Characterization of Residual Conduction Gaps After HotBalloon-Based Antral Ablation of Atrial Fibrillation　- Evidence From Ultra-High-Resolution 3-Dimensional Mapping.

BACKGROUND: The electrophysiological characteristics of residual conduction gaps between the left atrium (LA) and pulmonary veins (PVs) after HotBalloon-based wide antral ablation (HBWA) of atrial fibrillation (AF) remain incompletely understood. This study aimed to characterize the residual gaps by means of ultra-high-resolution mapping.Methods and Results:A total of 55 AF patients underwent HBWA by a predetermined protocol (6-shot total-based antral approach). LA-PV maps were created using 64-electrode minibasket catheters. In total, 55 residual gaps were identified among 26 (47%) patients. Residual gaps included 33 left superior (LS: 60%), 10 left inferior (18%), 6 right superior (11%), and 6 right inferior (11%) PVs. Those gaps demonstrated both extremely lower bipolar amplitudes (0.11 [interquartile range: 0.06-0.27] mV) and conduction velocities (0.75±0.27 m/s); however, the length was confined (10.3±4.1 mm) except for the LSPV anterior carina (12.2±2.4 mm) region. Among the carina regions, all gaps had far-field potentials consistently added to the PV potentials. Left atrial appendage pacing to split the far-field activity identified confined gap regions (6.7±1.9 mm). Touch-up ablation eliminated the residual PV potentials in all cases. CONCLUSIONS: HBWA resulted in a certain degree of residual gap conduction in particular antral regions. These gaps exhibited narrow lengths with lower amplitudes, and often had far-field recordings from the left atrial appendage. Combined with pacing maneuvers, ultra-high-resolution activation maps could both visualize all confined gaps and ensure a bare minimum of touch-up ablations in all patients with gap conduction.

Influence of the left atrial contact areas on fixed low-voltage zones during atrial fibrillation and sinus rhythm in persistent atrial fibrillation.

BACKGROUND: Atrial low-voltage zones (LVZ) are suggested as important factors for maintaining persistent atrial fibrillation (PsAF). The relationship between LVZs and left atrial (LA) contact areas (CoAs) is still unclear. OBJECTIVE: To assess whether CoA regions were involved in atrial substrate properties maintaining PsAF. METHODS: A total of 50 patients with PsAF (36 long-lasting) were analyzed. Three representative CoA detection areas (ascending aorta-anterior-LA, descending aorta-left pulmonary vein antrum, and vertebrae-posterior-LA) were registered on the mapping geometry. Electrograms during AF and sinus rhythm (SR) were acquired, and the fractionated electrograms (CFE; < 80milliseconds) and voltages were analyzed regarding the CoAs. RESULTS: After SR conversion, 76% (38/50) had a significant LVZ (>5% of the total LA surface area). Patients with long-lasting PsAF versus PsAF had larger CoA areas (7.7 ± 3.0 vs. 4.5 ± 2.5cm2 , P < 0.05) and overlapped-LVZs (8.2 [3.2-11.0] vs. 2.1 [0.7-3.7] cm2 , P = 0.0126) between the SR-LVZs (<0.5 mV) and AF-LVZs (<0.2 mV). Overlapped-LVZs were frequently observed in CoA regions (anterior 76.4%; LIPV antrum 78.8%, and vertebrae 39.2%), and those LVZs had smaller unipolar voltages than those distant from the CoA regions (0.64 ± 0.16 vs. 2.5 ± 1.5 mV, P < 0.0001). SR-LVZ targeted ablation, including of CoA regions, rendered AF termination (n = 8, 21%), and 88% of the sites were not located immediately above, but adjacent to, the overlapped-LVZs. Significant AF slowing (6.0 ± 0.6 to 5.6 ± 0.6 Hz; P < 0.05) accompanied by unintentional CFE elimination (9.8-1.8 cm2 ; P < .0001) was achieved in patients without termination. CONCLUSION: Our data suggested that external structures in contact with the LA are involved in the creation of localized diseased myocardium necessary for PsAF maintenance.

Long-Term Favorable Course of Aspergillus Endo-, Myo-, and Pericarditis.

