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The pathogenesis of chronic active myocarditis remains unclear. A 65-year-old man underwent permanent pacemaker implantation for sick sinus syndrome and pulmonary vein isolation for paroxysmal atrial fibrillation. Four years later, the left ventricular ejection fraction decreased from 51â¯% to 35â¯%, and the apical left ventricular inferior wall developed akinesis. Isolated cardiac sarcoidosis was suspected; however, prednisolone and optimal medical therapy failed to improve the symptoms. Even after cardiac resynchronization therapy followed by atrioventricular junction ablation for untreatable atrial tachycardia, the patient died of heart failure eight years after referral. An autopsy revealed inflammatory cell infiltration accompanied by cardiac myocytolysis in both atria and ventricles. He was diagnosed with chronic active myocarditis based on pathological findings and a persistent increase in the blood high-sensitivity cardiac troponin levels before death. The myocardium around the sinus node showed extensive and severe fibrosis with mild inflammation, suggesting a chronic inflammatory phase. In contrast, the left atrium and both ventricles showed active myocardial inflammation with fibrosis, suggesting a persistently active inflammatory phase. This case demonstrated that atrial inflammation caused intractable atrial arrhythmia, while ventricular inflammation led to biventricular heart failure, and highlighted the presence of spatially and temporally heterogeneous inflammation in chronic active myocarditis. Learning objective: We describe a case of chronic active myocarditis with spatially and temporally heterogeneous lesions throughout the four cardiac chambers. Inflammatory cell infiltration was observed in both atria and ventricles. Extensive fibrosis replaced the myocardium around the sinus node, suggesting a chronic phase. The left atrium and ventricles showed active inflammation, suggesting an active phase. Atrial and ventricular inflammation led to atrial arrhythmia and heart failure, respectively.
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BACKGROUND: Pulmonary vein isolation (PVI) employing cryoballoon (CB) or contact force-guided radiofrequency (CF-RF) catheter ablation has been established as an effective strategy for managing atrial fibrillation (AF). However, its efficacy in hypertrophic cardiomyopathy (HCM) remains to be further explored. METHODS: This retrospective study analyzed 60 consecutive AF patients with HCM (average age 67 ± 10 years; 41 men) who were consecutively admitted to our hospital from January 2014 to December 2022 and underwent initial PVI. RESULTS: The patients were treated with CB (26 patients) or CF-RF (34 patients). Successful PVI was achieved in both groups without significant complications. In the CF-RF group, additional ablations were performed on the cavotricuspid isthmus (14.7% of patients) and the anterior line (2.9%). The CB group benefited from reduced procedural times (93 ± 31 vs. 165 ± 60 min, p < 0.05) and decreased saline irrigation requirements (77.5 ± 31.4 vs. 870 ± 281.9 mL, p < 0.0001). Using a contrast medium was exclusive to the CB group (33.8 ± 4.2 mL). In a 12-month follow-up, the atrial tachyarrhythmia recurrence-free rates in the CB and CF-RF groups were comparable (77% and 76%, respectively; p = 0.63 according to the log-rank test). Notably, pulmonary vein reconnection was prevalent in most (7 out of 8) patients requiring a secondary ablation procedure. CONCLUSION: PVI is feasible as a strategy for AF in patients with HCM employing either CB or CF-RF techniques. While the recurrence-free rates were comparable in both groups, differences were noted in procedure duration, saline usage, and the need for a contrast medium.
