Accessory posterior cerebral artery (hyperplastic anterior choroidal artery) associated with contralateral accessory middle cerebral artery incidentally diagnosed by magnetic resonance angiography.

PURPOSE: To describe a case of accessory posterior cerebral artery (PCA) [hyperplastic anterior choroidal artery (AChA)] associated with contralateral accessory middle cerebral artery (MCA) incidentally diagnosed by magnetic resonance (MR) angiography. METHODS: A 71-year-old man with paroxysmal atrial fibrillation underwent cranial MR imaging and MR angiography of the intracranial region using a 1.5-T scanner for the evaluation of brain and vascular lesions. RESULTS: On MR angiography, two right PCAs of equal size arose from the internal carotid artery instead of the basilar artery. Additionally, a small left MCA branch arose from the proximal A2 segment of the anterior cerebral artery (ACA). CONCLUSION: One of the branches of the PCA rarely arises from the AChA. This variation is referred to as a hyperplastic AChA or accessory PCA. The latter name was recently proposed and may be more appropriate than the former name. An MCA branch arising from the ACA is called an accessory MCA. It is a frontal branch of two types: proximal-origin and distal-origin. The distal-origin accessory MCA arises from the distal A1 segment, A1-A2 junction or proximal A2 segment. Distal-origin accessory MCAs are rare. Our patient had two rare variations: an accessory right PCA and a distal-origin accessory left MCA. To identify cerebral arterial variations, especially accessory MCA, volume-rendering images are more useful than maximum-intensity projection images on MR angiography.

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction.

Myocardial infarction causes sympathetic activation and parasympathetic dysfunction, which increase risk of sudden death due to ventricular arrhythmias. Mechanisms underlying parasympathetic dysfunction are unclear. The aim of this study was to delineate consequences of myocardial infarction on parasympathetic myocardial neurotransmitter levels and the function of parasympathetic cardiac ganglia neurons, and to assess electrophysiological effects of vagal nerve stimulation on ventricular arrhythmias in a chronic porcine infarct model. While norepinephrine levels decreased, cardiac acetylcholine levels remained preserved in border zones and viable myocardium of infarcted hearts. In vivo neuronal recordings demonstrated abnormalities in firing frequency of parasympathetic neurons of infarcted animals. Neurons that were activated by parasympathetic stimulation had low basal firing frequency, while neurons that were suppressed by left vagal nerve stimulation had abnormally high basal activity. Myocardial infarction increased sympathetic inputs to parasympathetic convergent neurons. However, the underlying parasympathetic cardiac neuronal network remained intact. Augmenting parasympathetic drive with vagal nerve stimulation reduced ventricular arrhythmia inducibility by decreasing ventricular excitability and heterogeneity of repolarization of infarct border zones, an area with known proarrhythmic potential. Preserved acetylcholine levels and intact parasympathetic neuronal pathways can explain the electrical stabilization of infarct border zones with vagal nerve stimulation, providing insight into its antiarrhythmic benefit.

Atrial and ventricular activation sequence after ventricular induction/entrainment pacing during fast-slow atrioventricular nodal reentrant tachycardia: New insight into the use of V-A-A-V for the differential diagnosis of supraventricular tachycardia.

BACKGROUND: The atrial and ventricular response observed immediately after cessation of ventricular induction/entrainment pacing is commonly analyzed to discriminate atrial tachycardia from other supraventricular tachycardias during electrophysiologic studies. However, the response in fast-slow atrioventricular nodal reentrant tachycardia (F/S-AVNRT) remains poorly investigated. OBJECTIVE: The purpose of this study was to analyze the atrial and ventricular activation patterns after ventricular pacing in F/S-AVNRT. METHODS: We enrolled 28 patients with F/S-AVNRT incorporating a typical slow pathway (typ-F/S-AVNRT) and 9 patients with F/S-AVNRT incorporating a superior slow pathway (sup-F/S-AVNRT). RESULTS: The V-A-A-V response was observed in 14 patients (38%) with F/S-AVNRT, more commonly in patients with sup-F/S-AVNRT than in those with typ-F/S-AVNRT (89% vs 21%, P = .0003). The underlying mechanisms included (1) a double atrial response (DAR) in 13 patients; (2) an anterograde block at the lower common pathway once after ventricular pacing in 2 patients; and (3) a pseudo-A-A-V response in 2 patients. The DAR was characterized by a V-A-A-V interatrial interval that was 55 ± 60 ms shorter than the tachycardia cycle length, whereas the block at the lower common pathway or infrahisian block had a V-A-A-V interatrial interval that was almost equal to or longer than the tachycardia cycle length. CONCLUSION: The V-A-A-V activation sequence immediately after ventricular induction/entrainment pacing is observed in patients with F/S-AVNRT, particularly in patients with sup-F/S-AVNRT, and is caused by multiple mechanisms, including a DAR, which is the major etiology.