Here, we report on a healthy 30-year-old man with no significant medical history, who tested negative for human immunodeficiency virus antigenemia but developed Aspergillus pancarditis. A case of this kind is extremely rare, and to the best of our knowledge, this is the first report of a patient with Aspergillus pancarditis, which generally leads to a very poor outcome, who had a long-term favorable clinical course. A biopsy from the right atrium of hypertrophied atrial septum was essential for obtaining the definitive diagnosis. Long-term administration of an effective antifungal oral agent might account for the patient's favorable outcome.

Spatial Relation Between Left Atrial Anatomical Contact Areas and Circular Activation in Persistent Atrial Fibrillation.

INTRODUCTION: Atrial low-voltage zones (LVZs) may be related to maintenance of atrial fibrillation (AF). The influence of left atrial (LA) contact areas (CoAs) on reentrant or rotor-like sources maintaining AF has not been investigated. METHODS AND RESULTS: Forty patients with persistent AF (PsAF) were analyzed. Three representative CoA regions in the LA (ascending aorta: anterior wall; descending aorta: left inferior pulmonary vein; and vertebrae: posterior wall) were visualized by enhanced CT. Using circular catheters, the LVZs (<0.5 mV) were assessed after restoration of SR, and local activation mapping and frequency domain analyses were performed after induction of AF. Circular activation during AF was visually defined as sites with ≥2 rotations by serial electrograms encompassing >80% of the mean AF cycle length. A pivot was defined as the core of the localized circular activation. Anterior (39/40 patients, 98%), left pulmonary vein antrum (27/40, 68%), and posterior (19/40, 48%) CoAs were identified, and 80% (68/85) of those sites were overlapped by or close (<3 mm) to LVZs. Thirty-six (90%) patients demonstrated circular activation (3.1±1.7 sites/patients) along with significantly higher organized dominant frequencies (6.3 ± 0.5 Hz, regularity-index: 0.26 [0.23-0.41]) within the LA, and the average electrogram amplitude of those pivots was 0.30 mV (0.18-0.52). Of those sites, 55% (66/120) were located at or close to CoA regions. Catheter ablation including of LVZs neighboring CoAs terminated AF in 9 (23%) patients. CONCLUSIONS: External anatomical structures contacting the LA may be related to unique conduction properties in diseased myocardium necessary for PsAF maintenance.

Insulin Resistance as a Predictor of the Late Catch-up Phenomenon After Drug-Eluting Stent Implantation.

BACKGROUND: Percutaneous coronary intervention (PCI) is an effective treatment for patients with ischemic heart disease. In particular, restenosis is suppressed after drug-eluting stent (DES) implantation. However, several problems remain. Previously, we reported neointimal proliferation after DES implantation, which was associated with insulin resistance (IR). The aim of the present study was to clarify whether IR is associated with mortality and major adverse cardiac and cerebrovascular events (MACCE) after 1st-generation DES implantation. METHODS AND RESULTS: We researched the clinical records of 109 patients who had undergone elective PCI and DES implantation between May 2007 and December 2010. We segregated these patients according to the value of the homeostasis model assessment of IR (HOMA-IR) into Group P (n=63; HOMA-IR ≥2.5, positive) and Group N (n=46; HOMA-IR <2.5, negative), and examined the relationship between HOMA-IR and MACCE. The observation period was 7.4±1.6 years. There were no differences between the 2 groups in the occurrence of all-cause death, cardiac death, restenosis, myocardial infarction, stroke, heart failure, or stent thrombosis. However, the late catch-up phenomenon was significantly more common in Group P than in Group N (12.7% vs. 2.2% P=0.048). CONCLUSIONS: IR is a useful predictor of the late catch-up phenomenon after DES implantation, and improvement of IR may help to prevent the phenomenon. (Circ J 2016; 80: 657-662).

Percutaneous Removal of Inferior Vena Cava Filter after Migration to Pulmonary Artery using an 8-Fr Multipurpose Catheter.

An inferior vena cava filter migrated to the left pulmonary artery during removal. The legs of the filter were not open adequately due to thrombus accumulating around the legs and resulted in the filter floating up and migrating to the pulmonary artery through the right atrium and ventricle. The hook for retrieval placed at the top of the filter faced proximal in the pulmonary artery and the legs of filter remained closed, consequently the filter could be removed safely from the pulmonary artery. An 8-Fr multipurpose catheter with its flexibility was useful to retrieve the filter from the pulmonary artery.