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Giant cell myocarditis (GCM) is a potentially lethal subtype of myocarditis. Herein, we report a case of a 22-year-old woman with GCM who was successfully treated with prednisolone monotherapy. The patient had a fever and shortness of breath and was referred to our hospital. Laboratory test results revealed elevated troponin I levels. Cardiac magnetic resonance (CMR) showed high intensity in the inferoseptal segment of the left ventricle on T2-weighted short tau inversion recovery imaging without late gadolinium enhancement (LGE), suggesting predominant edema rather than necrosis. The patient was diagnosed with GCM based on an endomyocardial biopsy, which revealed lymphocyte infiltration and multinucleated giant cells in the absence of granuloma formation. Subsequently, the patient received intravenous methylprednisolone at 1000â¯mg/day for 3â¯days followed by oral prednisolone at 30â¯mg/day, which normalized troponin levels. Follow-up CMR revealed improved cardiac inflammation; therefore, the patient was discharged without prescribing another immunosuppressive agent. Prednisolone was tapered and terminated three years after discharge. The patient went one year without medication and had no recurrence of GCM on follow-up. This case highlights the presence of mild GCM, successfully treated by steroid monotherapy, in which the mismatch between high-intensity T2 areas and LGE suggests mild inflammation. Learning objective: Giant cell myocarditis (GCM) is potentially lethal and usually requires multiple immunosuppressive agents. Here, we report a patient with GCM with preserved left ventricular ejection fraction. Cardiac magnetic resonance revealed focal high T2 signal intensity areas without late gadolinium enhancement, indicating myocardial edema without necrosis. The patient remained in remission with prednisolone monotherapy for 2â¯years. Our report indicates that "mild" GCM may be treated with prednisolone monotherapy.
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A patient with hypertrophic cardiomyopathy experienced cardiopulmonary arrest. An automated external defibrillator administered defibrillation for ventricular fibrillation (A). The pacemaker recorded atrial tachycardia with a rapid ventricular response before the patient collapsed (B). After a few minutes, the pacemaker records dual tachyarrhythmia, characterized by the simultaneous presence of ventricular fibrillation (VF) and atrial fibrillation (AF) (C). This case demonstrates that VF induced by atrial tachyarrhythmia could contribute to AF-related sudden cardiac death.
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Introduction: During ventricular pacing, a fusion of atrial activation may occur owing to the simultaneous retrograde conduction of the atrioventricular (AV) node and accessory pathway (AP), potentially leading to an inaccurate mapping of the atrial AP insertion site. Objective: We tested the hypothesis that landiolol, an ultra-short-acting intravenous ß1-blocker, could dissociate a fusion of atrial activation. Methods: We conducted a prospective before-and-after study to investigate the effect of landiolol on retrograde conduction via the AV node and AP. We enrolled 21 consecutive patients with orthodromic AV reciprocating tachycardia who underwent electrophysiological studies at our hospital between January 1, 2018, and August 31, 2020. Results: Six patients exhibited a fusion of atrial activation. After landiolol administration (10 µg/kg/min), the effective refractory period was unchanged in AP (280 [240-290] ms vs. 280 [245-295] ms, p = .91), whereas that of the AV node was prolonged (275 [215-380] ms vs. 332 [278-445] ms, p = .03). The Wenckebach pacing rate via retrograde AV node decreased after landiolol administration (180 [140-200] beats per minute [bpm] vs. 140 [120-180] bpm, p = .02). Thus, landiolol decreased the minimum ventricular pacing rate required to dissociate a fusion of atrial activation (180 [160-200] bpm vs. 140 [128-155] bpm, p = .007). Radiofrequency catheter ablation under landiolol administration successfully eliminated AP in all patients during ventricular pacing without complications or recurrence. Conclusion: Landiolol inhibited the AV node without affecting the AP and helped dissociate a fusion of atrial activation at a lower ventricular pacing rate.
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BACKGROUND: The characteristics and clinical outcomes associated with sustained ventricular tachycardia and fibrillation (VT/VF) in Japanese acute myocardial infarction (AMI) patients remain unknown.MethodsâandâResults: Consecutive AMI patients (n=1,941) transferred to the Hirosaki University Hospital and treated with primary percutaneous coronary intervention (PCI) within 12 h of onset were retrospectively studied. The incidence of VT/VF during hospitalization was 8.3%, and 75% of cases occurred by the end of PCI. Independent predictors associated with VT/VF occurrence by the end of PCI and after PCI, respectively, were identified. Additionally, the differences between patients with VT and VF were examined, which revealed that the characteristics of patients and predictors for VT and VF were clearly different. Additionally, the QRS duration during VT was measured, which demonstrated the possible involvement of Purkinje fibers for VT in the acute phase of AMI. Of the patients with VT/VF, 12% required ECMO support due to refractory VT/VF despite intravenous antiarrhythmic agents such as ß-blockers, amiodarone, and nifekalant. Among the patients discharged alive, 1,690 were followed up for a mean of 3.7 years. VT/VF occurrence during hospitalization did not affect the mid-term clinical outcomes even in patients with VT. CONCLUSIONS: The results clearly indicated that VT/VF is still a serious complications of AMI. We need to identify patients at high risk of developing VT/VF for careful observation and appropriate intervention.