Premature Ventricular Contraction Coupling Interval Variability Destabilizes Cardiac Neuronal and Electrophysiological Control: Insights From Simultaneous Cardioneural Mapping.

BACKGROUND: Variability in premature ventricular contraction (PVC) coupling interval (CI) increases the risk of cardiomyopathy and sudden death. The autonomic nervous system regulates cardiac electrical and mechanical indices, and its dysregulation plays an important role in cardiac disease pathogenesis. The impact of PVCs on the intrinsic cardiac nervous system, a neural network on the heart, remains unknown. The objective was to determine the effect of PVCs and CI on intrinsic cardiac nervous system function in generating cardiac neuronal and electric instability using a novel cardioneural mapping approach. METHODS AND RESULTS: In a porcine model (n=8), neuronal activity was recorded from a ventricular ganglion using a microelectrode array, and cardiac electrophysiological mapping was performed. Neurons were functionally classified based on their response to afferent and efferent cardiovascular stimuli, with neurons that responded to both defined as convergent (local reflex processors). Dynamic changes in neuronal activity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed long, and variable CI. PVC delivery elicited a greater neuronal response than all other stimuli (P<0.001). Compared with fixed short and long CI, PVCs with variable CI had a greater impact on neuronal response (P<0.05 versus short CI), particularly on convergent neurons (P<0.05), as well as neurons receiving sympathetic (P<0.05) and parasympathetic input (P<0.05). The greatest cardiac electric instability was also observed after variable (short) CI PVCs. CONCLUSIONS: Variable CI PVCs affect critical populations of intrinsic cardiac nervous system neurons and alter cardiac repolarization. These changes may be critical for arrhythmogenesis and remodeling, leading to cardiomyopathy.

Cardiac sympathetic innervation via middle cervical and stellate ganglia and antiarrhythmic mechanism of bilateral stellectomy.

Cardiac sympathetic denervation (CSD) is reported to reduce the burden of ventricular tachyarrhythmias [ventricular tachycardia (VT)/ventricular fibrillation (VF)] in cardiomyopathy patients, but the mechanisms behind this benefit are unknown. In addition, the relative contribution to cardiac innervation of the middle cervical ganglion (MCG), which may contain cardiac neurons and is not removed during this procedure, is unclear. The purpose of this study was to compare sympathetic innervation of the heart via the MCG vs. stellate ganglia, assess effects of bilateral CSD on cardiac function and VT/VF, and determine changes in cardiac sympathetic innervation after CSD to elucidate mechanisms of benefit in 6 normal and 18 infarcted pigs. Electrophysiological and hemodynamic parameters were evaluated at baseline, during bilateral stellate stimulation, and during bilateral MCG stimulation in 6 normal and 12 infarcted animals. Bilateral CSD (removal of bilateral stellates and T2 ganglia) was then performed and MCG stimulation repeated. In addition, in 18 infarcted animals VT/VF inducibility was assessed before and after CSD. In infarcted hearts, MCG stimulation resulted in greater chronotropic and inotropic response than stellate ganglion stimulation. Bilateral CSD acutely reduced VT/VF inducibility by 50% in infarcted hearts and prolonged global activation recovery interval. CSD mitigated effects of MCG stimulation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts, without causing hemodynamic compromise. These data demonstrate that the MCG provides significant cardiac sympathetic innervation before CSD and adequate sympathetic innervation after CSD, maintaining hemodynamic stability. Bilateral CSD reduces VT/VF inducibility by improving electrical stability in infarcted hearts in the setting of sympathetic activation.NEW & NOTEWORTHY Sympathetic activation in myocardial infarction leads to arrhythmias and worsens heart failure. Bilateral cardiac sympathetic denervation reduces ventricular tachycardia/ventricular fibrillation inducibility and mitigates effects of sympathetic activation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts. Hemodynamic stability is maintained, as innervation via the middle cervical ganglion is not interrupted.

Detection of sequential activation of left atrium and coronary sinus musculature in the general population.