Influence of left atrium anatomical contact area in persistent atrial fibrillation-relationship between low-voltage area and fractionated electrogram.

BACKGROUND: Atrial low-voltage areas are suggested to be related to maintenance of atrial fibrillation (AF). The influence of the left atrium (LA) contact area (CoA) has not been investigated. METHODS AND RESULTS: Twenty-two persistent AF patients underwent high-density mapping during AF and sinus rhythm (SR). Three representative CoA regions in the LA (ascending aorta: anterior wall; descending aorta: left inferior pulmonary vein [LIPV]; and vertebrae: posterior wall) were identified. Electrogram analysis of both high dominant frequency (high-DF; >8 Hz) and complex fractionated atrial electrogram (con-CFAE; <50 ms) regions during SR was done. The anatomical relationship between CoA and both the very low-voltage areas (vLVA; <0.2 mV) and high-frequency sources was determined. Forty-seven vLVA (194.4 cm(2)) and 60 CoA (337.0 cm(2)) were documented, and 32 vLVA directly overlapped CoA. The vLVA were preferentially found in the anterior (45%) and posterior (13%) walls of the LA, and in the LIPV (13%), and corresponded to CoA sites. The mean voltage during SR at high-DF sites was significantly lower than that at con-CFAE sites (0.62 vs.1.54 mV; P<0.0001). Seventy-two percent of high-DF sites overlapped CoA, while 54% of con-CFAE did. Furthermore, 44% of high-DF surface area directly overlapped CoA, while only 19% of con-CFAE did. CONCLUSIONS: Very low-voltage regions had a strong association with CoA. Sites with CoA had a higher incidence of fractionated electrograms both during SR and AF.

Ectopic cycle length estimation from the quantified distribution patterns of ventricular bigeminy and trigeminy.

BACKGROUND: Ectopic cycle length (ECL) and the distribution patterns of ventricular bigeminy and trigeminy, expressed as their postextrasystolic intervals (PEIs) and interectopic intervals (IEIs), have been poorly pursued. OBJECTIVE: Based on modulation theory, we hypothesized that the PEIs of bigeminy and trigeminy determine their IEIs and ECL. METHODS: Ambulatory electrocardiograms of 1290 patients with ventricular premature complexes (≥3000/day) were studied. To quantify their distribution pattern on the PEI vs IEI curve (PIC), we introduced the following 2 ratios: PEI of trigeminy to PEI of bigeminy ratio (T/B-PEI) and IEI of trigeminy to IEI of bigeminy ratio (T/B-IEI). Distribution patterns were divided into 3 types by T/B-PEI: standard type (<0.90), intermediate type (between 0.90 and 1.20), and reverse type (>1.20). ECL was defined as the average of the bigeminy and trigeminy intervals in the standard type, and bigeminy intervals in the other 2 types. RESULTS: T/B-IEI disclosed significant linear relationship with T/B-PEI (P < .0001). ECLs were longest in the standard type (1905 ± 347 ms; n = 426), followed by the intermediate type (1520 ± 239 ms; n = 607) and reverse type (1317 ± 227 ms; n = 227) (P < .0001). Trigeminy PEI/ECL in the standard type (0.450 ± 0.074) was significantly shorter than that of the other 2 types (P < .0001). CONCLUSION: We confirmed that T/B-PEI determines T/B-IEI and ECL by discriminating the 3 distribution patterns. Among them, trigeminy PEI/ECL decided the 2 types of modulation by the first sinus QRS, starting at the early delay phase or the later acceleration phase.

Subtle Cardiovascular Abnormalities in Prader-Willi Syndrome Might Begin in Young Adulthood.