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Fibrilación Atrial , Accidente Cerebrovascular , Humanos , Rivaroxabán/uso terapéutico , Fibrilación Atrial/tratamiento farmacológico , Fibrilación Atrial/genética , Receptor X de Pregnano/genética , Sistema Enzimático del Citocromo P-450 , Anticoagulantes/uso terapéutico , Inhibidores del Factor Xa/uso terapéuticoRESUMEN
INTRODUCTION: The authors aimed to examine the impact of single nucleotide polymorphisms in P-glycoprotein, the hepatic uptake transporter organic anion transporter protein 1B1, cytochrome P450 ( CYP ) 3A5, and carboxylesterase-1 ( CES1 ) on the steady-state dose-adjusted trough concentrations of edoxaban (C Edo /D) and M-4 (C M-4 /D). They also investigated whether C M-4 and C Edo affect prothrombin time (PT). METHODS: The analyses included 152 patients with nonvalvular atrial fibrillation (NVAF) undergoing AF catheter ablation. The CYP3A5*3 ; CES1 c.1168-33A>C, c.257+885T>C; SLCO1B1 c.388A>G, c.521T>C; and ABCB1 c.3435C>T, c.2677G>A/T, c.1236C>T genotypes were determined. RESULTS: Stepwise selection multiple linear regression analyses demonstrated that creatinine clearance (Ccr), concomitant use of amiodarone, and SLCO1B1*15 haplotype status were independent factors influencing C M-4 /D (partial R2 = 0.189, 0.098, 0.067, respectively, all P values < 0.005). Ccr and concomitant use of amiodarone were independent factors influencing C Edo /D (partial R2 = 0.260, 0.117, respectively, both P value < 0.001). C Edo and C M-4 showed a weak correlation with PT (ρ = 0.369 and 0.315, both P values < 0.001). CONCLUSIONS: Although information concerning Ccr, concomitant use of amiodarone, and SLCO1B1*15 haplotype may be useful in assessing the pharmacokinetics of edoxaban, further studies are needed to clarify the requirement of PT monitoring at the trough level for dose adjustment of edoxaban in patients with NVAF.
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Amiodarona , Fibrilación Atrial , Humanos , Haplotipos , Fibrilación Atrial/tratamiento farmacológico , Fibrilación Atrial/genética , Tiempo de Protrombina , Transportador 1 de Anión Orgánico Específico del Hígado/genéticaRESUMEN
PURPOSE: We examined the impact of polymorphisms in genes encoding cytochrome P450 (CYP) 3A5 (gene code CYP3A5), P-glycoprotein (ABCB1), breast cancer resistance protein (ABCG2), cytochrome P450 oxidoreductase (POR), and pregnane X receptor (PXR; NR1I2) on the daily dose-adjusted steady-state trough concentrations (C0h/D) of apixaban. METHODS: The analyses included 104 patients with non-valvular atrial fibrillation (NVAF) undergoing AF catheter ablation. The CYP3A5*3; ABCG2 421C > A; ABCB1 1236C > T, 2677G > A/T, 3435C > T, and 2482-2236G > A; NR1I2 11156A > C, 11193T > C, and 8055C > T; and POR*28 genotypes were determined. The combination of the noted NR1I2 genotypes determined the PXR*1B haplotype. RESULTS: Multiple linear regression analyses demonstrated that decreased creatinine clearance (Ccr) and the PXR*1B/*1B haplotype correlated with increased C0h/D of apixaban, while the presence of the POR*28 allele correlated with decreased C0h/D of apixaban (partial R2 = 0.168, 0.029, and 0.044, all P < 0.05). The mean (95% CI) of estimated marginal means of apixaban C0h/D calculated using Ccr as a covariate was the highest in POR*28 noncarriers with PXR*1B/*1B (23.5 [21.0-25.9] ng/mL/[mg/day]) and lowest in POR*28 carriers with other haplotypes (16.6 [15.5-17.7] ng/mL/[mg/day]). CONCLUSION: The PXR*1B haplotype and POR*28 genotype statuses, which involve genes that impact the expression of multiple drug-metabolizing enzymes and drug-transporters, may have modest effects on the C0h/D of apixaban, but these effects were found to be small.
