The coronary artery calcium score correlates with left atrial low-voltage area: Sex differences.

INTRODUCTION: In patients with coronary artery disease, a high coronary artery calcium score (CACS) correlates with atrial fibrillation (AF); however, the association between left atrial (LA) remodeling progression and coronary arteriosclerosis is unclear. This study aimed to evaluate the relationship between LA remodeling progression and the CACS. METHODS: This retrospective study enrolled 148 patients with AF (paroxysmal AF, n = 94) who underwent catheter ablation. Voltage mapping for the left atrium and coronary computed tomography for CACS calculations were performed. The ratio of the LA low-voltage area (LA-LVA), defined by values less than 0.5 mV divided by the total LA surface without pulmonary veins, was calculated. Patients with LA-LVA (<0.5 mV) >5% and ≤5% were classified as the LVA (n = 30) and non-LVA (n = 118) groups, respectively. Patient characteristics and CACS values were compared between the two groups. RESULTS: LA volume, age, CHA2 DS2 VASc score, and percentage of female patients were significantly higher, and the estimated glomerular filtration rate was lower in the LVA group than in the non-LVA group. The CACS was significantly higher in the LVA group (248.4 vs. 13.2; p = .001). Multivariate analysis identified the LA volume index and CACS as independent predictors of LA-LVA (<0.5 mV) greater than 5%. The areas under the receiver operating characteristic curves for predicting LA-LVA (<0.5 mV) greater than 5% with CACS were 0.695 in the entire population, 0.782 in men, and 0.587 in women. CONCLUSION: Progression of LA remodeling and coronary artery calcification may occur in parallel. A high CACS may indicate advanced LA remodeling, especially in men.

Characteristics of ventricular intracardiac electrograms of ventricular tachycardias originating from the epicardia in patients with an implantable cardioverter defibrillator.

INTRODUCTION: While characteristic waveforms of 12-lead electrocardiograms have been reported to predict the epicardial origin of ventricular tachycardia (VT), it has not been fully examined whether ventricular intracardiac electrograms (VEGMs) recorded from the implantable cardioverter defibrillator (ICD) via telemetry can determine the origin of VT or not. The aim of this study was to investigate the VEGM characteristics of VT originating from the epicardia. METHOD AND RESULTS: Intracardiac VEGMs of the induced VTs, with detected sites of origin during the VT study, were recorded in 15 (23 VTs) of the 46 patients. The characteristics of the 23 VTs were evaluated using far-field and near-field VEGMs recorded via telemetry. Five of 23 VTs were found to be focused on the epicardial site (epi group) and 18 VTs were focused on the endocardium (endo group). VTs of the epi group had longer VEGM duration in far-field EGM than those of the endo group (epi group: 240 ± 49 ms vs endo group: 153 ± 45 ms; P = 0.002) and the duration from the onset to the peak of VEGM was also longer than that of the endo group (epi group: 153 ± 53 ms vs endo group: 63 ± 28 ms; P < 0.001). There was no difference in the V wave duration in tip-ring EGM between both groups (epi group: 122 ± 52 ms vs endo group: 98 ± 6 ms; P = 0.377). CONCLUSION: Evaluation of intracardiac VEGM before VT ablation may be helpful to predict the epicardial origin of VT in patients with an ICD.

The relationship between obstructive sleep apnea and recurrence of atrial fibrillation after pulmonary vein isolation using a contact force-sensing catheter.

PURPOSE: Our aim was to elucidate the relationship between obstructive sleep apnea (OSA) and atrial fibrillation (AF) recurrence after repeated pulmonary vein isolation (PVI). METHODS: We conducted a non-randomized observational study, with the data prospectively collected. One hundred patients (paroxysmal AF, n = 89) underwent PVI using a contact force-sensing catheter. All patients underwent an electrophysiological study and additional ablation for left atrium-pulmonary vein (PV) reconnection and non-PV foci, 6 months after the first treatment session, regardless of AF recurrence. Those with an apnea-hypopnea index ≥ 15 were diagnosed with OSA. Continuous positive air pressure (CPAP) therapy was initiated after the second treatment session, based on results of a sleep study. For analysis, patients were classified into the non-OSA (n = 66), treated OSA (OSA patients undergoing CPAP; n = 11), and untreated OSA (n = 23) groups, and between-group differences evaluated. RESULTS: After the first session, AF recurrence was observed in 18.2% (12/66) and 14.7% (5/34) of patients without and with OSA, respectively (P = 0.678). After the second procedure, the rate of AF recurrence was 12.1% (8/66) in the non-OSA group, 9.1% (1/11) in the treated OSA group, and 8.7% (2/23) in the untreated OSA group (log-rank P = 0.944). CONCLUSIONS: The rate of AF recurrence might not be greater in patients with untreated OSA than in those without OSA and those with treated OSA after repeated PVI, using a contact force-sensing catheter, for patients with paroxysmal or short-term persistent AF.

