with inherited CCD and DCM.Of the five family members investigated, four had either CCD/DCM or CCD alone, while one subject had no cardiovascular disease and acted as a normal control. We performed targeted resequencing of 174 inherited cardiovascular disease-associated genes in this family and pathological mutations were confirmed using Sanger sequencing. The degree of clinical severity and variability were also evaluated using long-term medical records. We discovered a novel heterozygous truncating lamin A/C (LMNA) mutation (c.774delG) in all four subjects with CCD. Because this mutation was predicted to cause a frameshift mutation and premature termination (p.Gln258HisfsTer222) in LMNA, we believe that this LMNA mutation was the causal mutation in this family with CCD and laminopathies. In addition, gender-specific intra-familiar clinical variability was observed in this Japanese family where affected males exhibited an earlier onset of CCD and more severe DCM compared to affected females. Using targeted resequencing, we discovered a novel truncating LMNA mutation associated with CCD and DCM in this family characterized by gender differences in clinical severity in LMNA carriers. Our results suggest that in patients with laminopathy, clinical severity may be the result of multiple factors.

Forward Projected Model-based Iterative Reconstruction SoluTion (FIRST) is a new reconstruction technique using CT, which provides successful reconstruction of high-quality CT images, especially in low contrast imaging. To evaluate improvements in the diagnostic accuracy of the detection of abnormal late enhancement (LE) in left-ventricular myocardium (LVM) using 320-slice CT with FIRST, we compared this modality with previous CT methods in patients with non-ischemic cardiomyopathy or a cardiac tumor.

This was a retrospective study of 88 patients (56 males; 57 ± 15 years) suspected of having non-ischemic myocardial disease or a cardiac tumor. The first 52 consecutive patients (Group 1) underwent 16-slice CT at 140 kV tube voltage and an average tube current of 337 ± 20 mA, and 1.5 T MRI. The next 18 patients (Group 2) underwent 1st generation 320-slice CT at 120 kV tube voltage and an average tube current of 255 ± 106 mA, and 1.5T MRI; the remaining 18 patients (Group 3) underwent 2nd generation 320-slice CT with FIRST, at 80 kV tube voltage and a tube current of 800 mA, and 1.5T or 3T MRI.

On patient-based analysis, no significant differences were observed between the 3 groups. For segment-based analysis, the specificity and overall accuracy were significantly higher (both P < 0.05) in Group 3 than in Group 1. Positive predictive value (PPV) was significantly higher in Group 3 than in Groups 1 and 2.

The diagnostic accuracy of LE on CT for detecting myocardial fibrosis determined by late gadolinium-enhanced MRI was improved with the use of 2nd generation 320-slice CT with FIRST, in particular regarding specificity, PPV, and overall accuracy.

Asymptomatic carotid stenosis is common and is associated with increased risk of stroke. The relative efficacy and safety of carotid endarterectomy (CEA) and carotid stenting (CAS) in patients with asymptomatic carotid stenosis remain unclear. Five studies that recruited patients with asymptomatic but significant carotid stenosis, who underwent CEA or CAS, were included in this systematic review and meta-analysis. The analyzed outcomes included risks of stroke, myocardial infarction (MI), and death. Risk ratio (RR) and 95% confidence interval (95% CI) were calculated and pooled for meta-analysis. Pooled analysis demonstrated that compared with CEA, CAS was associated with a decreased risk of MI (RR = 0.49, 95%CI = 0.26-0.91, P = 0.023) and slightly increased risk of stroke, although not significant (RR = 1.69, 95% CI = 0.97-2.92, P = 0.063). There was no difference in the death rates between the groups (RR = 0.60, 95% CI = 0.17-2.18, P = 0.436). In the subgroup analysis, CAS was associated with a decreased risk of MI in mixed patients (RR = 0.45, 95% CI = 0.26-0.78, P = 0.005), but not in asymptomatic patients (RR = 0.549, 95% CI = 0.26-1.17, P = 0.119). Compared with CAS, CEA was associated with decreased risk of perioperative stroke and increased risk of MI; it did not affect the risk of death in patients with asymptomatic carotid stenosis. In the subgroup analysis, the decreased risk of MI after CAS was significant only in the mixed patients group. CAS was associated with higher risk of stroke but lower risk of MI than those with CEA. Both procedures appeared equivalent in terms of the risk of death.