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Fibrilación Atrial , Citocromo P-450 CYP3A , Humanos , Citocromo P-450 CYP3A/genética , Citocromo P-450 CYP3A/metabolismo , Receptor X de Pregnano/genética , Fibrilación Atrial/tratamiento farmacológico , Fibrilación Atrial/genética , Transportador de Casetes de Unión a ATP, Subfamilia G, Miembro 2/genética , Proteínas de Neoplasias/genética , Polimorfismo Genético , Genotipo , Polimorfismo de Nucleótido SimpleRESUMEN
Complex coronary vein morphology impedes the insertion of the left ventricular (LV) lead and reduces the effectiveness of cardiac resynchronization therapy (CRT). A 77-year-old woman underwent dual-chamber pacemaker implantation via the left subclavian approach for a complete atrioventricular block 17 years previously. She was hospitalized due to decompensated heart failure, and her cardiac rhythm completely depended on ventricular pacing at that time. Transthoracic echocardiography showed thinning of the ventricular septum in the basal region and pacing-induced dyssynchrony. She was clinically diagnosed with cardiac sarcoidosis with severe LV systolic dysfunction. She was referred for an upgrade to CRT. Given that prior contrast venography showed occlusion of the left subclavian vein, an additional LV lead was inserted through the right subclavian vein. Coronary venography showed a lateral vein that branched from the great cardiac vein with an acute angle and had multiple tortuosities in the peripheral branches. Since the LV lead placement was unsuccessful with the conventional method, we attempted the lead placement using the balloon occlusion technique (BOT). Lead delivery into the anatomical optimal lateral vein was successful by using BOT, and LV pacing from the most delayed basal region was achieved in combination with the active fixation LV lead.
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BACKGROUND: The PRAETORIAN score was developed to evaluate the implant position and predict defibrillation success in patients implanted with a subcutaneous implantable cardioverter-defibrillator (S-ICD). However, usefulness of the PRAETORIAN score for Japanese patients is unknown. METHODS: We evaluated usefulness of this score, which was determined by width of sub-coil fat, sub-generator fat, and anterior positioning of the S-ICD generator by post-operative chest X-ray, in consecutive 100 Japanese S-ICD implanted patients [78 men, median age 59 (IQR 46.5-67.0) years, median body mass index (BMI) 24.2 (21.3-27.2) kg/m2]. RESULTS: The median PRAETORIAN score was 30 (30-45) and 93 patients were classified as a low risk of conversion failure. The remaining seven were at an intermediate risk. Almost all patients were classified as an optimal pulse-generator position in the second and third steps of the PRAETORIAN score. The only difference observed was in the width of sub-coil fat in the first step. To further evaluate its significance, patients were divided into the Thicker group (sub-coil fat >1 coil width, nâ¯=â¯19) and the Thinner group (sub-coil fat ≤1 coil width, nâ¯=â¯81). BMI and post-shock impedance were both higher in the Thicker group than in the Thinner group [27.1 (25.6-31.6) versus 23.1 (20.9-25.7) kg/m2, pâ¯<â¯0.001, and 75 (68-88) versus 63 (55-74) Ω, pâ¯=â¯0.003, respectively]. During the median follow-up periods of 888 (523-1418) days, 7 patients experienced appropriate shock therapy for spontaneous ventricular tachyarrhythmias, who were all at a low risk. No conversion failure was observed. Inappropriate shock (IAS) occurred in 11 patients, and there was no difference in IAS rate between the Thicker group (nâ¯=â¯2) and the Thinner group (nâ¯=â¯9) (pâ¯=â¯0.747 by log-rank test). CONCLUSIONS: Most Japanese patients were classified as at low risk of conversion failure. The PRAETORIAN score may be useful for the evaluation of conversion failure in Japanese S-ICD implanted patients.