Objective Patients with Prader-Willi syndrome (PWS) are known to have a high mortality rate. However, little is known about the exact reason for this, particularly in adults, because so few reports have been published. The present study examined cardiovascular abnormalities to determine the cause of death in adults with PWS. Methods From September 2017 to April 2019, a total of 18 adults with PWS, and, no history of cardiovascular diseases, were enrolled. We investigated the levels of the cardiovascular biomarkers: high-sensitivity C-reactive protein (hs-CRP) and troponin T (TnT). To estimate the cardiac function, we measured the left ventricular ejection fraction (LVEF), global longitudinal systolic strain (GLS) of the left ventricle, ratio of peak early mitral filling velocity (E) to early diastolic mitral annular velocity (E/e' ratio), mitral annular plane systolic excursion (MAPSE) and tricuspid annular plane systolic excursion (TAPSE) using standard and tissue Doppler echocardiography. Results The mean patient age was 28±9 years old. There were 11 men, and the mean body mass index was 45.1 kg/m2. Dyslipidemia (82%), diabetes mellitus (82%) and hypertension (83%) were commonly found as comorbidities. Most patients had elevated levels of hs-CRP (mean 1.007±0.538 mg/dL). The LVEF (mean 61%±5%) showed normal values, while the GLS (mean 15.0%±3.0%) was decreased. The TAPSE was mildly reduced (mean 16±3 mm). Conclusion These results suggest that subtle cardiovascular abnormalities have already begun in young adults with PWS. We need to manage obesity and the resultant obesity-related disorders in order to prevent heart failure and coronary atherosclerosis in PWS patients.

Impact of low-voltage zones on the left atrial anterior wall on the reduction in the left atrial appendage flow velocity in persistent atrial fibrillation patients.

BACKGROUND: The reduction in the left atrial appendage (LAA) flow velocity is related to the presence of emboli in atrial fibrillation (AF) patients. The LAA is located on the left superior side of the left atrial (LA) anterior wall, and we investigated the relationship between the reduction in the LAA flow velocity (LAAFV) and low voltage zones (LVZs < 0.5 mV) on the LA anterior wall. METHODS: In 146 persistent AF patients, LAAFV measurements, by transesophageal echocardiography, and catheter ablation were performed. LA mapping was performed before ablation during sinus rhythm, and the locations of any anterior-LVZs were documented. RESULTS: Eighty-one patients had a documented LVZ on the LA anterior wall, and those with an LVZ had a significantly lower LAAFV compared to those without (anterior-LVZ(+) vs. anterior-LVZ(-) = 26 ± 11 vs. 34 ± 10 cm/s, p < 0.001), while no significant difference was observed when compared to the other LVZ regions. A low-LAAFV (≦ 20 cm/s) was observed in 36 patients, and the CHADS2-vasc score and existence of an anterior-LVZ were associated with a low-LAAFV. In patients with anterior-LVZs, the distance between the anterior-LVZ and LAA orifice correlated with a low LAAFV (r = 0.534, p < 0.001) as compared to the surface area of the anterior-LVZ (r = - 0.288, p = 0.009). CONCLUSIONS: In persistent AF patients, an LVZ on the LA anterior wall was associated with a low LAAFV. In addition, an anterior-LVZ located near the LAA orifice was further related to a reduction in the LAAFV.

Causes of an increased pressure gradient through the left ventricular outflow tract: a West Coast experience.

BACKGROUND: Left ventricular outflow tract obstruction (LVOTO) occurs from not only obstructive hypertrophic cardiomyopathy but also other conditions such as sigmoid septum or post mitral valve repair. However, the changes of the LVOT pressure gradient (LVOT PG) in LVOTO with various conditions remain unclear. METHODS: The clinical characteristics and echocardiographic parameters of 73 patients with LVOT PG ≥50 mmHg at rest on Doppler ultrasound were retrospectively investigated. RESULTS: In these patients (age 69 ± 15 years, 38% male), high prevalences of hypertension (66%) and anemia (43%) were observed. The most frequent clinical disease causing LVOTO was hypertrophic obstructive cardiomyopathy (HOCM) (74%). There were other conditions, including hypertensive left ventricular hypertrophy (9%), post-open heart surgery (7%), sigmoid septum (4%), hyperkinetic LV (3%), takotsubo cardiomyopathy (1.5%), and discrete subaortic membrane (1.5%). Significant improvement or reduction of LVOTO was observed in 93% of cases at follow-up (mean 44 months) echocardiography compared with the initial one with the use of medications and transcatheter procedures. CONCLUSIONS: The causes of LVOTO are diverse. However, the occurrence of LVOTO might depend on the coexistence of primary morphological LV characteristics and hemodynamic LV status. Specific factors causing LVOTO need to be investigated, and efforts for improvement of each individual status by the appropriate approach are required.

Limitation of the bandpass filter in preventing oversensing of pectoral myopotentials over the long-term follow-up.

