Efficacy and safety of uninterrupted rivaroxaban taken preoperatively for radiofrequency catheter ablation of atrial fibrillation compared to uninterrupted warfarin.

PURPOSE: Data on uninterrupted rivaroxaban taken preoperatively for radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF) is limited. The aim was to evaluate safety and efficacy of rivaroxaban taken in the morning for AF ablation, especially with regard to asymptomatic cerebral emboli (ACE) and anticoagulation parameters. METHODS: We prospectively evaluated 147 consecutive patients who underwent RFCA (mean age 66, 110 patients with paroxysmal AF), 76 of whom were on rivaroxaban, 71 on warfarin. The drugs were continued throughout the periprocedural period, including the morning of RFCA. Heparin infusion was maintained during RFCA to achieve an activated clotting time (ACT) of >300 s. RESULTS: There were no significant differences in basic patient characteristics and ablation procedure between the two groups. ACT during the procedure correlated significantly with prothrombin time and international normalized ratio in each group (correlation coefficient 0.799 in rivaroxaban, 0.705 in warfarin, p < 0.01). D-dimer level was more elevated after RFCA in the warfarin group than in the rivaroxaban group (warfarin 0.37 ± 0.28 to 0.67 ± 0.81, rivaroxaban 0.41 ± 0.33 to 0.51 ± 0.25, p = 0.02). One major bleeding event (1.3%), a cardiac tamponade, was observed in the warfarin group. No symptomatic thromboembolic complications were observed in either group. Two patients (3%) in each group had minor bleeding, specifically, groin hematoma. Postprocedural MRI indicated ACE in 5/46 (11%) patients in the rivaroxaban group and 4/39 (10%) in the warfarin group (p = 0.99). CONCLUSIONS: Uninterrupted rivaroxaban taken preoperatively for AF ablation is clinically effective and safe. Its ACE profile is similar to warfarin. ACT is sufficient for monitoring anticoagulation.

Intracoronary electrocardiogram ST-segment elevation in patients with non-ST-segment elevation myocardial infarction and its association with culprit lesion location and myocardial injury.

AIMS: An intracoronary electrocardiogram (IC-ECG) is a sensitive method to detect local myocardial ischaemia. We investigated the prevalence of IC-ECG ST-segment elevation (STE) with respect to culprit lesion location in patients with non-ST-segment elevation myocardial infarction (NSTEMI) and its relationship with elevated levels of cardiac biomarkers. METHODS AND RESULTS: We examined 87 NSTEMI patients who underwent IC-ECG recording by locating the insulated polymer-coated guidewire distal to the culprit lesion before percutaneous coronary intervention (PCI). Cardiac biomarkers were serially examined. IC-ECG STE was observed in 24 patients (27.6%) before PCI, and was significantly more frequent in patients with LCx culprit lesions (LAD vs. LCx vs. RCA, 12.1% vs. 53.3% vs. 16.7%; p<0.001). Peak cardiac troponin I (cTnI) values were associated with IC-ECG STE, ejection fraction (EF), cTnI values on admission, and type B2/C lesions. In multivariate analysis, IC-ECG STE (odds ratio [OR], 5.04; 95% confidence intervals [CI]: 1.51-16.85; p=0.009), and EF (OR, 0.95; 95% CI: 0.90-1.00; p=0.043) were predictors of greater peak cTnI values. CONCLUSIONS: IC-ECG STE was not uncommon in NSTEMI patients, particularly those with LCx culprit lesions. IC-ECG monitoring before PCI may help identify NSTEMI patients with high risk of greater myocardial injury.

In vivo detection of lipid-rich plaque by using a 40-MHz intravascular ultrasound: a comparison with optical coherence tomography findings.

iMAP™ has recently been introduced as a new tissue characterization method using the 40-MHz intravascular ultrasound (IVUS). However, few data have been published on the comparative findings of other imaging modalities in vivo. We examined 108 matched lesions from 70 patients (35 with stable angina and 35 with acute coronary syndrome) that underwent percutaneous coronary intervention (PCI) using pre-PCI OCT and IVUS. Identification of OCT-derived lipid-rich plaques and thin-cap fibroatheroma (TCFA) was performed using iMAP™. OCT-derived lipid-rich plaques and TCFAs were detected in 56 (51.8 %) and 20 (18.6 %) lesions, respectively. The iMAP™ analysis identified significantly greater percentage of necrotic area (%NA) in the lesions with lipid-rich plaques than in those without [46.5 (29.4-56.9) vs. 24.6 (10.3-41.6) %, p < 0.01]. In the receiver operating characteristic (ROC) analysis, the optimal %NA cut-off value for identifying lipid-rich plaques was 33 % (AUC: 0.75; sensitivity: 73.2 %; specificity: 67.3 %). A greater plaque burden and a larger necrotic area were detected using iMAP™ in the OCT-derived TCFAs than in the non-TCFAs [81.5 (77.3-86.8) vs. 72.7 (60.6-81.0) %, p < 0.01; 7.6 (4.3-9.6) mm(2) vs. 2.7 (1.0-6.0) mm(2), p < 0.01]. For the iMAP™-derived TCFAs, combinations of variables such as necrotic area, % plaque burden, and absolute plaque area showed a relatively low positive predictive value and high negative predictive value (plaque burden >75 % and confluent luminal necrotic area >4.0 mm(2); sensitivity: 75.0 %; specificity: 71.6 %; PPV: 37.5 %; NPV: 92.6 %; and diagnostic accuracy: 72.2 %). The results showed that iMAP™ tissue characterization may help to detect lipid-rich plaque and rule out TCFAs in vivo.