Endothelial dysfunction is observed in several cardiovascular diseases, where endothelium-dependent vasodilation is impaired by oxidative stress. However, the time course of endothelial function during the perioperative period of a minor-to-moderate surgery, and the effects of atherosclerotic risk factors and employed general anesthetics on recovery of endothelial function, are unknown. Endothelial function of 30 patients was evaluated as the reactive hyperemia index (RHI) of reactive hyperemia peripheral arterial tonometry. RHI was measured on day before surgery (control), immediately after surgery (Day 0), day after surgery (Day 1), and day 4 after surgery (Day 4) in patients with no functional limitations who were scheduled for oral and maxillofacial surgery of around 3 hours. Sevoflurane- or propofol-based anesthesia supplemented with an opioid analgesic remifentanil was employed. The control RHI was 2.26 ± 0.64. The RHI significantly decreased to the lowest level on Day 0 (1.52 ± 0.28), recovered on Day 1 (2.07 ± 0.58), and improved further on Day 4 (2.55 ± 0.83). Multiple linear regression analysis revealed that recovery of the RHI from Day 0 to Day 4 was impaired by diabetes mellitus (P = 0.0313), obesity (BMI ≥ 25; P = 0.0166), hyperuricemia (uric acid ≥ 6.0 mg/dL; P = 0.0416) and sevoflurane-based anesthesia (P = 0.0308). These findings suggest that endothelial function as evaluated by the RHI is severely suppressed on the day of a minor-to-moderate surgery, and that it improves until the 4th postoperative day on average. Recovery of endothelial function is impaired by diabetes mellitus, obesity, hyperuricemia, and sevoflurane-based anesthesia.

An increase in the ratio of the brachial pre-ejection period to brachial ejection time [pre-ejection period (PEP)/ET] is correlated with a decrease of left ventricular ejection fraction (LVEF). The current study was designed to test the hypothesis that the change value (Δ) of PEP/ET is a useful indicator of Δ LVEF in patients with left ventricular systolic dysfunction.

We consecutively enrolled 104 patients with left ventricular systolic dysfunction (LVEF < 45%). PEP/ET, B-type natriuretic peptide (BNP), and LVEF were evaluated at baseline and at 6-month follow-up. Compared with the baseline measurements, the 6-month values of ΔLVEF, ΔBNP, and ΔPEP/ET were 9.8% ± 9.0% (from 36.3% ± 9.2% to 46.3% ± 12.5%, P < 0.001), -168.5 ± 255.4 (from 271.4 ± 282.5 to 104.1 ± 129.6, P < 0.001), and -0.060 ± 0.069 (from 0.413 ± 0.097 to 0.358 ± 0.079, P < 0.001), respectively. There were significant correlations between LVEF and PEP/ET and between LVEF and BNP in both the initial (r = -0.316, P = 0.001 and r = -0.598, P < 0.001, respectively) and 6-month follow-up (r = -0.307, P = 0.003 and r = -0.701, P < 0.001, respectively). The Steiger's Z test showed that BNP had a significantly stronger correlation with LVEF compared with the correlations between LVEF and PEP/ET in both the initial and 6-month studies (Z = 2.471, P = 0.013 and Z = 3.575, P < 0.001, respectively). There were also significant correlations between ΔLVEF and ΔPEP/ET (r = -0.515, P < 0.001) and between ΔLVEF and ΔBNP (r = -0.581, P < 0.001); however, there was no difference between the correlations for ΔLVEF and ΔPEP/ET versus ΔLVEF and ΔBNP (Steiger's Z = 0.600, P = 0.545).

In patients with left ventricular systolic dysfunction not only ΔBNP but also ΔPEP/ET could be a simple indicator of predicting change of LVEF.

Decongestion is an important goal of heart failure (HF) management. Blood cell concentration is a recognized indicator for guiding decongestive treatment for HF. We aimed to assess the clinical impact of hemodilution and hemoconcentration after initial treatment in acute decompensated HF (ADHF) patients. We retrospectively evaluated hemoglobin levels and body weight obtained before admission, on admission, 3 days after admission, and at discharge in 102 consecutive patients admitted with ADHF. Patients were then stratified into hemodilution (n = 55) and hemoconcentration (n = 47) groups based on whether their hemoglobin levels decreased or increased, respectively, during the first 3 days after admission. From before admission to admission, hemoglobin levels decreased less in the hemodilution group (-0.16 ± 0.98 g/dL) than in the hemoconcentration group (-0.88 ± 1.11 g/dL) (P < 0.001); however, there was no significant difference in body weight (P≥ 0.05). More patients in the hemodilution group (85%) had grade III/IV pulmonary edema (Turner's criteria) compared with the hemoconcentration group (63%) (P < 0.01). Rate of readmission for HF within 180 days of discharge was higher in the hemodilution group (34%) compared with the hemoconcentration group (9%) (P < 0.01). Hemodilution after initial treatment for ADHF was associated with severe pulmonary edema at admission and higher readmission rates.