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Desfibriladores Implantables , Índice de Masa Corporal , Desfibriladores Implantables/efectos adversos , Cardioversión Eléctrica/efectos adversos , Impedancia Eléctrica , Humanos , Japón , Masculino , Persona de Mediana Edad , Resultado del TratamientoRESUMEN
Calcium antagonists are used for coronary spastic angina (CSA) treatment. We previously identified a phospholipase C (PLC) -δ1 gene variant that results in enhanced PLC activity in patients with CSA and developed a CSA animal model by generating vascular smooth muscle cell-specific human variant PLC-δ1 overexpression (PLC-TG) mice. In this study, we investigated the molecular mechanism of CSA using the PLC-TG mice and the inhibitory effect of a calcium antagonist, diltiazem hydrochloride (DL).We treated the PLC-TG and wild-type (WT) mice with oral DL or trichlormethiazide (TM) (control) for 2 weeks. Ergometrine injection-induced coronary spasm was observed on the electrocardiogram in all 5 PLC-TG mice treated with TM, but only in 1 of 5 PLC-TG mice treated with DL. Voltage-dependent calcium channel (Cav1.2) phosphorylation and protein kinase C (PKC) activity were enhanced in the aortas of PLC-TG mice treated with TM. DL treatment significantly inhibited Cav1.2 phosphorylation and PKC activity. Although total Cav1.2 expression was similar between WT and PLC-TG mice treated with TM, DL treatment significantly increased its expression in PLC-TG mice. Furthermore, its expression remained high after DL discontinuation. DL and PKC inhibitor suppressed intracellular calcium response to acetylcholine in cultured rat aortic smooth muscle cells transfected with variant PLC-δ1.These results indicate that enhanced PLC activity causes coronary spasm, presumably via enhanced Cav1.2 phosphorylation and PKC activity, both of which were inhibited by DL. Enhanced total Cav1.2 expression after DL discontinuation and high PKC activity may be an important mechanism underlying the calcium antagonist withdrawal syndrome.
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Bloqueadores de los Canales de Calcio/uso terapéutico , Canales de Calcio Tipo L/metabolismo , Vasoespasmo Coronario/tratamiento farmacológico , Diltiazem/uso terapéutico , Proteína Quinasa C/metabolismo , Animales , Bloqueadores de los Canales de Calcio/farmacología , Vasoespasmo Coronario/metabolismo , Diltiazem/farmacología , Evaluación Preclínica de Medicamentos , Activación Enzimática/efectos de los fármacos , Masculino , Ratones Transgénicos , Fosforilación/efectos de los fármacosRESUMEN
Rivaroxaban is excreted from the body via multiple pathways involving glomerular filtration, drug-metabolizing enzymes and transporters. In this study, we aimed to examine the impact of single nucleotide polymorphisms in P-glycoprotein, breast cancer resistance protein, cytochrome P450 (CYP) 3A5 and CYP2J2 on the pharmacokinetics of rivaroxaban. Eighty-six patients with non-valvular atrial fibrillation (NVAF) undergoing AF catheter ablation were enrolled in this study. In these analyses, the dose-adjusted plasma trough concentration ratio (C0h /D) of rivaroxaban was used as the pharmacokinetic index. The median (quartile range) rivaroxaban C0h /D was 3.39 (2.08-5.21) ng/mL/mg (coefficient of variation: 80.5%). The C0h /D did not differ significantly among ABCB1 c.3435C>T, c.2677G>A/T, c.1236C>T, ABCG2 c.421C>A, CYP3A5*3 and CYP2J2*7 genotypes. Stepwise selection multiple linear regression analysis showed that the estimated glomerular filtration rate was the only independent factor influencing the C0h /D of rivaroxaban (R2 = 0.152, P < 0.001). There was a significant correlation between the C0h of rivaroxaban and prothrombin time (PT) (rho = 0.357, P = 0.001). In patients with NVAF, pharmacokinetic genotype tests are unlikely to be useful for prediction of the C0h of rivaroxaban.