BACKGROUND: The direction of impulse propagation across the coronary sinus (CS) musculature (CSM) is an important piece of the mechanistic puzzle underlying atrial tachyarrhythmias. We hypothesized that in the general population, the sequence of left atrial (LA) to CSM electrograms recorded in the CS reflects the direction of impulse propagation over the CSM. METHODS: We studied 19 patients with atrioventricular (AV) reentrant tachycardia (RT) utilizing a left-sided accessory pathway (AP) and 21 patients with typical counterclockwise atrial flutter (AFL). Conduction through the CSM during AVRT and AFL is from the left atrial (LA) to the right atrial (RA) and from the RA to LA direction, respectively. CS recordings of retrograde conduction over the AP and of AFL were analyzed in search of far-field, LA potentials. RESULTS: Among 19 patients with AP, LA potentials were visible in 7 (37%), all in an LA → CSM activation sequence, while among the 21 patients with AFL, LA potentials were visible in 14 (67%), all in a CSM-LA activation sequence (P<0.0001). The prevalence of LA potentials was similar between both study groups (P=0.1119), and the overall prevalence was 53%. CONCLUSIONS: Far-field LA potentials are often recorded in the CS during sequential LA and CSM activation in the general population. The timing of LA potentials in CS recordings reflected the direction of conduction across the CSM.

Atypical Fast-Slow Atrioventricular Nodal Reentrant Tachycardia Incorporating a "Superior" Slow Pathway: A Distinct Supraventricular Tachyarrhythmia.

BACKGROUND: The existence of an atypical fast-slow (F/S) atrioventricular nodal reentrant tachycardia (AVNRT) including a superior (sup) pathway with slow conductive properties and an atrial exit near the His bundle has not been confirmed. METHODS AND RESULTS: We studied 6 women and 2 men (age, 74 ± 7 years) with sup-F/S-AVNRT who underwent successful radiofrequency ablation near the His bundle. Programmed ventricular stimulation induced retrograde conduction over a superior SP with an earliest atrial activation near the His bundle, a mean shortest spike-atrial interval of 378 ± 119 milliseconds, and decremental properties in all patients. sup-F/S-AVNRT was characterized by a long-RP interval; a retrograde atrial activation sequence during tachycardia identical to that over a sup-SP during ventricular pacing; ventriculoatrial dissociation during ventricular overdrive pacing of the tachycardia in 5 patients or atrioventricular block occurring during tachycardia in 3 patients, excluding atrioventricular reentrant tachycardia; termination of the tachycardia by ATP; and a V-A-V activation sequence immediately after ventricular induction or entrainment of the tachycardia, including dual atrial responses in 2 patients. Elimination or modification of retrograde conduction over the sup-SP by ablation near the right perinodal region or from the noncoronary cusp of Valsalva eliminated and confirmed the diagnosis of AVNRT in 4 patients each. CONCLUSIONS: sup-F/S-AVNRT is a distinct supraventricular tachycardia, incorporating an SP located above the Koch triangle as the retrograde limb, that can be eliminated by radiofrequency ablation.

Measurement of the ventriculoatrial interval from the coronary sinus during para-Hisian pacing may fail to distinguish ventriculoatrial nodal conduction from conduction over a septal accessory pathway.

BACKGROUND: Para-Hisian pacing (PHP) helps differentiate retrograde conduction over an accessory pathway (AP) from retrograde conduction over the atrioventricular (AV) node. This study examined a potential limitation of this technique, focusing on the measurement of the ventriculoatrial (V-A) interval from the coronary sinus (CS) during PHP. METHODS: Our subjects were 9 patients undergoing electrophysiological studies before successful catheter ablation of a posteroseptal AP. During PHP, retrograde conduction occurred over an AP when the pacing stimulus to atrium (S-A) interval recorded near the AP remained unchanged whether the His bundle (HB) was captured or not (pattern 1), or when a loss of HB capture was associated with an increase in the S-A interval and no change in the V-A interval near the AP (pattern 2). RESULTS: Patterns 1 and 2 were observed in 5 (56%) and 2 (22%) patients, respectively. However, in the remaining 2 patients (22%), loss of HB capture during PHP was associated with an increase in the S-A interval (as in pattern 2), whereas the V-A interval near the AP could not be measured because no ventricular electrogram was visible on the CS recording (pattern 3); therefore, the presence of AP could not be confirmed by PHP. In patterns 2 and 3, the atrial activation sequence remained unchanged whether the HB was captured or not. CONCLUSIONS: PHP may not be able to discriminate between a retrograde septal AP and AV nodal conduction in patients whose proximal CS recording shows no visible ventricular electrogram.