A 60-year-old male experienced an inappropriate shock from an implantable cardioverter-defibrillator (ICD) because of oversensing of pectoral myopotentials. Battery depletion was also observed, and a generator change was performed. A single-chamber ICD (VENTAK PRIZM II 1860) was changed to a new ICD (INCEPTA VR F161). The myopotentials were clearly eliminated by the difference in the band pass filter (PRIZM; 21-171 Hz, INCEPTA; 20-85 Hz), but unfortunately, new noise was documented 4 years later. The utility of the bandpass filter for preventing oversensing of myopotentials was observed, but the limitation of its use for long-term follow-up was also indicated.

Investigation of the atrial conduction time measured by tissue Doppler imaging at the left atrial appendage and the actual electrical conduction time: consideration of left atrial remodeling in atrial fibrillation patients.

PURPOSE: The atrial conduction time measured by echocardiography using tissue Doppler imaging (TDI) has been reported as a predictive factor of left atrial (LA) remodeling. We investigated the P wave to LA appendage (LAA) conduction time defined by transthoracic echocardiography using TDI (P-LAA TDI), and directly compared the actual LA electrical conduction time determined by the electrophysiological data. Additionally, we confirmed the clinical utility of the P-LAA TDI by examining the relationship to the electroanatomical LA remodeling data. METHODS: Sixty-three AF patients (22 paroxysmal AF, 41 persistent AF) underwent ablation and electroanatomical LA mapping. The P-LAA TDI was measured after the ablation and was compared with the electrophysiological data during sinus rhythm, including the actual electrical conduction time. RESULTS: A strong linear correlation (r = 0.776, p < 0.001, y = 1.28x + 49) was observed between the P-LAA TDI (161 ± 24 ms) and electrophysiological P-LAA time (87 ± 15 ms). The P-LAA TDI was also strongly correlated with the LA volume (173 ± 52 ml, r = 0.632, p < 0.001) and LA conduction velocity index (1.07 ± 0.19 mm/ms, r = -0.735, p < 0.001), but less to the focal anterior-LVA region surface area (2.2 [0.4-5.0] cm2, r = 0.380, p = 0.002). Additionally, a stepwise multiple linear regression demonstrated that both the LA volume and LA conduction velocity index were strongly associated with the value of the P-LAA TDI (p < 0.001). CONCLUSIONS: The P-LAA TDI was useful for estimating the actual electrophysiological conduction time and represented both electrical and anatomical LA remodeling.

Identification of stimulation site of pacemaker lead using tissue tracking method.

PURPOSE: We aimed to identify the electrical stimulation sites of pacemaker leads using a tissue tracking method of tissue Doppler imaging. METHODS: The study group consisted of 30 patients who had undergone permanent pacemaker implantation. During tissue Doppler imaging, the initial contraction site was seen as a red area stimulated by the pacemaker lead. This red area was analyzed precisely using time-distance curves generated by tissue tracking. RESULTS: The initial contraction site of the myocardium was located in the interventricular septum in seven patients and in the apical portion of the right ventricle in 11 patients. Furthermore, analysis of time-distance curves demonstrated that one point within the red area started to move earlier than the others. CONCLUSION: The site of electrical stimulation within the myocardium can be determined from the time-distance curves generated by the tissue tracking method.

Temporal sinus node modification by high-dose continuous intravenous administration of landiolol in a patient with persistent inappropriate sinus tachycardia.

A 20-year-old woman underwent an electrophysiological study for drug-resistant persistent inappropriate sinus tachycardia (IST). Use of a high-dose continuous intravenous administration of landiolol, a short-acting beta-adrenoreceptor blocker, made the patient׳s heart rate suddenly drop with a slight change in the P-wave morphology. Three-dimensional right atrial (RA) activation mapping revealed that the earliest activation site moved 8 mm to a lower anterior site around the high lateral RA. Radiofrequency energy applied to the earliest activation site during tachycardia was successful. A temporal sinus node modification with landiolol administration was useful for mapping and for safe catheter ablation of IST.

Impact of catheter tip-tissue contact on three-dimensional left atrial geometries: Relationship between the external structures and anatomic distortion of 3D fast anatomical mapping and high contact force guided images.

