上岡 正志

AIMS: The relationship between local unipolar voltage (UV) in the pulmonary vein (PV)-ostia and left atrial wall thickness (LAWT) and the utility of these parameters as indices of outcome after atrial fibrillation (AF) ablation remain unclear. METHODS AND RESULTS: Two-hundred seventy-two AF patients who underwent AF ablation were enrolled. Unipolar voltage of PV-ostia was measured using a CARTO system, and LAWT was measured using computed tomography. The primary endpoint was atrial tachyarrhythmia (ATA) recurrence including AF. The ATA recurrence was documented in 74 patients (ATA-Rec group). The UV and LAWT of the bilateral superior PV roof to posterior and around the right-inferior PV in the ATA-Rec group were significantly greater than in patients without ATA recurrence (ATA-Free group) (P < 0.001). The UV had a strong positive correlation with LAWT (R2 = 0.446, P < 0.001). The UV 2.7 mV and the corresponding LAWT 1.6 mm were determined as the cut-off values for ATA recurrence (P < 0.001, respectively). Multisite LA high UV (HUV, ≥4 areas of >2.7 mV) or multisite LA wall thickening (≥5 areas of >1.6 mm), defined as LA hypertrophy (LAH), was related to higher ATA recurrence. Among 92 LAH patients, 66 had HUV (LAH-HUV) and the remaining 26 had low UV (LAH-LUV), characterized by history of non-paroxysmal AF and heart failure, reduced LV ejection fraction, or enlarged LA. In addition, LAH-LUV showed the worst ablation outcome, followed by LAH-HUV and No LAH (log-rank P < 0.001). CONCLUSION: Combining UV and LAWT enables us to stratify recurrence risk and suggest a tailored ablation strategy according to LA tissue properties.

Purpose: To elucidate the electrophysiological predictors of the intramural origins of left ventricular outflow tract-ventricular tachyarrhythmias (LVOT-VAs), and to clarify the involvement of anatomical factors. Methods: Twenty-nine successfully ablated LVOT-VAs patients with origins in the aortomitral continuity (AMC) (n = 8), aortic sinus of valsalva (ASV) (n = 9), great cardiac vein (GCV) (n = 5), and intramural myocardium (n = 7) were enrolled. Intramural origins were defined as when effective ablation from AMC and epicardium (ASV and/or GCV) was needed. The local activation time difference (LATD) was calculated as follows: (earliest AMC activation) − (earliest epicardial activation), and was presented as an absolute value. Electrophysiological parameters and anatomical factors predisposing the intramural origins were investigated. Results: LATD of intramural origins was significantly shorter than that of AMC and GCV (4.5 ± 2.6 vs. 12.1 ± 7.4 vs. 17.4 ± 4.7, P &lt 0.05), respectively. In multivariate logistic regression analysis, LATD was associated with intramural origins (odds ratio: 0.711, confidence interval: 0.514−0.985, P = 0.040). ROC analysis revealed LATD of 7 ms as cut-off value. In computed tomography analysis, some patients who had thick fat tissue below the GCV, and an unusual GCV running pattern might be misdiagnosed as intramural origins. Conclusion: LATD ≤ 7 ms was associated with intramural origins, but with some anatomical limitations.

Purpose: Atrial fibrillation (AF) often coexists with atrial septal defects (ASD). Each of the transcatheter closure for ASD and radiofrequency catheter ablation (RFCA) for AF have been established as the first-line therapy. However, there are limited data about therapeutic effect RFCA plus transcatheter ASD closure on AF recurrence in AF patients with ASD. The aim of the current study was to investigate the clinical impact of ASD closure following RFCA on AF recurrence. Methods: Forty-two ASD patients (17 males and 54 ± 20 years old) were enrolled and classified into three groups: ASD occlusion-sinus rhythm (ASO-SR) (n = 26), no AF history prior to ASD closure ASO-AF-RFCA (n = 11), RFCA was performed due to AF history before ASD closure and ASO-AF-anti-arrhythmic drug (ASO-AF-AAD) (n = 5), AF was treated with AAD before and after ASD closure. AF occurrence among the 3 groups was evaluated. Results: Kaplan-Meier analysis showed that ASO-SR and ASO-AF-RFCA groups showed a lower AF occurrence ratio than ASO-AF-AAD group during the 14- ± 9-month follow-up periods (P = 0.013). AF occurrence in ASO-SR and ASO-AF-RFCA groups was comparable (P = 0.480). Bi-atrial reverse remodeling, such as decrease in left atrial volume index (P = 0.049) and right atrial area (P = 0.046), and significant decrease in high-sensitivity C-reactive protein levels (P = 0.049) were identified in ASO-AF-RFCA group, but not in ASO-AF-AAD group. Conclusion: A combination of two percutaneous therapies was proven to be effective and induced bi-atrial reverse remodeling in association with inflammatory reaction.