Ischemic reperfusion (I/R) injury is a serious problem in the treatment of ischemic heart disease. MicroRNA-208a (miR-208a) is a cardiac-specific or cardiac-enriched miRNA. This study was aimed to assess the role of miR-208a in I/R injury. H9c2 cells were used to simulate I/R injury in vitro. miR-208a expression level was measured by qPCR. H9c2 cells after simulated I/R injury were transfected with miR-208a mimic, AOS-miR-208a or negative controls. LDH release, MDA and SOD contents were measured by corresponding purchased detection kits, respectively. Cell apoptosis were measured by flow cytometry. Then binding effect of miR-208a on CHD9 3'UTR was detected by Dual-Luciferase activity assay. After miRNA or CHD9 overexpression transfections, expressions of apoptosis-related factors, CHD9, Notch 1, IκBα, and p65 in H9c2 cells after I/R injury were measured by Western blot assay. Results showed that in H9c2 cells after simulated I/R injury, miR-208a was upregulated. The elevated miR-208a expression enhanced the injury of cells and promoted cell apoptosis. miR-208a directly target 3'UTR of CHD9 and negatively regulated CHD9 expression. Overexpression of CHD9 rescued I/R injury that was enhanced by miR-208a mimic transfection. miR-208a was positively related with activation of Notch/NF-B signal pathways via CHD9. In conclusion, miR-208a was a cardiac-enriched miRNA and CHD9 is a direct target of miR-208a, which was also related with Notch/NFB signal pathway during I/R injury. miR-208a has potential to be a biomarker for early diagnosis of I/R injury and might be used as a treatment target in clinical treatment of ischemic heart disease.

Ca⁺⁺-channel antagonist verapamil and ATP-sensitive K⁺-channel opener pinacidil are known to decrease the rise in extracellular K⁺ ([K⁺]_e) level and pH (pH_e) that occurs during reversible acute myocardial ischemia and to lessen the accompanying activation delay. Verapamil is also known to decrease the incidence of ventricular tachycardia (VT)/fibrillation (VF) during acute myocardial ischemia; however, the effects of ATP-sensitive K⁺-channel opener on the incidence of VT/VF are controversial. We studied, in an in vivo pig model, the effects of verapamil and pinacidil on the changes in [K⁺]_e level and pH_e, local activation, and the incidence of VT/VF during 60 minutes of ischemia. Thirty-one pigs were divided into 2 groups: a verapamil group (9 control pigs and 8 verapamil-treated pigs) and pinacidil group (5 control pigs and 9 pinacidil-treated pigs). In the verapamil group, VF developed in 1 of the 9 control pigs, whereas no VF developed in 8 verapamil-treated pigs. In the pinacidil group, VF developed in 3 of the 5 control pigs and all 9 pinacidil-treated pigs. Under verapamil treatment (versus the control condition), onset of the second rise in [K⁺]_e level was delayed, and the maximum rise in [K⁺]_e level was decreased. Under pinacidil treatment (versus the control condition), time to the onset of VT/VF was shorter than that under the control condition, and VT/VF developed at lower [K⁺]_e level and higher pH_e. In conclusion, VF may develop at a lesser [K⁺]_e rise and pH_e fall in the presence of pinacidil during acute myocardial ischemia.

The present study was performed to identify the genetic abnormalities in a family with familial hypertrophic cardiomyopathy.

Peripheral blood samples were collected from 22 members of a Chinese family with hypertrophic cardiomyopathy and 307 healthy controls. A total of 26 candidate pathogenic genes were analyzed in the proband using targeted capture sequencing. Identified mutations were analyzed using Sanger sequencing in all family members and healthy controls.

A missense mutation (c.1172A>C, p. Asn391Thr) in exon 12 of MYH7 was identified in eight family members, among which six of them were hypertrophic cardiomyopathy carriers. Three carriers presented with cardiac dysfunction. Four members of this pedigree died suddenly, three of whom were diagnosed with hypertrophic cardiomyopathy.