BACKGROUND: A high catheter tip-tissue contact force (CF) with the myocardium may cause 3-dimensional (3D) map distortion, however, the influence of external structures surrounding the left atrium (LA) on that distortion remains unknown. This study characterized the impact of high CF mapping on the local LA geometry distortion. METHODS: Thirty AF patients underwent 3D-ultrasound merged with CT images (3D-Merge-CT). The LA area in contact with external structures was identified by enhanced CT. Fast-electroanatomical-mapping (FAM) geometries were created by two methods, point-by-point mapping with high (>10g) CFs (high-CF guided-FAM), followed by that with multielectrode-mapping catheters (conventional-FAM). The resulting geometries were compared with the 3D-Merge-CT images. RESULTS: Three representative anatomical contact areas (ascending aorta-vs.-anterior wall, descending aorta-vs.-left pulmonary vein [PV], and vertebrae-vs.-posterior wall) were identified. The PV antrum distorted distance on the 3D-Merge-CT was significantly longer for high-CF guided-FAMs than conventional-FAMs (1.7[0-3.6] vs. 0[0-1.8]mm, P<0.0001). In high-CF maps, the distorted distance significantly differed between regions with and without contact areas in both the PV antrum (0[0-0.17] vs. 1.7[0-3.9]mm, P=0.0201) and LA body region (0[0-1.5] vs. 1.7[0.7-2.2]mm, P<0.005). The catheter tip-tissue CF did not correlate with the distorted distance (r=0.08, P=0.46), and a multivariate analysis revealed that the absence of anatomical contact areas was strongly associated with significant local distortion, independent of the CF. CONCLUSIONS: High-CF guided mapping yields greater 3D-image anatomical distortion than conventional-FAM methods. That distortion was attenuated by regions with anatomical contact areas, suggesting that regional anatomic distortion is involved in the existence of external structures surrounding the LA.

Stent-induced expression and activation of the leukocyte integrin Mac-1 is associated with neointimal thickening and restenosis.

BACKGROUND: Increased expression of the beta2 integrin Mac-1 (CD11b/CD18, alphaMbeta2), which is responsible for firm leukocyte adhesion to platelets and fibrinogen at injured vessels, is found in association with neointimal hyperplasia after coronary interventions. The role of Mac-1 in the pathophysiology of restenosis is incompletely defined. To clarify further the role of Mac-1, we determined whether coronary stenting induced activation of Mac-1, which is required for high-affinity receptor-ligand interactions. METHODS AND RESULTS: Expression of CD11b (alpha-subunit of Mac-1) and binding of 8B2 (monoclonal antibody against an activation-dependent neoepitope of Mac-1) on the surface of polymorphonuclear leukocytes were analyzed in 62 patients undergoing coronary stenting using flow cytometric analysis of whole blood obtained from the coronary sinus and femoral vein. Transcardiac CD11b expression increased significantly at 24 hours and maximally at 48 hours after stenting; 8B2 began to increase at 10 minutes and was maximally increased at 48 hours after stenting. These changes were more prominent in patients with subsequent restenosis. Multiple regression analysis showed that the late lumen loss by quantitative coronary angiographic analysis was independently correlated with the CD11b increase (R=0.42, P<0.01) and the 8B2 increase (R=0.55, P<0.001) 48 hours after the procedure. Mac-1 activation, as assessed by 8B2 binding, was the most powerful predictor of late lumen loss. CONCLUSIONS: Coronary stenting produced upregulation and early activation of the leukocyte integrin Mac-1, which is associated with late lumen loss and restenosis. These data support a role for inflammation in neointimal thickening and suggest the validity of targeting leukocyte recruitment for preventing clinical restenosis.

Impact of Insulin Resistance on Neointimal Tissue Proliferation after 2nd-Generation Drug-Eluting Stent Implantation.

