Qualitative study of barriers and facilitators encountered by individuals with physical diseases in returning and continuing to work.

BACKGROUND: The number of employees with physical diseases is increasing, and there is a need for support to help them return and continue to work. To provide effective support, it is important to identify barriers and facilitators for individuals in returning and continuing to work. Previous studies have reported barriers and facilitators for specific diseases. However, few reports have dealt with these issues across various diseases. To identify a range of barriers and facilitators that may apply to different physical diseases, we conducted a qualitative analysis by interviewing patients with diverse characteristics being treated for diseases. METHODS: We conducted semi-structured interviews based on the criteria for qualitative research. We investigated three disease groups to obtain details of barriers and facilitators: impairments that were visible to other people (mainly stroke); impairments invisible to others (mainly heart disease); and impairments that changed over time (mainly cancer). Interview transcripts were analyzed and the results reported using systematic text condensation. RESULTS: We extracted 769 meaning units from 28 patient interviews. We categorized barriers and facilitators that were generalizable to various diseases into three themes (personal factors, workplace factors, and inter-sectoral collaboration and social resources) and 10 sub-themes (work ability, psychological impacts, health literacy, social status, family background, workplace structure, workplace system, workplace support, inter-sectoral collaboration, and social resources). CONCLUSIONS: This study identified 10 sub-themes that can be applied for workers with physical diseases; those sub-themes may be used as a basis for communicating with those individuals about returning and continuing to work. Our results suggest that various barriers and facilitators for workers with physical diseases should be understood and addressed at medical institutions, workplaces, and support sites.

"Carryover phenomenon" in subcutaneous implantable cardioverter-defibrillator: Residual energy caused early shock to subsequent ventricular tachycardia.

We reported a case of early S-ICD shock due to the carryover of previously charged energy. Depending on the interval with the preceding event, an early shock may occur for the subsequent event. Especially, in cases where non-sustained VTs occur frequently, the indication for S-ICD surgery should be considered carefully.

Relationship between device displacement distance toward the caudal side during standing and pocket position laterality.

BACKGROUND: The displacement of cardiac implantable electronic devices (CIEDs) toward the caudal side during standing after CIED implantation could cause lead dislodgement. This study investigated the relationship between supine pocket position and standing CIEDs' displacement distance after the implantation. METHODS: After CIED surgeries performed at 2 hospitals between 2012 and 2020, 134 patients underwent postoperative chest x-rays in the supine and standing positions during hospitalization. To measure the displacement distance of CIEDs from the supine to the standing position, we identified the first thoracic vertebrae (Th1) in the supine position using the first rib as an index, drew a horizontal line at the lower edge of the Th1, and calculated the distance from that point to the upper edge of the CIED. The difference between measures for the two positions was compared. At the position of the pocket in the thorax in the supine position, the ratio of the distance between the thorax and the device is defined as the device thorax ratio (DTR). We examined the relationship between DTR and CIED displacement distance. RESULTS: In this study, we included 134 patients (53% men; median age, 79 years, body mass index, 22.3 ± 3.4; pacemaker 93%, left implantation 96%). We found that the more lateral the position of the CIED pocket, the more the CIED fell when standing (confidence interval = 0.34-0.60, P < .001). CONCLUSIONS: The farther the CIED was implanted outside the thorax in the supine position, the more significantly the CIED was displaced in the standing position.

Adenosine revives catheter-induced mechanical blocks in radiofrequency ablation.

Adenosine can hyperpolarize the atrial action potential, which helps rapidly re-establish the membrane potential in ablated sites and unmask "dormant conduction." It has been reported that pharmacological agents, including adenosine, were unable to revive traumatized tissues. We present the first case of the catheter-induced mechanical block ("bump" phenomenon) that was unmasked with adenosine administration in the working myocardium of the superior vena cava. This result may be because, unlike before, we could determine the force of contact between the tip of the ablation catheter and the myocardial tissue. This case suggests the clinical usefulness of adenosine for unmasking bumped sites.

Rate-dependent pacing failure after pacemaker implantation: Novel insights into the mechanism of using adenosine.

An 82-year-old woman received pacemaker implantation for sick sinus syndrome. Two days after the implantation, electrocardiography showed 2:1 atrial pacing failure, followed by a bradycardia-dependent increase in the atrial pacing threshold during a pacemaker examination. However, transient 1:1 atrial pacing capture recovered by adenosine triphosphate (ATP) administration, which was performed to evaluate the bradycardia-dependent pacing failure mechanism. We considered this phenomenon to be caused by Phase 4 depolarization and avoided replacing this atrial lead. Three weeks later, the atrial pacing threshold had improved. We report the potential role of Phase 4 depolarization in a bradycardia-dependent increase in pacing threshold by using ATP.

Prevention of serious air embolism during cryoballoon ablation; risk assessment of air intrusion into the sheath by catheter selection and change in intrathoracic pressure: An ex vivo study.