Usefulness of epicardial impedance evaluation for epicardial mapping and determination of epicardial ablation site for ventricular tachycardia: A pilot study.

BACKGROUND: During epicardial mapping, determination of appropriate ablation sites in low voltage areas (LVA) is challenging because of large epicardial areas covered by adipose tissue. OBJECTIVE: To evaluate the impedance difference between epicardial fat and the epicardial LVA using multiple detector computed tomography (MDCT). METHODS: We enrolled patients who underwent ventricular tachycardia (VT) ablation via the epicardial approach after endocardial ablation failure. After the procedure, MDCT-derived images of epicardial fat were loaded to the mapping system. Then, all points acquired during sinus rhythm were retrospectively superimposed and analyzed. RESULTS: This study included data from 7 patients (62.5 ± 3.9 years old) who underwent eight epicardial VT ablation procedures. After the procedure, MDCT-derived images of epicardial fat were registered in eight procedures. Retrospective analysis of 1,595 mapping and 236 ablation points was performed. Of the 1,595 mapping points on the merged electroanatomical and epicardial fat maps, normal voltage area (NVA) and low voltage area (LVA) without fat had lower impedance than those with fat (NVA without fat 182 ± 46 Ω vs. NVA with fat 321 ± 164.0 Ω, P  =  0.001, LVA without fat 164 ± 69 Ω vs. LVA with fat 248 ± 89 Ω, P  =  0.002). Of the 236 ablation points, initial impedance before ablation was higher on epicardial fat than on epicardial LVA without fat (134 ± 16 Ω vs. 156 ± 28 Ω, P  =  0.01). CONCLUSIONS: Real time epicardial impedance evaluation may be useful to determine effective epicardial ablation sites and avoid adipose tissue. However, the number of patients in the present study is limited. Further investigation with a large number of patients is needed to confirm our result.

Prevalence and electrophysiological characteristics of typical atrial flutter in patients with atrial fibrillation and chronic obstructive pulmonary disease.

AIMS: Chronic obstructive pulmonary disease (COPD) is one of the important underlying diseases of atrial fibrillation (AF). However, the prevalence and electrophysiological characteristics of typical atrial flutter (AFL) in patients with AF and COPD remain unknown. The purpose of the present study was to investigate those characteristics. METHODS AND RESULTS: We investigated 181 consecutive patients who underwent catheter ablation of AF. Twenty-eight patients were diagnosed with COPD according to the Global Initiatives for Chronic Obstructive Lung Disease (GOLD) criteria. Forty patients with no lung disease served as a control group. We analysed the electrophysiological characteristics in these groups. Typical AFL was more common in the COPD group (19/28, 68%) than in the non-COPD group (13/40, 33%; P = 0.006). The prevalence of AFL increased with the severity of COPD: 4 (50%) of 8 patients with GOLD1, 13 (72%) of 18 patients with GOLD2, and 2 (100%) of 2 patients with GOLD3. Atrial flutter cycle length and conduction time from the coronary sinus (CS) ostium to the low lateral right atrium (RA) during CS ostium pacing before and after the cavotricuspid isthmus ablation were significantly longer in the COPD group than in the non-COPD group (285 vs. 236, 71 vs. 53, 164 vs. 134 ms; P = 0.009, 0.03, 0.002, respectively). CONCLUSION: In COPD patients with AF, conduction time of RA was prolonged and typical AFL was commonly observed.

Prophylactic catheter ablation for induced monomorphic ventricular tachycardia in patients with implantable cardioverter defibrillators as primary prevention.

AIMS: Prophylactic catheter ablation (CA) has been established to reduce the incidence of appropriate implantable cardioverter-defibrillator (ICD) therapy (anti-tachycardia pacing or shock) in secondary prevention patients. The aim of this study was to determine whether prophylactic CA for induced ventricular tachycardia (VT) reduces the incidence of appropriate ICD therapy in primary prevention patients. METHODS AND RESULTS: We retrospectively investigated 66 consecutive patients with structural heart disease who had undergone ICD implantation as primary prevention and electrophysiological study. Patients with hypertrophic cardiomyopathy or no inducible monomorphic VT had been excluded, and the remaining 38 patients were divided into two groups; those who had undergone prophylactic CA for induced monomorphic VT (the CA group, n = 18), and those who had not undergone CA (the non-CA group, n = 20). During a mean follow-up of 50 ± 38 months, 1 patient (5%) received appropriate ICD therapy in the CA group and 13 (65%) in the non-CA group. Kaplan-Meier survival analysis revealed a significantly higher event-free survival rates for appropriate ICD therapy in the CA group compared with the non-CA group (P = 0.003). Among the patients, one patient (5%) in the CA group and nine patients (45%) in the non-CA group suffered appropriate shock (P = 0.018). CONCLUSIONS: Prophylactic CA for induced monomorphic VT reduces the incidence of appropriate ICD therapy including shock in primary prevention patients. These results indicate that prophylactic CA may be considered for structural heart disease patients who are candidates for ICD implantation as primary prevention.