From the results of this study, we concluded that the Asn391Thr mutation of MYH7 is a malignant mutation for HCM and that mutation carriers should get effective treatment to prevent sudden death.

A biological pacemaker is expected to solve the persisting problems of an artificial cardiac pacemaker including short battery life, lead breaks, infection, and electromagnetic interference. We previously reported HCN4 overexpression enhances pacemaking ability of mouse embryonic stem cell-derived cardiomyocytes (mESC-CMs) in vitro. However, the effect of these cells on bradycardia in vivo has remained unclear. Therefore, we transplanted HCN4-overexpressing mESC-CMs into bradycardia model animals and investigated whether they could function as a biological pacemaker. The rabbit Hcn4 gene was transfected into mouse embryonic stem cells and induced HCN4-overexpressing mESC-CMs. Non-cardiomyocytes were removed under serum/glucose-free and lactate-supplemented conditions. Cardiac balls containing 5 × 10³ mESC-CMs were made by using the hanging drop method. One hundred cardiac balls were injected into the left ventricular free wall of complete atrioventricular block (CAVB) model rats. Heart beats were evaluated using an implantable telemetry system 7 to 30 days after cell transplantation. The result showed that ectopic ventricular beats that were faster than the intrinsic escape rhythm were often observed in CAVB model rats transplanted with HCN4-overexpressing mESC-CMs. On the other hand, the rats transplanted with non-overexpressing mESC-CMs showed sporadic single premature ventricular contraction but not sustained ectopic ventricular rhythms. These results indicated that HCN4-overexpressing mESC-CMs produce rapid ectopic ventricular rhythms as a biological pacemaker.

Vascular cells have a finite lifespan and eventually enter irreversible growth arrest called cellular senescence. We have previously suggested that vascular cell senescence contributes to the pathogenesis of human atherosclerosis. Amlodipine is a mixture of two enantiomers, one of which (S- enantiomer) has L-type channel blocking activity, while the other (R+ enantiomer) shows ~1000-fold weaker channel blocking activity than S- enantiomer and has other unknown effects. It has been reported that amlodipine inhibits the progression of atherosclerosis in humans, but the molecular mechanism of this beneficial effect remains unknown. Apolipoprotein E-deficient mice on a high-fat diet were treated with amlodipine, its R+ enantiomer or vehicle for eight weeks. Compared with vehicle treatment, both amlodipine and the R+ enantiomer significantly reduced the number of senescent vascular cells and inhibited plaque formation to a similar extent. Expression of the pro-inflammatory molecule interleukin-1β was markedly upregulated in vehicle-treated mice, but was inhibited to a similar extent by treatment with amlodipine or the R+ enantiomer. Likewise, activation of p53 (a critical inducer of senescence) was markedly suppressed by treatment with amlodipine or the R+ enantiomer. These results suggest that amlodipine inhibits vascular cell senescence and protects against atherogenesis at least partly by a mechanism that is independent of calcium channel blockade.

We report a novel technique for retrieving an entrapped Gaia guidewires in severely calcified coronary chronic total occlusion (CTO) using a rotational atherectomy device. By successfully cutting the entrapped and untangled guidewire within the CTO with the use of a rotational atherectomy device, we could effectively remove the Gaia guidewire from the right coronary artery.

The mechanism of atrial lead dysfunction varies in patients receiving pacemaker implantation and this needs to be investigated, especially when the causes are reversible. We report and discuss a 76-year-old female who had atrial lead dysfunction caused by acute myocardial infarction and who was recovered after primary percutaneous coronary intervention. The sequential electrocardiographic changes were demonstrated and the possible mechanisms were discussed.

Allergic reactions to contrast media are a frequently reported complication of coronary angiography. The majority of patients experience mild, self-limited episodes, but in rare cases patients may experience severe, persistent symptoms. A strategy of premedication with corticosteroids and anti-histamines and an optimal selection of contrast agent is almost always successful in averting contrast reactions, yet a select few patients will continue to have breakthrough events. This is a case of recurrent, severe allergy to contrast media despite standard precautions complicating the treatment of non-ST elevation myocardial infarction (NSTEMI). Our patient was successfully managed with a strategy of rapid desensitization to iodinated contrast media achieved by administering progressively incremental doses of the media.