INTRODUCTION: One cause of cerebral infarction during cryoballoon ablation is the entry of air into a sheath due to the use of inappropriate catheters. It is known that the left atrial pressure of patients with obstructive sleep apnea syndrome can be negative. However, the effects of catheter selection and negative pressure changes in the sheath on air intrusion are not yet well understood. The aim of this study was to evaluate how catheter selection and negative pressure changes affect air intrusion and to perform countermeasures for air intrusion. METHODS AND RESULTS: This experiment used siphon principle to create negative pressure in the sheath. Noncryoablation catheters (not designed exclusively for cryoballoon ablation) and cryoballoon catheters were investigated. Catheters were inserted into the sheath and then removed. Thereafter, the amount of air in the sheath was measured. For catheters producing significantly larger amounts of air intrusion, the catheters were inserted via a long sheath in the sheath (sheath-in-sheath technique) and the same procedures were repeated. We found that the amount of air intrusion through most of the noncryoablation catheters was significantly larger than that through cryoablation catheters. An increase in the magnitude of negative pressure in the sheath resulted in a proportional increase in air intrusion, but the sheath-in-sheath technique significantly reduced air intrusion. CONCLUSION: The amount of air intrusion increased when using catheters with complicated tip shapes and thin outer diameters and when the magnitude of negative pressure in the sheath increased. The sheath-in-sheath technique may be an effective countermeasure.

Prognostic impact of lead tip position confirmed via computed tomography in patients with right ventricular septal pacing.

BACKGROUND: Although fluoroscopy-guided right ventricular (RV) lead placement in the ventricular septum is a widely performed procedure, variation in true RV lead tip position confirmed via computed tomography (CT) and its prognostic implications in patients with atrioventricular block (AVB) are not well understood. OBJECTIVE: The purpose of this study was to evaluate the prognostic impact of CT-confirmed RV lead tip position. METHODS: We retrospectively enrolled 228 consecutive patients (age 77 ± 10 years; 125 men) with AVB who underwent fluoroscopy-guided RV septal lead implantation and thoracic CT after pacemaker implantation. Patients were classified into septal and free-wall groups according to RV lead tip position. The primary endpoint was the composite outcome of cardiac death and heart failure hospitalization. RESULTS: The RV lead tip was located at the free wall in 18 patients (8%). The primary endpoint occurred in 37 patients (16%) over median follow-up of 41 months. Electrocardiographic analysis found that R amplitude >0.53 mV in lead I was significantly predictive of free-wall pacing, with sensitivity of 70% and specificity of 77%. Multivariate Cox regression analysis demonstrated that the lead tip in the free wall (hazard ratio 2.93; 95% confidence interval 1.21-7.11; P = .018) was an independent predictor of the primary endpoint. CONCLUSION: Fluoroscopy-guided RV lead placement carries potential risk of unexpected RV free-wall pacing and may increase the risk of cardiac death and heart failure-related hospitalization in patients undergoing RV septal pacing due to AVB and receiving thoracic CT for medical reasons.

Clinical Manifestations and Long-Term Mortality in Lamin A/C Mutation Carriers From a Japanese Multicenter Registry.

BACKGROUND: Mutation in the lamin A/C gene (LMNA) is associated with several cardiac phenotypes, such as cardiac conduction disorders (CCD), atrial arrhythmia (AA), malignant ventricular arrhythmia (MVA) and left ventricular dysfunction (LVD), leading to sudden cardiac death (SCD) and/or end-stage heart failure. We investigated how these phenotypes are associated with each other and which of them are most important for total mortality. Methods and Results: A multicenter registry included 110 LMNA mutation carriers (age, 43±15 years, male: 62%) from 60 families. After genetic diagnosis of LMNA mutation (missense: 27%, non-missense: 73%), patients or subjects were followed to evaluate the manifestations of their phenotypes and the risk of total mortality; 90 patients could be followed (median: 5 [0-35] years). Prevalence of the 4 clinical phenotypes was significantly increased during follow-up. Among these phenotypes, AA was significantly associated with MVA. CCD was significantly associated with LVD. LVD, meanwhile, was significantly associated with CCD and MVA. Male sex was significantly associated with MVA. Furthermore, during follow-up, 17 patients died: 12 end-stage heart failure, 4 SCD and 1 stroke. LVD was the only independent predictor for all-cause death (OR: 41.7, 95% CI: 4.1-422.3; P=0.0016). CONCLUSIONS: Several cardiac phenotypes were age-dependently increased in LMNA mutation carriers, suggesting that ICD or CRT-D could suppress SCD after middle age; however, LVD leading to end-stage heart failure was the only independent predictor for total mortality.

Gene-Based Risk Stratification for Cardiac Disorders in LMNA Mutation Carriers.