Macroreentrant atrial tachycardia in patients without previous atrial surgery or catheter ablation: clinical and electrophysiological characteristics of scar-related left atrial anterior wall reentry.

INTRODUCTION: Macroreentrant atrial tachycardia (MRAT) has been described most frequently in patients with prior cardiac surgery. Left atrial tachycardia and flutter are common in patients who undergo atrial fibrillation ablation; however, few reports describe left atrial MRAT involving the regions of spontaneous scarring. Here, we describe left atrial MRAT in patients without prior cardiac surgery or catheter ablation (CA) and discuss the clinical and electrophysiological characteristics of tachycardia and outcome of CA. METHODS AND RESULTS: An electrophysiological study and CA were performed in 6 patients (3 men; age 76 ± 6 years) with MRAT originating from the left atrial anterior wall (LAAW). No patient had a history of cardiac surgery or CA in the left atrium. Spontaneous scars (areas with bipolar voltage ≤ 0.05 mV) were observed in all patients. The activation map showed a figure-eight circuit with loops around the mitral annulus (4 counterclockwise and 2 clockwise) and a low-voltage area with LAAW scarring. The mean tachycardia cycle length was 303 ± 49 milliseconds. The conduction velocity was significantly slower in the isthmus between the scar in the LAAW and the mitral annulus than in the lateral mitral annulus (0.17 ± 0.05 m/s vs 0.94 ± 0.35 m/s; P = 0.003). Successful ablation of the isthmus caused interruption of the tachycardia and rendered it noninducible in all patients. CONCLUSION: Spontaneous LAAW scarring is an unusual cause of MRAT, showing activation patterns with a figure-eight configuration. Radiofrequency CA is a feasible and effective treatment in such cases.

Clinical and electrophysiological characteristics in patients with sustained monomorphic reentrant ventricular tachycardia associated with dilated-phase hypertrophic cardiomyopathy.

AIMS: Little is known about sustained monomorphic ventricular tachycardia (SMVT) associated with dilated-phase hypertrophic cardiomyopathy (DHCM). The purpose of this study was to clarify the clinical characteristics and effectiveness of catheter ablation for SMVTs in DHCM patients. METHODS AND RESULTS: Five patients with DHCM (mean age; 67.0 years old, five males) who underwent catheter ablation for drug-refractory SMVTs were included the study. Four of five patients suffered from electrical storm. When the endocardial ablation failed, epicardial and/or intracoronary ethanol ablation, or surgical cryoablation was performed. We reviewed all ablation procedures and electrocardiogram (ECG) of targeted SMVTs. A total of 13 SMVTs were targeted for ablation. Mechanism of all ventricular tachycardias (VTs) was diagnosed as reentry. Endocardial ablation successfully eliminated all VTs in two patients. The remaining three patients needed epicardial ablation, intracoronary ethanol ablation, and surgical cryoablation. All but one VT arose from the basal septum, basal anterior to anterolateral left ventricle (LV). Although the ECGs demonstrated similar features of idiopathic outflow or mitral annulus VTs reflecting the origins, there were characteristic multiple QRS deflections. Following the ablation, four (80%) of the five patients are free from VT recurrence during 18 months of the follow-up period. CONCLUSIONS: In DHCM patients, VT circuits predominantly distributed in the basal septum and the basal anterior to anterolateral LV. In addition to the endocardial ablation, alternative approaches were required in some patients.

Reciprocal control of hERG stability by Hsp70 and Hsc70 with implication for restoration of LQT2 mutant stability.

RATIONALE: The human ether-a-go-go-related gene (hERG) encodes the α subunit of the potassium current I(Kr). It is highly expressed in cardiomyocytes and its mutations cause long QT syndrome type 2. Heat shock protein (Hsp)70 is known to promote maturation of hERG. Hsp70 and heat shock cognate (Hsc70) 70 has been suggested to play a similar function. However, Hsc70 has recently been reported to counteract Hsp70. OBJECTIVE: We investigated whether Hsc70 counteracts Hsp70 in the control of wild-type and mutant hERG stability. METHODS AND RESULTS: Coexpression of Hsp70 with hERG in HEK293 cells suppressed hERG ubiquitination and increased the levels of both immature and mature forms of hERG. Immunocytochemistry revealed increased levels of hERG in the endoplasmic reticulum and on the cell surface. Electrophysiological studies showed increased I(Kr). All these effects of Hsp70 were abolished by Hsc70 coexpression. Heat shock treatment of HL-1 mouse cardiomyocytes induced endogenous Hsp70, switched mouse ERG associated with Hsc70 to Hsp70, increased I(Kr), and shortened action potential duration. Channels with disease-causing missense mutations in intracellular domains had a higher binding capacity to Hsc70 than wild-type channels and channels with mutations in the pore region. Knockdown of Hsc70 by small interfering RNA or heat shock prevented degradation of mutant hERG proteins with mutations in intracellular domains. CONCLUSIONS: These results indicate reciprocal control of hERG stability by Hsp70 and Hsc70. Hsc70 is a potential target in the treatment of LQT2 resulting from missense hERG mutations.