Percutaneous coronary intervention is established as an effective treatment for patients with ischemic heart disease; in particular, drug-eluting stent implantation is known to suppress in-stent restenosis. Diabetes mellitus is an independent risk factor for restenosis, so reducing insulin resistance is being studied as a new treatment approach. In this prospective study, we sought to clarify the factors associated with in-stent restenosis after percutaneous coronary intervention, and we evaluated the homeostasis model assessment of insulin resistance (HOMA-IR) index as a predictor of restenosis. We enrolled 136 consecutive patients who underwent elective percutaneous coronary intervention at our hospital from February 2010 through April 2013. All were implanted with a 2nd-generation drug-eluting stent. We distributed the patients in accordance with their HOMA-IR index values into insulin-resistant Group P (HOMA-IR, ≥2.5; n=77) and noninsulin-resistant Group N (HOMA-IR, <2.5; n=59). Before and immediately after stenting, we measured reference diameter, minimal lumen diameter, and percentage of stenosis, and after 8 months we measured the last 2 factors and late lumen loss, all by means of quantitative coronary angiography. After 8 months, the mean minimal lumen diameter was smaller in Group P than that in Group N (1.85 ± 1.02 vs 2.37 ± 0.66 mm; P=0.037), and the mean late lumen loss was larger (0.4 ± 0.48 vs 0.16 ± 0.21 mm; P=0.025). These results suggest that insulin resistance affects neointimal tissue proliferation after 2nd-generation drug-eluting stent implantation.

The influence of the external structures in atrial fibrillation patients: Relationship to focal low voltage areas in the left atrium.

INTRODUCTION: Left atrial (LA) low voltage areas (LVAs) are suggested as an important factor for maintaining atrial fibrillation (AF). The relationship between focal LVAs and anatomical contact is still unclear. METHODS: Thirty paroxysmal AF (PAF) and 30 persistent AF (PsAF) patients underwent high density voltage mapping during sinus rhythm before any radiofrequency applications were performed. The relationship between the LVA (<0.5mV) and contact area (CoA) demonstrated by enhanced CT and the distance to near external structures were investigated. RESULTS: The anterior region, posterior wall and left pulmonary vein (LPV) antrum were the three most frequent LVA sites that corresponded to CoA sites, and LVAs mostly overlapped with CoAs (PAF 47/61: 77%, PsAF 63/74: 85%). In the PAF group, patients with posterior-LVAs had a shorter distance to the vertebrae than those without (2.8 ± 1.1 vs. 4.4 ± 1.9 mm; P=0.0086). The distance to the vertebrae was the only predictive factor of the existence of a posterior-LVA and the cut-off value was ≤2.9 mm (P<0.0001). Similarly, an LPV-LVA also had the same results (2.0 ± 0.5 vs. 2.7 ± 0.8mm, P=0.0127) and the cut-off value was ≤2.6mm (P=0.0391). In contrast, the PsAF patients had no difference in the distance when compared to the existence of an LVA. CONCLUSIONS: Anatomical CoAs demonstrated a spatial relationship to the LVAs in AF patients. In PAF patients, the distance to near external structures in the posterior region was a predictive factor for the existence of an LVA and may have had some influence on maintaining AF, while in PsAF patients no relationship was suggested.

Impact of irbesartan, an angiotensin receptor blocker, on uric acid level and oxidative stress in high-risk hypertension patients.

Hyperuricemia is a known cardiovascular risk factor. The angiotensin II receptor blocker (ARB) losartan is known to decrease serum uric acid (UA) level. A recent in vitro study demonstrated a strong interaction between irbesartan and UA transporters that exceeded that of losartan. The purpose of the present study was to evaluate the hypouricemic effect of irbesartan in a clinical setting. A total of 40 high-risk hypertensive outpatients with coronary artery disease, cerebrovascular disease and/or diabetes complications who were taking ARBs other than irbesartan and losartan were enrolled in this study. After a 4-week control period, the patients' prescribed ARBs were exchanged for an equivalent dose of irbesartan. We assessed blood pressure, heart rate, serum UA level, parameters of lipid and glucose metabolism, cardiac and renal function and inflammatory and oxidative stress markers in blood samples taken immediately before the initiation of irbesartan treatment and again after 12 weeks of treatment. All 40 recruited patients were followed (31 men and 9 women, mean age: 68 years) without any dropouts. During the 12 weeks of irbesartan treatment, no significant changes in blood pressure, heart rate, parameters of lipid or glucose metabolism or other biomarkers of cardiac function, renal function, or inflammation were observed. However, UA level (5.9±1.6 to 5.5±1.6 mg ml(-1), P=0.028) and the oxidative stress marker derivative reactive oxygen metabolites (dROMs) (354±83 to 310±65 U.CARR, P<0.001) were significantly lower at 12 weeks of treatment compared with before treatment. These results suggest that irbesartan has beneficial effects on hyperuricemia and oxidative stress.