BACKGROUND: Mutations in LMNA (lamin A/C), which encodes lamin A and C, typically cause age-dependent cardiac phenotypes, including dilated cardiomyopathy, cardiac conduction disturbance, atrial fibrillation, and malignant ventricular arrhythmias. Although the type of LMNA mutations have been reported to be associated with susceptibility to malignant ventricular arrhythmias, the gene-based risk stratification for cardiac complications remains unexplored. METHODS AND RESULTS: The multicenter cohort included 77 LMNA mutation carriers from 45 families; cardiac disorders were retrospectively analyzed. The mean age of patients when they underwent genetic testing was 45±17, and they were followed for a median 49 months. Of the 77 carriers, 71 (92%) were phenotypically affected and showed cardiac conduction disturbance (81%), low left ventricular ejection fraction (<50%; 45%), atrial arrhythmias (58%), and malignant ventricular arrhythmias (26%). During the follow-up period, 9 (12%) died, either from end-stage heart failure (n=7) or suddenly (n=2). Genetic analysis showed truncation mutations in 58 patients from 31 families and missense mutations in 19 patients from 14 families. The onset of cardiac disorders indicated that subjects with truncation mutations had an earlier occurrence of cardiac conduction disturbance and low left ventricular ejection fraction, than those with missense mutations. In addition, the truncation mutation was found to be a risk factor for the early onset of cardiac conduction disturbance and the occurrence of atrial arrhythmias and low left ventricular ejection fraction, as estimated using multivariable analyses. CONCLUSIONS: The truncation mutations were associated with manifestation of cardiac phenotypes in LMNA-related cardiomyopathy, suggesting that genetic analysis might be useful for diagnosis and risk stratification.

Impact of additional intracoronary nicorandil administration during fractional flow reserve measurement with intravenous adenosine 5'-triphosphate infusion.

BACKGROUND: Fractional flow reserve (FFR) is a useful index for determining the functional severity of epicardial coronary artery stenosis as an invasive physiological method. Although intravenous adenosine 5'-triphosphate (ATP) is generally used as a hyperemic agent for FFR measurement in Japan, there are some concerns about the variability of FFR measurement (short half-life, effect of caffeine, cyclic change). It is difficult to confirm sufficient maximum hyperemia after ATP infusion. Recent studies reported that nicorandil (NIC) could be an alternative to ATP as a hyperemic agent. METHODS: Patients who underwent FFR assessments of angiographically intermediate lesions were included. All patients were asked to refrain from caffeine-containing products more than 12hours before FFR measurements. All patients first received intravenous (IV) ATP infusion (180µg/kg/min) for 3min to measure FFR (ATP-FFR). After additional intracoronary (IC) NIC administration (2mg/30s) during ATP infusion, FFR was measured again (NIC-FFR). To check cyclic change in FFR, we measured minimum and maximum FFR values during both ATP and NIC hyperemic phase. RESULTS: In this study, 94 patients with 94 lesions were enrolled. Mean FFR value was 0.81±0.10 in ATP-FFR infusion and 0.80±0.09 in NIC-FFR, respectively. ATP-FFR and NIC-FFR had a strong correlation on the whole (r=0.92, p<0.001). In 18 patients (19%), FFR values were significantly lower in NIC-FFR than in ATP-FFR. In one-third of those patients (6%), it was possible to change therapeutic strategy from deferral range (>0.80) to interventional range (≦0.80) after NIC-FFR measurements. Cyclic change in FFR was smaller in NIC-FFR than in ATP-FFR (0.03±0.02 vs. 0.06±0.05, p<0.0001). CONCLUSION: Additional IC NIC might be useful to confirm sufficient maximum hyperemia after IV ATP infusion in daily clinical practice. Furthermore, IC NIC could reduce cyclic change in FFR; thus, physicians might find it easier to determine FFR value during the procedure.

Differential modulation of late sodium current by protein kinase A in R1623Q mutant of LQT3.

AIMS: In the type 3 long QT syndrome (LQT3), shortening of the QT interval by overdrive pacing is used to prevent life-threatening arrhythmias. However, it is unclear whether accelerated heart rate induced by beta-adrenergic agents produces similar effects on the late sodium current (I(Na)) to those by overdrive pacing therapy. We analyzed the beta-adrenergic-like effects of protein kinase A and fluoride on I(Na) in R1623Q mutant channels. MAIN METHODS: cDNA encoding either wild-type (WT) or R1623Q mutant of hNa(v)1.5 was stably transfected into HEK293 cells. I(Na) was recorded using a whole-cell patch-clamp technique at 23 degrees C. KEY FINDINGS: In R1623Q channels, 2 mM pCPT-AMP and 120 mM fluoride significantly delayed macroscopic current decay and increased relative amplitude of the late I(Na) in a time-dependent manner. Modulations of peak I(Na) gating kinetics (activation, inactivation, recovery from inactivation) by fluoride were similar in WT and R1623Q channels. The effects of fluoride were almost completely abolished by concomitant dialysis with a protein kinase inhibitor. We also compared the effect of pacing with that of beta-adrenergic stimulation by analyzing the frequency-dependence of the late I(Na). Fluoride augmented frequency-dependent reduction of the late I(Na), which was due to preferential delay of recovery of late I(Na). However, the increase in late I(Na) by fluoride at steady-state was more potent than the frequency-dependent reduction of late I(Na). SIGNIFICANCE: Different basic mechanisms participate in the QT interval shortening by pacing and beta-adrenergic stimulation in the LQT3.