Low risk for arrhythmic events in asymptomatic patients with drug-induced type 1 ECG. Do patients with drug-induced Brugada type ECG have poor prognosis? (Con).

The type 1 ST-segment elevation is diagnostic for Brugada syndrome (BS) and its presence may sometimes be associated with a high risk of arrhythmic events. The type 1 ECG is also known to be unmasked by administration of sodium-channel blockers in equivocal or suspected cases of BS, and the drug-challenge test is frequently used in the diagnostic approach. In large cohort studies the spontaneous appearance of the type 1 ECG with symptoms of aborted sudden death or unexplained syncope are indicative of a poor prognosis for patients with BS compared with not having clinical symptoms. Therefore, the spontaneous type 1 ECG appears to represent an important predictive sign for cardiac events. It is unknown, however, whether or not the drug-induced type 1 ECG is as useful as the spontaneous type 1 for predicting cardiac events in asymptomatic subjects showing non-type 1 ECG. Review of the literature for large cohort studies indicates that there is a low incidence of arrhythmic events in asymptomatic patients with either the spontaneous or drug-induced type 1 ECG compared with symptomatic subjects, and the drug-induced type 1 ECG in asymptomatic patients does not add to an increase in arrhythmic risk. Therefore, drug testing to unmask the type 1 ECG in asymptomatic patients with a non-type 1 BS ECG does not have an additional value for risk stratification of cardiac events, although it might be useful in symptomatic patients showing only the non-type 1 ECG.

Bidirectional ventricular tachycardia caused by a reentrant mechanism with left bundle branch block configuration on electrocardiography.

Reentrant bidirectional ventricular tachycardia (VT) with left bundle branch block (LBBB) configuration was diagnosed in a 54-year-old woman who showed 2 types of VT: QRS morphologies of LBBB with inferior axis and LBBB with superior axis. The development of VT with a superior axis was preceded by VT with inferior axis and/or both configurations of VT in alternate beats exhibiting bidirectional VT. The electrophysiological study demonstrated reproducible induction of both types of VT by programmed ventricular stimulation and both types of VT were entrained. Using conventional pace mapping and electro-anatomical mapping methods, radiofrequency energy applications at the 2 exit sites of the reentry path successfully terminated both types of VT and the patient was free from VT attacks for more than 15 months.

ST-T wave changes in a patient complicated with vasospastic angina and Brugada syndrome: differential responses to acetylcholine in right and left coronary artery.

A 49-year-old man with chest pain and syncope presented saddleback or occasionally coved type ST elevation in V1-V3. Coronary spasm in the left anterior descending artery was induced by acetylcholine injection and ST elevation changed from saddleback to coved type in V2-V3 together with ST depression in V4-V5, whereas acetylcholine injection into the right coronary artery did not provoke spasm, but induced augmented and coved type ST elevation in V2 without ST-T changes in V4-V5. These electrocardiographic changes in response to acetylcholine administration into each coronary artery are compatible with pathogenesis of vasospastic angina and Brugada syndrome, respectively.

Autonomic and pharmacological responses of idiopathic ventricular tachycardia arising from the left ventricular outflow tract.

BACKGROUND: It is well recognized that the mechanism of idiopathic ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) is mostly due to cyclic AMP-mediated triggered activity. The mechanism of VT arising from the left ventricular outflow tract (LVOT) has not been well clarified whether it is the same as VT of RVOT. METHODS: We studied autonomic modulations and pharmacological interventions on VT/premature ventricular contractions (PVCs) from LVOT to explore its possible mechanism in six patients (age: 49 +/- 14, three males). None of them had structural heart diseases. RESULTS: Isoproterenol application easily induced VT and/or PVCs from LVOT. Valsalva maneuvers suppressed isoproterenol-induced VT in two and PVCs in two, and carotid sinus massage (CSM) suppressed PVCs in one patient. Adenosine triphosphate inhibited both VT and PVCs in all six patients. Propranolol, lidocaine, and procainamide eliminated VT/PVCs in four, three, and four patients, respectively. Verapamil terminated VT in one and PVCs in another one patient, but aggravated PVCs to VT in one patient. CONCLUSION: The results suggest that the mechanism of VT from LVOT is mostly due to cAMP-mediated triggered activity as similar to that in VT from RVOT.