Masaomi Chinushi

Blood Pressure and Autonomic Responses to Electrical Stimulation of the Renal Arterial Nerves Before and After Ablation of the Renal Artery

Radiofrequency (RF) catheter ablation of the renal artery is therapeutic in patients with drug-refractory essential hypertension. This study was designed to examine the role of the renal autonomic nerves and of RF application from inside the renal artery in the regulation of blood pressure (BP). An open irrigation catheter was inserted into either the left or right renal artery in 8 dogs. RF current (17±2 watts) was delivered to one renal artery. Electrical autonomic nerve stimulation was applied to each renal artery before and after RF ablation. BP, heart rate, indices of heart rate variability, and serum catecholamines were analyzed. Before RF ablation, electrical autonomic nerve stimulation of either renal artery increased BP from 150±16/92±15 to 173±21/105±16 mm Hg. After RF ablation, BP increased similarly when the nonablated renal artery was electrically stimulated, although the rise in BP was attenuated when the ablated renal artery was stimulated. Serum catecholamines and sympathetic nerve indices of heart rate variability increased when electrical autonomic nerve stimulation was applied before RF ablation and to the nonablated renal artery after RF ablation, although it changed minimally when the ablated renal artery was stimulated, suggesting interconnectivity between afferent renal nerve stimulation and systemic sympathetic activity. Renal artery angiogram showed no apparent injury after RF ablation. In conclusion, electrical stimulation of the renal arterial autonomic nerves increases BP via an increase in central sympathetic nervous activity. This response might be used to determine the target ablation site and end point of renal artery RF ablation.

Analysis of J waves during myocardial ischaemia

AIMSnThe aim of this study was to investigate the relationship between J-wave dynamics and arrhythmias during myocardial ischaemia in patients with vasospastic angina (VSA).nnnMETHODS AND RESULTSnSixty-seven consecutive patients diagnosed with VSA by a provocation test for coronary spasm were grouped according to whether they had a J wave in the baseline electrocardiograms or not (VSA-JW group, n = 14; VSA-non-JW group: n = 53). We retrospectively studied the associations between J-wave and ST-segment dynamics and induced ventricular fibrillations (VFs) during coronary spasm. xa0In the VSA-JW group, 7 of the 14 patients showed changes in J-wave morphology and/or gains in J-wave voltage, followed by VF in 4 patients. Compared with patients without VF, the four patients with VF showed similar maximal voltage in the baseline J waves but a higher voltage during induced coronary spasms (0.57 ± 0.49 vs. 0.30 ± 0.11 mV; P = 0.011). In three patients with VF, J waves progressively increased and were accompanied by the characteristic coved-type or lambda-shaped ST-segment elevations. In the VSA-non-JW group, only four patients showed new appearances of J waves during coronary spasms and another patient without a distinct J wave developed VF. Ventricular fibrillations were induced more frequently in the VSA-JW group than in the VSA-non-JW group [4/14 (29%) vs. 1/53 (2%); P = 0.012].nnnCONCLUSIONnJ-wave augmentations were caused by myocardial ischaemia during coronary spasms. The presence and augmentation of J waves, especially prominent J waves with the characteristic ST-elevation patterns, were associated with VF.

Role of mineralocorticoid receptor on atrial structural remodeling and inducibility of atrial fibrillation in hypertensive rats

Hypertension is well known to increase atrial fibrillation (AF) and the development of AF is associated with atrial chamber remodeling. Although mineralocorticoid receptor (MR) inhibition provides cardiovascular protection, the role of MR on atrial structural remodeling and inducibility of AF in hypertension remains unclear. Here, we investigated roles of the MR on atrial structural remodeling and inducibility of AF in hypertensive rats by using MR antagonist eplerenone (EPL). Dahl salt-sensitive (DS) rats were fed a normal-salt or a high-salt (HS) diet from 7 weeks, and a non-antihypertensive dose of EPL or vehicle was administrated from 13 weeks, at which time myocytes hypertrophy, interstitial fibrosis in the atrium and AF inducibility had increased, until 20 weeks. There was no significant difference in systolic blood pressure between DS+HS (186±4u2009mmu2009Hg) and DS+HS+EPL (184±5u2009mmu2009Hg) at 20 weeks. Burst atrial pacing demonstrated decreased AF inducibility in DS+HS+EPL (0 of 10) compared with DS+HS (7 of 10). Fibrosis and myocytes hypertrophy in the atrium were decreased in DS+HS+EPL with the reduction of atrial inflammatory cytokines. These beneficial effects of EPL were associated with less atrial oxidative stress, as assessed by 4-hydroxy-2-nonenal staining, and reduced activation of the Rho GTPase Rac1 in the atrium. Thus, MR has important roles in atrial structural remodeling and AF inducibility in Dahl rats. The effects of MR are associated, at least in part, with activation of Rac1-oxidative stress/inflammatory axis.