A cardiac resynchronization therapy defibrillator (CRT-D) (Medtronic Inc. Protecta XT) was implanted in a 67-year-old man who had cardiac sarcoidosis with extremely low cardiac function. He had ventricular tachycardia which was controlled by catheter ablation, medication and pacing. The programmed mode was DDI, lower rate was 90 beats/minute, paced AV delay was 150 ms, and the noncompetitive atrial pacing (NCAP) function was programmed as 300 ms.

After his admission for pneumonia and heart failure, we changed his DDI mode to a DDD mode because he had atrial tachycardia, which led to inadequate bi-ventricular pacing. After a while, there were cycle lengths which were longer than his device setting and alternately varied. We were able to avoid this phenomenon with AV delay of 120 ms and NCAP of 200 ms.

NCAP is an algorithm which creates a gap above a certain period after the detection of an atrial signal during the postventricular atrial refractory period of the pacemaker. This is to prevent atrial tachycardia and repetitive non-reentrant ventriculoatrial (VA) synchrony in the presence of retrograde VA conduction. But in this case, NCAP algorithm induced much lower rate than the programmed basic lower rate. This situation produced some arrhythmias and exacerbated symptoms of heart failure. This had to be paid attention to, especially when the device was programmed at high basic heart rate.

A 78-year-old woman had paroxysmal atrial fibrillation and effort angina. Two months before she was admitted for a coronary angiography, she had been feeling dizzy. A Holter 24-hour electrocardiography monitor exhibited an asymptomatic episode of 2.9 seconds of RR interval. She underwent a coronary angiography, which showed intermediate stenosis in the left descending artery. Fractional flow reserve (FFR) measurement using intracoronary papaverine administration was performed. After intracoronary papaverine (12 mg) administration, pause of 4 seconds led to polymorphic ventricular tachycardia (VT), although the VT terminated spontaneously. Premature ventricular beat occurred and led to sustained polymorphic VT. In cardiac electrophysiology study, pacing from the right atrium showed that the maximum sinus node recovery time (SRT) was 910 ms. After procainamide (10 mg/kg) administration, the maximum SRT was 16.3 seconds with some junctional escapes. After intravenous papaverine administration, there was a slight change. Intracoronary papaverine administration induced about 9-seconds pause with some junctional escapes. We conclude that intracoronary papaverine administration reveals potential sinus node dysfunction. The patient has been asymptomatic since the implantation of the pacemaker. Patients with suspicious sinus dysfunction should be careful.

An 88-year-old woman was diagnosed with aortic stenosis and an aortic annulus that was too narrow to perform transcatheter aortic valve implantation. Surgery was performed through a 7-cm right mini-thoracotomy at the fourth intercostal space. A 19-mm aortic valve bioprosthesis was implanted after root enlargement. The fourth intercostal space was a suitable site for aortic root enlargement because of the shorter skin-to-root distance and the detailed exposure of the aortic valve after cutting the aortic wall. This study concluded that minimally-invasive aortic valve replacement following root enlargement can be an option for the treatment of elderly patients with aortic stenosis accompanied by an annulus that is too small to perform transcatheter aortic valve implantation.

Transaortic septal myectomy is a procedure that involves a learning curve for surgeons because the bulging interventricular septum usually interferes with the visualization of the deep parts of the left ventricular chamber. In this case report, we demonstrate computed tomography virtual endoscopy for preoperative simulation, which enabled us to clearly image the relationship among the bulging septum, the expected myectomy area, and the structures deep in the left ventricle, such as the papillary muscle and abnormal muscular bundles, which are hidden by the hypertrophic septum, thus preventing visualization. This approach could make minimally invasive transaortic septal myectomy safe and easy.

We present the case of a patient with acute necrotizing eosinophilic myocarditis (ANEM) who rapidly recovered after receiving high-dose corticosteroid therapy. A previously healthy 29-year-old woman presented to our hospital with abdominal pain, nausea, and fever that had lasted for two days. Her clinical condition progressively declined and she ultimately presented with cardiogenic shock due to fulminant heart failure and atrioventricular dissociation due to sinus bradycardia, which required inotropic and ventilatory support. Endomyocardial biopsy results were consistent with ANEM. High-dose corticosteroids were promptly initiated, and her cardiac function rapidly improved, with almost complete cardiac recovery one week later. She survived with completely normalized left ventricular systolic and diastolic function after high-dose corticosteroid therapy. The prompt and definite pathological diagnosis based on endomyocardial biopsy in the acute phase might have been instrumental in improving the outcome.

