Kenichi Iijima

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.

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

VT Associated with HCM. Objective: 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

BACKGROUND Previous 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. OBJECTIVE We 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. METHODS Using 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. RESULTS This 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. CONCLUSION During 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.

A post-QRS potential in Brugada syndrome: its relation to electrocardiographic pattern and possible genesis.

To the Editor: Brugada syndrome (BS) has been established as a clinical entity of idiopathic ventricular fibrillation (VF) and is characterized by the peculiar electrocardiographic (ECG) pattern in V1 and/or V2 ([1][1]). The characteristic ECG patterns, coved- or saddleback-type ST-segment elevation

Antiarrhythmic vs. pro-arrhythmic effects depending on the intensity of adrenergic stimulation in a canine anthopleurin-A model of type-3 long QT syndrome

AIMS The effects of adrenergic activity and beta-blockade were studied in a canine experimental model of type-3 long QT syndrome (LQT3) induced by application of anthopleurin-A. METHODS AND RESULTS Boluses of epinephrine at 0.5 and/or 1.0 microg/kg were administered before and after propranolol, 0.3 mg/kg, and the distribution of the ventricular repolarization and the development of polymorphic ventricular tachyarrhythmia (VA) were assessed. Using needle electrodes, transmural unipolar electrograms were recorded across the left ventricle (LV) and right ventricle (RV). Activation-recovery interval (ARI) was measured in each electrogram to estimate local repolarization during RV pacing at the cycle length of 750 ms after the creation of complete atrioventricular block. Before propranolol, epinephrine, 0.5 microg/kg, did not induce VA in any experiment. However, a dose of 1.0 microg/kg induced polymorphic VA following multiple premature ventricular complex (PVC) in four of six experiments. Epinephrine, 0.5 microg/kg, shortened ARI at all sites and lessened LV transmural ARI dispersion. Neither ARI nor its dispersion could be determined after 1.0 microg/kg of epinephrine because of the induction of PVC, polymorphic VA, or both. Propranolol (i) prevented epinephrine-induced PVC and polymorphic VA in all experiments, (ii) slightly prolonged ARI at all sites, along with a decrease in LV transmural ARI dispersion, and (iii) reversed the epinephrine-induced shortening of ARI. CONCLUSION In this LQT3 model, an increase in adrenergic activity by epinephrine had dose-dependent, opposite effects on ventricular electrical stability. Since beta-adrenergic blockade suppressed epinephrine-induced PVC and polymorphic VA, it might be considered for supplemental therapy to suppress VA in patients presenting with LQT3.

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

PURPOSE This 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. RESULTS Verapamil 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. CONCLUSION In some BS patients, calcium channel blockade may modify the electrical characteristics of VF.

Electrical stimulation–based evaluation for functional modification of renal autonomic nerve activities induced by catheter ablation

BACKGROUND Catheter ablation of the renal artery can be performed without apparent angiographic stenosis. This suggests that renal nerve function can be attenuated with minor structural damage to the renal artery. OBJECTIVE To clarify this hypothesis, we examined the relationship between electrical nerve stimulation (ENS)-induced blood pressure (BP) response and severity of histological injury of the renal artery using an acute canine model of renal artery ablation. METHODS An irrigation catheter was inserted into the renal arteries of 8 dogs, and radiofrequency current was delivered at 15, 20, or 25 W. ENS was applied to each artery before and after ablation. RESULTS Before ablation, ENS increased the BP and heart rate from 145 ± 15/86 ± 13 to 189 ± 21/111 ± 19 mm Hg and from 116 ± 9 to 130 ± 6 beats/min, respectively. Heart rate variability indices and serum catecholamine levels were elevated concomitantly. After ablation, the ENS-induced increase in BP and heart rate were markedly attenuated after 15 W ablation and those were nearly completely inhibited after 20 or 25 W ablation. An increase in heart rate variability indices and serum catecholamine levels became insignificant regardless of the applied energy. Renal artery angiograms revealed stenotic lesions only after 25 W ablation procedures. Histological studies showed mild to moderate injury of the arterial wall and autonomic nerves caused by 20 and 25 W ablation procedures, whereas only minor changes caused by 15 W ablation. CONCLUSION Functional renal autonomic nerve ablation is potentially performable with the guidance of ENS.

Is the coexistence of sustained ST-segment elevation and abnormal Q waves a risk factor for electrical storm in implanted cardioverter defibrillator patients with structural heart diseases?

AIM The aim of this study was to determine whether or not the coexistence of sustained ST-segment elevation and abnormal Q waves (STe-Q) could be a risk factor for electrical storm (ES) in implanted cardioverter defibrillator (ICD) patients with structural heart diseases. METHODS AND RESULTS In all, 156 consecutive patients received ICD therapy for secondary prevention of sudden cardiac death and/or sustained ventricular tachyarrhythmias were included. Electrical storm was defined as ≥3 separate episodes of ventricular tachycardia (VT) and/or ventricular fibrillation (VF) terminated by ICD therapies within 24 h. During a mean follow-up of 1825 ± 1188 days, 42 (26.9%) patients experienced ES, of whom 12 had coronary artery disease, 15 had idiopathic dilated cardiomyopathy, 6 had hypertrophic cardiomyopathy, 4 had arrhythmogenic right ventricular cardiomyopathy, 4 had cardiac sarcoidosis, and 1 had valvular heart disease. Sustained ST-segment elevation and abnormal Q waves in ≥2 leads on the 12-lead electrocardiography was observed in 33 (21%) patients. On the Kaplan-Meier analysis, patients with STe-Q had a markedly higher risk of ES than those without STe-Q (P< 0.0001). The multivariate Cox proportional hazards regression model indicated that STe-Q and left ventricular ejection fraction (LVEF) (<30%) were independent risk factors associated with the recurrence of VT/VF (STe-Q: HR 1.962, 95% CI 1.24-3.12, P= 0.004; LVEF: HR 1.860, 95% CI 1.20-2.89, P= 0.006), and STe-Q was an independent risk factor associated with ES (HR 4.955, 95% CI 2.69-9.13, P< 0.0001). CONCLUSION Sustained ST-segment elevation and abnormal Q waves could be a risk factor of not only recurrent VT/VF but also ES in patients with structural heart diseases.

Automatic R-wave and impedance testing with the modern patient alert system to reduce inappropriate implantable cardioverter defibrillator shocks due to lead fracture

A 62-year-old man was afflicted with implantable cardioverter defibrillator (ICD) shocks during sinus rhythm. Stored ICD data revealed that sensing of noise due to fracture of the ventricular lead triggered the delivery of shocks. Since the lead fracture developed suddenly, it is suggested that close, early attention should be paid to the potential of such events during follow-up of ICD leads.