Ventricular Tachyarrhythmia Associated with Hypertrophic Cardiomyopathy: Incidence, Prognosis, and Relation to Type of Hypertrophy

VT Associated with HCM.u2002Objective: To assess the incidence, characteristics, and prognosis of ventricular tachyarrhythmia in hypertrophic cardiomyopathy (HCM).

The peak-to-end of the T wave in the limb ECG leads reflects total spatial rather than transmural dispersion of ventricular repolarization in an anthopleurin-A model of prolonged QT interval

BACKGROUNDnPrevious studies have showed that the interval between the peak and the end of the T wave (Tp-e) is a marker of transmural dispersion of ventricular repolarization.nnnOBJECTIVEnWe studied the relationship between (a) the Tp-e on local pseudo transmural electrograms (pseudo transmural Tp-e) or limb leads of body surface electrocardiogram (surface Tp-e) and (b) the intracardiac left ventricular (LV) repolarization during a drug-induced QT-interval prolongation.nnnMETHODSnUsing open-chested canine intact hearts treated by anthopleurin-A, transmural LV electrograms were recorded via needle electrodes placed in the basoanterior, midanterior, apicoanterior, basolateral, midlateral, and apicolateral LV wall. Recovery time (RT) was calculated as an index of local repolarization at each transmural unipolar electrode.nnnRESULTSnThis model showed slower heart rate-dependent heterogeneous distribution of ventricular repolarization both along the basal to apical axis and along the transmural axis. RT was longer at the LV apex than at the base and longer in the lateral than in the anterior wall during the slower heart rate. A high correlation was found between surface Tp-e and total LV dispersion. In contrast, pseudo transmural Tp-e correlated with transmural RT dispersion. The shortest RT in the heart roughly corresponded to the peak, as did the longest RT with the end of the T wave on the surface electrocardiogram.nnnCONCLUSIONnDuring drug-induced QT-interval prolongation with a large apicobasal and anterolateral dispersion of ventricular repolarization, the Tp-e in the limb leads expresses spatial (total) distribution of repolarization in the whole left ventricle.

The prevalence of early repolarization in Wolff-Parkinson-White syndrome with a special reference to J waves and the effects of catheter ablation

We determined the prevalence of J waves in the electrocardiograms (ECG) of 120 patients with Wolff-Parkinson-White syndrome in comparison with J-wave prevalence in a control group of 1936 men and women with comparable demographic and ECG characteristics and with normal atrioventricular conduction. J waves were present only during manifest preexcitation in 22 of 120 patients (18.3%), disappearing after catheter ablation and suggesting that J waves were associated with the presence of preexcitation. J waves were present in 19 (15.8%) of 120 patients only after ablation, apparently having been masked by early depolarization of the preexcited myocardial region, and in 22 patients (18.3%), J waves were not altered significantly by preexcitation. Thus, the overall J-wave prevalence was 52.5% (63/120) and, excluding those apparently due to preexcitation, 34.8% (41/120), both substantially higher than the prevalence (11.5%) in the control group (P < .001 for both). The patients with J waves appearing only during preexcitation were younger, predominantly females. The presence of J waves after ablation was associated with a history of atrial fibrillation and shorter ventricular effective refractory period. It is concluded that the prevalence of J waves is high in patients with Wolff-Parkinson-White syndrome and is influenced by manifest preexcitation.