BACKGROUND: To investigate the clinical implication of the temporal difference in atrial fibrillation (AF)-onset in acute decompensated heart failure (ADHF) and its impact on post-discharge prognosis. METHODS: 336 new-onset ADHF patients without any history of AF before admission were enrolled (201 males, 63 ± 16 year-old) and classified into two groups based on their history of AF: the Control group (No AF was detected during hospitalization, n = 278), and the In-hos-AF group (AF occurred during hospitalization, n = 58). Post discharge prognosis including rehospitalization due to worsening HF, cardiac death, all-cause death and cerebrovascular event were compared. RESULTS: Kaplan-Meier analysis demonstrated that the incidence of rehospitalization due to HF, cardiac death, all-cause death and cerebrovascular event in the In-hos-AF group was not significantly different from that in the Control group (P > 0.05 respectively). However, when AF recurred in the In-hos-AF group patients (n = 24, 41%) after discharge, the incidence of rehospitalization due to HF and cardiac deaths were higher than those without AF recurrence (P = 0.018 and P = 0.027 respectively). Cox proportional analysis revealed that AF developing after discharge was proven to be an independent risk factor for rehospitalization due to HF (HR 1.845, P = 0.043), cardiac death (HR 3.562, P = 0.013) and all-cause deaths (HR 2.138, P = 0.020). CONCLUSION: Clinical outcomes of new-onset in-hospital AF patients were as good as those without AF history until AF recurrence. However, AF recurrence led to worse prognosis. Therefore, treatment for new-onset in-hospital AF in ADHF patients might be postponed until AF recurrence.

BACKGROUND: The mechanism of esophageal thermal injury (ETI; esophageal mucosal injury and periesophageal nerve injury leading to gastric hypomotility) remains unknown when using a high-power short-duration (HP-SD) setting. This study sought to evaluate the characteristics of esophageal injuries in atrial fibrillation ablation using a HP-SD setting. METHODS: After exclusion of 5 patients with their esophagus at the right portion of left atrium and 21 patients with additional ablations such as box isolation and low voltage area ablation in left atrium posterior wall, 271 consecutive patients (62±10 years, 56 women) who underwent pulmonary vein isolation by radiofrequency catheter ablation were analyzed. In the 101 patients, a HP-SD setting at 45 to 50 W with an Ablation Index module was used (HP-SD group). In the remaining 170 patients before introduction of the HP-SD setting, a conventional power setting of 20 to 30 W with contact force monitoring was used (conventional group). We performed esophagogastroduodenoscopy after pulmonary vein isolation in all patients and investigated the incidence and characteristics of ETI. RESULTS: Although the incidence of ETI was significantly higher in the HP-SD group compared with the conventional group (37% versus 22%, P=0.011), the prevalence of esophageal lesions did not differ between the groups (7% versus 8%). Multivariate logistic regression analysis revealed that the use of the HP-SD setting (odds ratio, 6.09, P<0.001), and the parameters that suggest anatomic proximity surrounding the esophagus, were independent predictors of ETI. However, the majority of ETI in the HP-SD group was gastric hypomotility, and the thermal injury was limited to the shallow layer of the periesophageal wall using the HP-SD setting. CONCLUSIONS: Although the use of the HP-SD setting was a strong predictor of ETI, it could avoid deeper thermal injuries that reach the esophageal mucosal layer.