Two distinct electrocardiographic forms of idiopathic ventricular arrhythmia originating in the vicinity of the His bundle.

AIM: The objective is to assess electrocardiographic characteristics predicting the precise location of ventricular arrhythmia (VA) origin within the right ventricle (RV) close to the His bundle (HB) region. METHODS AND RESULTS: Twenty-five patients (14 men, age 65 ± 14 years) underwent successful catheter ablation of para-Hisian VA. Ventricular arrhythmias were considered to arise in the vicinity of the HB region based on the criteria that mapping exhibited the earliest RV activation before QRS onset in the HB region. Surface 12-lead electrocardiogram during the para-Hisian VAs was analysed. Of the 25 patients, 8 originated from the RV antero-septum just above the HB region, and 17 arose from the RV mid-septum just below the HB region. There was no significant difference in precedence of the local ventricular electrogram of the HB region from the onset of surface QRS during VAs. Surface electrocardiographic findings were characterized according to R-wave amplitude in lead I (0.43 ± 0.18 vs. 0.67 ± 0.19 mV, P = 0.005), mean R-wave amplitude in inferior leads (1.12 ± 0.32 vs. 0.71 ± 0.24 mV, P = 0.002), R-wave amplitude ratio of leads III/II (0.77 ± 0.10 vs. 0.50 ± 0.23, P = 0.005), incidence of S-wave in lead III [1/8 (13%) vs. 16/17 (94%), P < 0.001], and QS morphology in lead V1 [3/8 (38%) vs. 17/17 (100%), P = 0.001]. CONCLUSIONS: Despite their adjacent locations, para-Hisian VAs could be classified into two subgroups with distinctive electrocardiographic characteristics according to origin either above or below the HB region. The present findings can be helpful for planning catheter ablation of para-Hisian VAs, and can reduce the risk of inadvertent atrioventricular block.

Impact of coronary plaque morphology assessed by optical coherence tomography on cardiac troponin elevation in patients with elective stent implantation.

BACKGROUND: Mild elevations of cardiac troponin frequently occur after percutaneous coronary intervention (PCI), and patients with elevated post-PCI biomarkers have a worse prognosis. We used optical coherence tomography (OCT) to study the relationship between pre-PCI plaque morphology and post-PCI cardiac troponin I elevations. METHODS AND RESULTS: One hundred thirty-one patients with normal pre-PCI cardiac troponin I levels underwent OCT before nonemergency stent implantation. Clinical and OCT findings were compared between patients with (n=31, 23.7%) and without (n=100, 76.3%) post-PCI cardiac troponin I of >3 × upper reference limit (post-PCI myocardial infarction [MI]). After PCI, long-term follow-up data were collected. Post-PCI MI was associated with angiographic lesion length, type B2/C lesions, presence of thin-cap fibroatheroma, and fibrous cap thickness. In multivariable analysis, presence of thin-cap fibroatheroma (odds ratio, 10.47; 95% confidence interval, 3.74 to 29.28; P<0.001) and type B2/C lesions (odds ratio, 3.74; 95% confidence interval, 1.41 to 9.92; P=0.008) were predictors of post-PCI MI. At a median follow-up of 12 months, cardiac event-free survival was significantly worse in patients with post-PCI MI (log-rank test χ(2)=8.9; P=0.003). Cox proportional hazards analysis showed that post-PCI MI (hazard ratio, 3.67; 95% confidence interval, 1.39 to 9.65; P=0.009) and ejection fraction (hazard ratio, 0.96; 95% confidence interval, 0.92 to 0.99; P=0.029) were independent predictors of adverse cardiovascular events during follow-up. CONCLUSIONS: Type B2/C lesions and the presence of OCT-defined thin-cap fibroatheroma can predict post-PCI MI in patients treated with elective stent implantation, who may require adjunctive therapy after otherwise successful PCI.

In vivo critical fibrous cap thickness for rupture-prone coronary plaques assessed by optical coherence tomography.

AIMS: The widely accepted threshold of <65 µm for coronary plaque fibrous cap thickness was derived from postmortem studies of ruptured plaques and may not be appropriate for in vivo rupture-prone plaques. We investigated the relationship between fibrous cap thickness and plaque rupture using optical coherence tomography (OCT). METHODS AND RESULTS: We studied 266 lesions (103 from patients with acute coronary syndrome and 163 from patients with stable angina) before percutaneous coronary intervention using OCT. Ruptured and non-ruptured lipid-rich plaques were identified and the thinnest and most representative fibrous cap thickness were determined. Cap thickness was reliably measured in 71 ruptured and 111 non-ruptured plaques. From the ruptured plaques, the median thinnest cap thickness was 54 µm (50-60). The median most representative cap thickness was 116 µm (103-136). For non-ruptured plaques, the median thinnest cap thickness was 80 µm (67-104) and 182 µm (156-216) for most representative cap thickness. In 95% of ruptured plaques, the thinnest cap thickness and most representative cap thickness were <80 and <188 µm, respectively. The best cut-offs for predicting rupture were <67 µm (OR: 16.1, CI: 7.5-34.4, P < 0.001) for the thinnest cap thickness and <151 µm (OR: 35.6, CI: 15.0-84.3, P < 0.001) for most representative cap thickness. These two measures were modestly correlated (r(2) = 0.39) and both independently associated with rupture. CONCLUSION: In vivo critical cap thicknesses were <80 µm for the thinnest and <188 µm for most representative fibrous cap thickness. Prospective imaging studies are required to establish the significance of these values.