Focal atrial tachycardia refractory to radiofrequency catheter ablation originating from right atrial appendage

A 44-year-old female presented with incessant, drug-refractory atrial tachycardia (AT). An electrophysiological study suggested focal abnormal automaticity, and localized the AT origin to the apex of the right atrial appendage (RAA). Repeated radiofrequency catheter ablation to the site of the earliest endocardial activation during AT failed. At surgery, right atrial appendectomy terminated the AT. On macroscopic findings, the cavity of the RAA became a dead-end before the apex. In patients with drug and radiofrequency catheter ablation, refractory focal AT arising from the RAA, especially the apex of the RAA, in our opinion surgical treatment could be considered in the lack of efficacy of ablation.

Ventricular Fibrillation and Ventricular Tachycardia Triggered by Late‐Coupled Ventricular Extrasystoles in a Brugada Syndrome Patient

Premature ventricular complexes (PVC) falling after the end of the T wave triggered ventricular fibrillation (VF) at night and monomorphic ventricular tachycardia (MVT) during daytime, in a recipient of implantable cardioverter defibrillator with Brugada syndrome. Treatment with bepridil (1) decreased the height of ST segment elevation in leads V1‐V3, (2) completely eliminated VF, and (3) markedly decreased the incidence of PVC and MVT. Albeit rare, VF can be triggered by late‐coupled PVC, due to a mechanism other than phase 2 reentry in some patients with Brugada syndrome. (PACE 2011; e1–e5)

Relationship between electroanatomical voltage mapping characteristics and breakout site of ventricular activation in idiopathic ventricular tachyarrhythmia originating from the right ventricular outflow tract septum

ObjectiveTo assess the electrophysiological characteristics of the breakout site of ventricular activation using electroanatomical voltage mapping (EVM) and its relation to the optimal ablation site in idiopathic ventricular tachyarrhythmias originating from the outflow tract of the (RVOT) septum.MethodsTwenty-eight patients with symptomatic drug-refractory premature ventricular complexes (PVCs) and/or ventricular tachycardia (VT) originating from the RVOT septum and 5 control subjects with WPW syndrome were included. Low-voltage areas (LVAs) were defined as signal amplitudes between 0.1 and 1.5xa0mV. The borderline between the normal area and the LVA was defined as “border,” and the distance from the LVA to the border (length of LVA) was measured.ResultsIn all 28 patients and control subjects, there was an LVA below the pulmonary valve. There was no significant difference in length of LVA between patients with idiopathic ventricular arrhythmias and control subjects (2.0u2009±u20090.6 vs. 1.9u2009±u20090.1xa0cm). In 19 of the 28 patients, the optimal ablation site was identical to the border area. In all 11 patients who had pre-potentials at the successful ablation site, there were two cases with polymorphic VT and/or ventricular fibrillation associated with PVCs. In these two cases, length of LVA was longer than in other patients (4.0 and 3.9xa0cm vs. 1.8u2009±u20090.5xa0cm (nu2009=u200926)), and the optimal ablation site was located at the border area.ConclusionThe border area, including the LVA, tends to be the breakout site and/or origin of ventricular arrhythmias in idiopathic ventricular tachyarrhythmia originating from the RVOT septum.

Effects of verapamil on anterior ST segment and ventricular fibrillation cycle length in patients with Brugada syndrome.

PURPOSEnThis study examined the effects of verapamil (5-10 mg intravenous) on the cardiac electrical activity of 10 Brugada syndrome (BS) patients having vasospastic angina, atrial fibrillation, and/or hypertension.nnnRESULTSnVerapamil showed no significant change in the ST-segment elevation. Likewise, there was no significant change in the lengths of QRS complex, HV and corrected QT intervals, or effective refractory period at the right ventricle. The conduction time between right ventricular apex and outflow tract, measured at 400-millisecond pacing, was mildly prolonged by verapamil. At baseline, induced ventricular fibrillation (VF) was terminated by a 200-J shock in all patients. After verapamil, VF was reinduced in 7, was noninducible in 2, and self-terminated in 1 patient. Mean F-F interval was shorter after than before verapamil, and a 360-J shock was required in 2 of the 7 patients.nnnCONCLUSIONnIn some BS patients, calcium channel blockade may modify the electrical characteristics of VF.