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Fibrilación Atrial/tratamiento farmacológico , Inhibidores del Factor Xa/sangre , Variantes Farmacogenómicas , Polimorfismo de Nucleótido Simple , Rivaroxabán/sangre , Subfamilia B de Transportador de Casetes de Unión a ATP/genética , Subfamilia B de Transportador de Casetes de Unión a ATP/metabolismo , Transportador de Casetes de Unión a ATP, Subfamilia G, Miembro 2/genética , Transportador de Casetes de Unión a ATP, Subfamilia G, Miembro 2/metabolismo , Adulto , Anciano , Anciano de 80 o más Años , Fibrilación Atrial/sangre , Biotransformación , Citocromo P-450 CYP2J2 , Citocromo P-450 CYP3A/genética , Citocromo P-450 CYP3A/metabolismo , Sistema Enzimático del Citocromo P-450/genética , Sistema Enzimático del Citocromo P-450/metabolismo , Monitoreo de Drogas , Inhibidores del Factor Xa/efectos adversos , Inhibidores del Factor Xa/farmacocinética , Femenino , Tasa de Filtración Glomerular , Humanos , Japón , Riñón/fisiopatología , Masculino , Tasa de Depuración Metabólica , Persona de Mediana Edad , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Farmacogenética , Pruebas de Farmacogenómica , Rivaroxabán/efectos adversos , Rivaroxabán/farmacocinética , Resultado del TratamientoRESUMEN
BACKGROUND: Direct oral anticoagulants (DOACs) are effective in reducing thromboembolism events in patients with non-valvular atrial fibrillation (NVAF). However, little is known about trends in NVAF prevalence and DOAC prescriptions in daily clinical practice. This study investigated the current status and trends in NVAF prevalence and DOAC prescriptions in a region of Japan.MethodsâandâResults:Annual data for the 4 years from May 2014 to May 2017 in the Tsugaru region of Aomori Prefecture, Japan, were obtained for analysis from the Japanese National Health Insurance database ("Kokuho" database [KDB]). The prevalence of NVAF in subjects aged 40-74 years increased gradually over the 4-year study period (1,094/57,452 [1.90%] in 2014, 1,055/56,018 [1.88%] in 2015, 1,072/54,256 [1.98%] in 2016, and 1,154/52,341 [2.20%] in 2017). The proportion of NVAF patients prescribed warfarin decreased (42%, 33%, 24%, and 21% in 2014, 2015, 2016, and 2017, respectively), the proportion of those prescribed DOACs increased (30%, 42%, 50%, and 57%, respectively), and the proportion not prescribed an oral anticoagulant (OAC) decreased (28%, 25%, 26%, and 22%, respectively). However, 17% of patients with a CHADS2score ≥2 were not prescribed an OAC in 2017. CONCLUSIONS: By using the KDB we found that the prevalence of NVAF has increased gradually from 2014 to 2017. In the Tsugaru region in Japan, DOACs prescriptions increased and warfarin prescriptions decreased over the 4-year period.
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Anticoagulantes/administración & dosificación , Fibrilación Atrial/tratamiento farmacológico , Inhibidores del Factor Xa/administración & dosificación , Pautas de la Práctica en Medicina/tendencias , Accidente Cerebrovascular/prevención & control , Warfarina/administración & dosificación , Administración Oral , Adulto , Anciano , Anticoagulantes/efectos adversos , Fibrilación Atrial/diagnóstico , Fibrilación Atrial/epidemiología , Estudios Transversales , Bases de Datos Factuales , Prescripciones de Medicamentos , Revisión de la Utilización de Medicamentos/tendencias , Inhibidores del Factor Xa/efectos adversos , Femenino , Humanos , Japón/epidemiología , Masculino , Persona de Mediana Edad , Programas Nacionales de Salud , Prevalencia , Estudios Retrospectivos , Factores de Riesgo , Accidente Cerebrovascular/diagnóstico , Accidente Cerebrovascular/epidemiología , Factores de Tiempo , Resultado del Tratamiento , Warfarina/efectos adversosRESUMEN
BACKGROUND: The subcutaneous implantable cardioverter-defibrillator (S-ICD) is effective in preventing sudden cardiac death. Compared with transvenous ICDs, S-ICDs have a lower rate of inappropriate shocks (IASs) for supraventricular arrhythmias, but such shocks for T-wave oversensing (TWO) and extracardiac myopotentials are more common. No screening tests to identify patients at risk for IAS due to myopotential interference (MPI) currently are available. OBJECTIVE: The purpose of this study was to assess the efficacy of a tube exercise test (TET) developed to detect MPI post S-ICD implantation. METHODS: TET includes 3 different maneuvers using an exercise tube. S-ICD electrograms were recorded to assess MPI while patients performed each of the maneuvers. RESULTS: TET was performed in 43 patients, and MPI was observed in 12 patients (28%). In 10 of the 12 TET-positive patients, the positive vector corresponded with a vector that did not show TWO on standard S-ICD preoperative screening. During median follow-up of 672 days (interquartile range 465-805 days), 3 patients (7%) experienced IAS due to MPI. Importantly, the vector at the time of IAS in all 3 patients passed standard preoperative screening for TWO but was positive with TET. Sensitivity and specificity of TET were 100% and 78%, respectively, and positive and negative predictive values were 25% and 100%, respectively. CONCLUSION: Postimplant screening for MPI identified patients at increased risk for IAS. TET may be helpful for guiding optimal programming to prevent IAS.