BACKGROUND: Cardiac amyloidosis (CA) is characterized by left ventricular hypertrophy (LVH) and autonomic nervous imbalance due to amyloid infiltration. However, autonomic dysfunction is often seen in heart failure (HF) with LVH from other etiologies. We aimed to characterize autonomic dysfunction in CA from other etiologies of LVH. METHODS: Fifty-five HF patients with LVH (35 males, mean age 65 ± 16 years) were enrolled. LVH was defined as left ventricular mass index measured by echocardiography >95 g/m2 in women and 115 g/m2 in men. The etiology was as follows: amyloid light chain (AL)-CA, n = 14; hypertrophic cardiomyopathy, n = 21; and aortic stenosis (AS), n = 20. With the patient in a clinically stable condition, heart rate variability (HRV) and heart rate turbulence (HRT), which reflect autonomic dysfunction, were measured using Holter monitoring and compared among the three groups. RESULTS: Brain natriuretic peptide levels, LVH severity, left ventricular ejection fraction, and tissue Doppler index E/e' did not differ among the three groups. However, severe abnormalities of HRV and HRT were obtained in AL-CA. In the ROC analysis to identify AL-CA in HF with LVH, the best cutoff value for standard deviation of all R-R intervals, standard deviation of the 5-min mean R-R intervals, turbulence onset, and turbulence slope were 68.5 ms (AUC: 0.865), 58.5 ms (AUC: 0.834), 0.25% (AUC: 0.813), and 1.00 ms/RR (AUC 0.736), respectively. CONCLUSION: Autonomic dysfunction is a hallmark of AL-CA, and its noninvasive assessment by Holter monitoring may be a useful tool for differential diagnosis of HF with LVH.

Background: The clinical significance of premature ventricular complexes (PVCs) in heart failure (HF) remains unclear. We aimed to clarify the associations of PVC burden with re-hospitalization and cardiac death in HF patients. Methods: We studied 435 HF patients (271 men, mean age 65 years). All patients were hospitalized for worsening HF. After optimal medications, echocardiography, 24 hours Holter monitoring and cardiopulmonary exercise testing were performed before discharge. The clinical characteristics and outcomes of the HF patients were investigated. Results: During a median follow-up period of 2.3 years, there were 125 (28.7%) cardiac events (re-hospitalization due to worsening HF, fatal arrhythmias, or cardiac death). The patients with cardiac events had higher PVC burden compared to those without (median 0.374%/d [interquartile range 0.013-1.510] vs median 0.026%/d [interquartile range 0.000-0.534], P &lt .001). We examined cutoff value of PVC burden for predicting cardiac events. Receiver-operating characteristic analysis showed PVC burden (&gt 0.145%/d) to be a predictive factor of cardiac events (area under the curve: 0.64). Kaplan-Meier analysis demonstrated that cardiac events were more frequent in patients with high-PVC burden (&gt 0.145%/d, n = 194) compared to those with low-PVC burden (≤0.145%/d, n = 241). Furthermore, the high-PVC burden patients had left ventricular (LV) and atrial dilatation, reduced LV ejection fraction, and impaired exercise capacity, compared to the low-PVC burden patients. In Cox proportional hazards analysis, high-PVC burden was significantly associated with cardiac events with a hazard ratio of 2.028 (95% confidence interval: 1.418-2.901, P &lt .001). Conclusion: These results suggest that PVC burden is an important predictor of cardiac events in HF patients.

Introduction: The relationship between insulin resistance and atrial fibrillation (AF) recurrence after pulmonary vein isolation (PVI) remains unclear. Methods: Drug-refractory 114 paroxysmal AF patients (89 males, 62 ± 8 years) who underwent successful PVI were enrolled. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated and a value of ≥2.5 was defined as insulin resistant. The left atrial volume index (LAVI) was measured using echocardiography before and 1 year after PVI. Tumor necrosis factor-α (TNF-α) and TGF-β1 serum levels were measured before PVI, and the left atrium (LA) conduction velocity was calculated. The patients were divided into two groups (group 1: HOMA-IR &lt 2.5, n = 81 group 2: HOMA-IR ≥ 2.5, n = 33). Results: The LAVI between the two groups before PVI did not significantly differ (P &gt 0.05), nor did TNF-α (7.7 ± 2.0 vs 7.5 ± 1.0 pg/mL P = 0.149) or TGF-β1 (28.4 ± 12.0 vs 27.6 ± 10.3 ng/mL P = 0.757). LAVI before and 1 year after PVI in each group did not change. The conduction velocity of group 2 was slower than that of group 1 (0.7 ± 0.1 vs 1.1 ± 0.3 m/s, P &lt 0.001). Kaplan-Meier analysis showed significantly higher AF recurrence in group 2 than that in group 1 (P = 0.019). Cox multivariable analysis revealed that insulin resistance was an independent predictor of recurrence (hazard ratio 1.287, P = 0.004). Conclusion: Our results suggest that insulin resistance promotes LA electrical remodeling and might be related to AF recurrence after PVI.