Fluorine-18 fluorodeoxygluose (¹⁸F-FDG) positron emission tomography (PET) is a useful tool for evaluating disease activity in sarcoidosis including cardiac involvement. A 67-year-old patient who developed atrioventricular block requiring permanent pacemaker implantation was diagnosed with cardiac sarcoidosis. The patient did not undergo steroid or immunosuppressive therapy but underwent serial ¹⁸F-FDG PET examination, which showed spontaneous reduction in the myocardial FDG uptake, indicating the remission of immune-inflammatory activity. Although the global systolic function remained preserved, thinning of the septal wall emerged during the clinical course of follow-up, which is characteristic for cardiac sarcoidosis.

A 61-year-old male patient was admitted to our hospital with recurrent palpitations and syncope. Electrocardiography, echocardiography, and contrast-enhanced computed tomography were performed. The patient was diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC) complicated by multiple thrombi, and ventricular tachycardia (VT) without typical left bundle branch block (LBBB) morphology. This case suggests that VT is not always the sole contributor to syncope and death in patients with ARVC, and pulmonary embolism should be considered. Furthermore, VT with typical LBBB morphology is not an absolute necessity as a major criterion for the diagnosis of ARVC when the right heart is extremely enlarged.

Purulent pericarditis is a rare disease in the antibiotic era. The common pathogens of purulent pericarditis are gram-positive species such as Staphylococcus aureus. Streptococcus pneumoniae, Salmonella, Haemophilus, fungal pathogens/tuberculosis can also result in purulent pericarditis. We report an old male case of purulent pericarditis by Escherichia coli. He came to our hospital suffering from leg edema for 3 months. Echocardiography revealed the large amount of pericardial effusion, and he was admitted to test the cause of pericardial effusion without high fever, tachycardia, and shock vital signs. On the third day, he suddenly presented vital shock. We performed emergency cardiopulmonary resuscitation and pericardiocentesis. Appearance of pericardial effusion was hemorrhagic and purulent. The gram stain revealed remarkable E. coli invasion to pericardial space. Antibiotic therapy was immediately started; however, he died on sixth day with septic shock. The cytological examination of pericardial effusion suggested the invasion of malignant lymphoma to pericardium. This case showed subacute or chronic process of pericarditis without severe clinical and laboratory sings before admission. Nevertheless, bacterial purulent pericarditis usually shows acute clinical manifestation; the first process of this case was very silent. Immunosuppression of malignant lymphoma might make E. coli translocation from gastrointestinal tract to pericardial space, and bacterial pericarditis was progressed to purulent pericarditis. In the latter process, this case showed unexpected rush progression to death by sepsis from purulent pericarditis. Immediate pericardiocentesis should be performed for a prompt diagnosis of purulent pericarditis, and it might have improved the outcome of this case.

A 69-year-old man on maintenance dialysis underwent endovascular therapy for a refractory wound due to critical limb ischemia in the popliteal and below-knee arteries. Because of bulky calcified nodules projecting into the popliteal artery, conventional balloon angioplasty alone did not seem to provide a sufficient lumen area, and we ablated the calcified nodules by using myocardial biopsy forceps for lesion preparation. Under roadmap guidance, we repeated ablation 39 times to carefully tear off the bulky calcified nodules, and subsequently performed balloon angioplasty in the popliteal artery. Neither flow-limiting dissection nor perforation occurred, and a sufficient lumen area was obtained. After treatment of the popliteal artery, conventional endovascular therapy was performed in the below-knee arteries. One month later, the wound was fully epithelialized. We report a case of critical limb ischemia with calcified nodules projecting into the popliteal artery, in which the use of myocardial biopsy forceps led to good results.

The intra-pericardial paraganglioma is very rare and most of them present with hypertension or palpitations. Here we reported an extraordinarily rare case of intra-pericardial paraganglioma presenting as faint, pitting edema, abdominal fullness with ascites, and hemopericardium with impending tamponade, which was treated successfully by emergent pericardiocentesis and surgical resection.

An error appeared in the article titled "Can Anti-inflammatory Therapy Prevent Atrial Fibrillation in Myocardial Infarction Patients?" by Yukiteru Nakayama and Katsuhito Fujiu (Vol. 59, No. 1, 3-5, 2018).

The name of the last author on page 3 should be "Katsuhito Fujiu" and not "Katushito Fujiu".