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BACKGROUND: The entirely subcutaneous implantable cardioverter defibrillator (S-ICD) was introduced as a new alternative to conventional transvenous ICD (TV-ICD) in Japan in February 2016, but its safety and efficacy are unclear.MethodsâandâResults:A total of 60 patients (48 men, median age, 60 years; IQR, 44-67 years; primary prevention, n=24) underwent S-ICD implantation between February 2016 and August 2017. The device pocket was formed in the intermuscular space between the serratus anterior muscle and the latissimus dorsi muscle, and the parasternal S-ICD lead was placed according to pre-implant screening. Defibrillation test was performed in 56 patients (93%). Ventricular fibrillation (VF) was induced in 55 patients and terminated by a single 65-J shock in all patients. The median time to shock therapy was 13.4 s (IQR, 12.1-14.9 s) and the median post-shock impedance of the S-ICD lead was 64 Ω (IQR, 58-77 Ω). There were no operation-related complications or subsequent infectious complications. During follow-up (median, 275 days; IQR, 107-421 days), 1 patient (1.7%) had appropriate shock for VF with successful termination, whereas 5 patients (8.3%) had inappropriate shock due to oversensing of myopotential (n=3) or T-wave (n=1), and detection of supraventricular tachycardia (n=1). CONCLUSIONS: S-ICD is a safe and effective alternative to conventional TV-ICD. The long-term safety and efficacy of the S-ICD need further investigation.
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Muerte Súbita Cardíaca/prevención & control , Desfibriladores Implantables/normas , Fibrilación Ventricular/terapia , Adulto , Anciano , Desfibriladores Implantables/efectos adversos , Cardioversión Eléctrica/métodos , Cardioversión Eléctrica/normas , Femenino , Humanos , Japón , Masculino , Persona de Mediana Edad , Prevención Primaria/métodos , Prevención Primaria/normas , Prevención Secundaria/métodos , Prevención Secundaria/normas , Taquicardia/diagnóstico , Resultado del Tratamiento , Fibrilación Ventricular/diagnósticoRESUMEN
We reported that coronary spasm was induced in the transgenic mice with the increased phospholipase C (PLC)-δ1 activity. We investigated the effect of enhanced PLC-δ1 on Ca2+ influx and its underlying mechanisms. We used human embryonic kidney (HEK)-293 and coronary arteries smooth muscle cells (CASMC). Intracellular free Ca2+ concentration ([Ca2+ ]i ; nm) was measured by fura-2, and Ca2+ influx was evaluated by the increase in [Ca2+ ]i after addition of extracellular Ca2+ . Acetylcholine (ACh) was used to induce Ca2+ influx. ACh-induced peak Ca2+ influx was 19 ± 3 in control HEK-293 cells and 71 ± 8 in the cells with PLC-δ1 overexpression (P < 0.05 between two groups). Nifedipine partially suppressed this Ca2+ influx, whereas either 2-APB or knockdown of classical transient receptor potential channel 6 (TRPC6) blocked this Ca2+ influx. In the human CASMC, ACh-induced peak Ca2+ influx was 29 ± 6 in the control and was increased to 45 ± 16 by PLC-δ1 overexpression (P < 0.05). Like HEK-293 cells, pretreatment with nifedipine partially suppressed Ca2+ influx, whereas either 2-APB or knockdown of TRPC6 blocked it. ACh-induced Ca2+ influx was enhanced by PLC-δ1 overexpression, and was blocked partially by nifedipine and completely by 2-APB. TRPC-mediated Ca2+ influx may be related to the enhanced Ca2+ influx in PLC-δ1 overexpression.