Background: To investigate the impact of uncontrolled blood pressure (BP) on left atrial (LA) remodeling and clinical outcome after pulmonary vein isolation (PVI) in paroxysmal atrial fibrillation (AF). Methods: One hundred and one symptomatic paroxysmal AF patients (85 males, 62.2 ± 8.4-year-old) who underwent successful PVI were classified as follows: group 1 (n = 46), no hypertension (HTN) group 2 (n = 36), HTN with controlled BP and group 3 (n = 19), HTN with uncontrolled BP. Uncontrolled BP was defined as BP &gt  140/90 mm Hg. LA dimension was measured by echocardiography before and 6 months after PVI. LA wall thickness along the ablation line was measured using computed tomography prior to PVI. Cox regression analysis was performed for the prediction of recurrence. Results: LA wall thickness in groups 2 and 3 was greater than that of group 1, except for the anterior right superior pulmonary vein (PV) and posterior left inferior PV. Kaplan-Meier analysis revealed a significantly higher recurrence in group 3 (52.6%). LA dimension only increased in group 3 (38.2 ± 5.6 mm to 41.3 ± 6.2 mm, P = 0.022). At the second procedure, all group 3 recurrent patients showed substrate degradation (low voltage area and/or dense scar formation) and required substrate modification. Uncontrolled BP was an independent risk factor for recurrence (hazard ratio: 2.350, P = 0.033). Conclusions: HTN induced heterogeneous LA hypertrophy regardless of whether HTN was controlled. Uncontrolled BP promoted atrial remodeling, and is therefore a strong predictor for recurrence of AF after PVI.

BackgroundIn catheter ablation of idiopathic ventricular arrhythmia (VA), it is still unclear whether pace mapping or activation mapping is more useful for successful catheter ablation. The depth of origin in the ventricular wall especially affects the success rate of endocardial-approached catheter ablation. Thus, we examined the relationship between these tactics and QRS morphology. MethodsWe evaluated the relationship among pace mapping score, activation time, and peak deflection index (PDI) in 28 patients, with a total of 30 origins, who underwent successful catheter ablation of idiopathic VA. ResultsAll origins were located in the ventricular outflow tract area, including three in the left coronary cusp (LCC). PDI, activation time, and pace mapping score at successful ablation sites were 0.60 0.08, 26.3 +/- 9.9 ms, and 19.1 +/- 4.6, respectively. The pace mapping score inversely correlated with the PDI (R = -0.540, P = 0.0017), but the activation time did not correlate with the PDI. When excluding the three VAs originating from the LCC, in which perfect pace mapping was obtained from epicardial sites despite high PDI, this correlation coefficient became more intensive (R = -0.734, P &lt; 0.0001). ConclusionsOur study suggests that pace mapping with an endocardial approach could not reproduce the precise QRS morphology for VA originating from the intramural site of the ventricular wall. With such origins, we should rely on activation mapping to detect the optimal ablation site.

Backgrounds: Although acute decrease of intrathoracic impedance measured by cardiac resynchronization therapy (CRT) is effective to detect pulmonary congestion, it is unclear about the association with long-term change of intrathoracic impedance and left ventricular (LV) function in chronic heart failure (CHF) patients with CRT. Methods: Twenty six CHF patients who received CRT-defibrillator (CRT-D) were enrolled. LV dimensions, LV ejection fraction (LVEF) and B-type natriuretic peptide (BNP) were measured before and 6 months after CRT-D implantation. LV reverse remodeling was defined as >15% reduction in LV end-systolic volume after 6 months. In addition, intrathoracic impedance at 1 and 6 months after CRT-D implantation was investigated. The study subjects were divided into 2 groups: 18 patients with increased levels of intrathoracic impedance (Group-A) and 8 patients with decreased (Group-B). We compared LVEF, BNP levels and LV reverse remodeling between two groups. Results: In Group-A, BNP levels decreased and LVEF increased at 6 months after CRT-D implantation (P=0.01, each). In contrast, BNP levels and LVEF did not change in group-B. In Group-A, 15 patients (83%) were classified as LV reverse remodeling despite of 3 patients (37%) in Group-B (P=0.01). Conclusions: These results suggest that long-term increase of intrathoracic impedance is a novel predictor for LV reverse remodeling in CHF patients with CRT.

Backgrounds: It has been recently shown that the monitoring of changes in Fluid Index (FI) calculated by intrathoracic impedance with cardiac resynchronization therapy (CRT) may be useful for early detection of decompensated heart failure (DHF). However, the relation of changing pattern in FI and DHF remains uncertain, because several factors other than pulmonary congestion may affect on intrathoracic impedance. Therefore, we investigated this issue in order to predict the manifestation of DHF correctly. Methods and Results: We studied 26 chronic heart failure patients (19 males, mean age 66±11 years) who had implanted CRT-defibrillator with impedance monitoring. In the observation term (10.9±4.2 months), 20 patients experienced 48 episodes of FI over 60ω-days. These episodes were divided into two groups whether medical treatment for DHF was required (group A, n=21) or not (group B, n=27). Based on daily FI, we determined linear approximate equation (Y=aX, Y: daily FI, a: the slope of increasing FI, X: the days from the beginning of increasing FI to crossing 60ω-days). We next compared the slope of increasing FI between two groups. The slope of increasing FI was significantly steeper in group A than in group B (3.68±0.88 vs. 2.84±0.96, P<0.01). Conclusions: These results suggest that the monitoring of the slope of increasing FI was helpful for predicting patients with DHF.

Sympathetic activation plays a critical role of Cheyne-Stokes respiration (CSR) with chronic heart failure (CHF) and has associated with adverse clinical outcome. Recently, several studies have shown that adaptive servo ventilation (ASV) therapy improves the prognosis of CHF patients with CSR. However, it remains unclear the effect of ASV on sympathetic nervous activity. A case is a 50's dilated cardiomyopathy man. He was diagnosed as severe CSR by polysomnography and treated with ASV. We performed new multifunction wireless holter ECG (CarPod^R) before and after ASV therapy, which is able to evaluate the heart rate variability, physical activity, body temperature and etc. ASV improved apnea hypopnea index (63.8/h to 12.1/h) and slow wave sleep (2.3% to 3.4%). In addition, ASV decreased the occurrence of PVC (0.07% to 0.04%), LF/HF (2.7 to 1.3 during sleeping, 5.2 to 4.2 during awaking) and heart rate increase index (33.9 to 15.3), and also increased physical activity in the daytime. These results obtained from new multifunction wireless holter ECG suggest that ASV might improve not only sympathetic function but also physical performance in CHF patients with CSR.

Backgrounds: It has been shown that the position of left ventricular (LV) pacing lead and viability of the LV wall may affect on the response to cardiac resynchronization therapy (CRT). However, little is known about the association between characteristics of LV pacing lead and LV reverse remodeling in chronic heart failure (CHF) patients with CRT implantation. Methods: The study subjects consisted of 32 CHF patients (23 males, mean age, 64±11 years) with CRT-defibrillator (CRT-D) implantation. We measured LV end-systolic volume (LVESV) by echocardiography before and 6 months after CRT-D implantation and defined the CRT responder as >15% reduction of LVESV at 6 months. The patients were divided into 2 groups based on CRT responder (group-A, n=20) or not (group-B, n=12). We compared the LV R-wave amplitude at CRT-D implantation and the change of LV pacing threshold 6 months after CRT-D implantation between 2 groups. Results: LV R-wave amplitude did not differ between 2 groups (A, 15.1±8.1 mV vs. B, 14.5±8.6 mV). In addition, the change in LV pacing threshold was similar between two groups (improving: 5% vs. 8%; worsening: 25% vs. 25%). Conclusions: These results suggest that electrophysiological properties of regional left ventricle at CRT implantation site do not predict the LV reverse remodeling in response to CRT in CHF patients.