Left intraventricular dyssynchrony caused by a false tendon.

Left ventricular (LV) false tendons are usually benign, intraventricular myocardial structures, which may cause functional malfunction or deformation of the LV cavity due to mechanical stretching and dilatation of the LV wall. We present a case of non-ischemic cardiomyopathy complicated with intraventricular dyssynchrony that was caused by complete left bundle branch block and the mechanical pressure exerted by the stiff false tendon on the weakened mid-septum during systole.

Characteristics and catheter ablation of focal atrial tachycardia originating from the interatrial septum.

BACKGROUND: Ablation of focal atrial tachycardia (AT) originating from the interatrial septum (IAS) is challenging because of its complex anatomy. METHODS: We studied the electrocardiographic and electrophysiologic characteristics of focal, septal AT in seven patients who underwent successful ablation. RESULTS: The site of successful ablation was at the site of earliest activation on the right side of the IAS in three patients and on the left side in four patients, >1cm away from the centre of the fossa ovalis in the septum secundum. A negative or +/- versus a positive or -/+ P wave in lead V1 during AT accurately predicted a right- versus left-sided origin of the AT, respectively. In the four left septal AT cases, right atrial activation mapping opposite the site of successful ablation revealed the presence of a small, low-frequency potential followed by a larger, high-frequency potential. In contrast, a high-frequency potential was not preceded by a low-frequency potential in the three right septal AT cases. CONCLUSIONS: Septal AT may originate from either side of the septum secundum. The P wave polarity in lead V1 accurately predicted the side of the IAS that the AT originated from. Left septal AT is characterised by the recording of double potentials reflecting far-field activation of the left-sided IAS, followed by near-field activation of the right-sided IAS, when recording from its right side, opposite the AT origin. These observations are particularly relevant when mapping an apparent right septal AT.

Relationship between sinus rhythm late activation zones and critical sites for scar-related ventricular tachycardia: systematic analysis of isochronal late activation mapping.

BACKGROUND: It is not known whether the most delayed late potentials are functionally most specific for scar-related ventricular tachycardia (VT) circuits. METHODS AND RESULTS: Isochronal late activation maps were constructed to display ventricular activation during sinus rhythm over 8 isochrones. Analysis was performed at successful VT termination sites and prospectively tested. Thirty-three patients with 47 scar-related VTs where a critical site was demonstrated by termination of VT during ablation were retrospectively analyzed. In those who underwent mapping of multiple surfaces, 90% of critical sites were on the surface that contained the latest late potential. However, only 11% of critical sites were localized to the latest isochrone (87.5%-100%) of ventricular activation. The median percentage of latest activation at critical sites was 78% at a distance from the latest isochrone of 18 mm. Sites critical to reentry were harbored in regions with slow conduction velocity, where 3 isochrones were present within a 1-cm radius. Ten consecutive patients underwent ablation prospectively guided by isochronal late activation maps, targeting concentric isochrones outside of the latest isochrone. Elimination of the targeted VT was achieved in 90%. Termination of VT was achieved in 6 patients at a mean ventricular activation percentage of 78%, with only 1 requiring ablation in the latest isochrone. CONCLUSIONS: Late potentials identified in the latest isochrone of activation during sinus rhythm are infrequently correlated with successful ablation sites for VT. The targeting of slow conduction regions propagating into the latest zone of activation may be a novel and promising strategy for substrate modification.

A Case of Type 2 Amiodarone-Induced Thyrotoxicosis That Underwent Total Thyroidectomy under High-Dose Steroid Administration.

Amiodarone is used commonly and effectively in the treatment of arrhythmia; however, it may cause thyrotoxicosis categorized into two types: iodine-induced hyperthyroidism (type 1 amiodarone-induced thyrotoxicosis (AIT)) and destructive thyroiditis (type 2 AIT). We experienced a case of type 2 AIT, in which high-dose steroid was administered intravenously, and we finally decided to perform total thyroidectomy, resulting in a complete cure of the AIT. Even though steroid had been administered to the patient (maximum 80 mg of prednisolone), the operation was performed safely and no acute adrenal crisis as steroid withdrawal syndrome was found after the operation. Few cases of type 2 AIT that underwent total thyroidectomy with high-dose steroid administration have been reported. The current case suggests that total thyroidectomy should be taken into consideration for patients with AIT who cannot be controlled by medical treatment and even in those under high-dose steroid administration.

Electrical storm in patients with brugada syndrome is associated with early repolarization.

BACKGROUND: Electrical storms (ESs) in patients with Brugada syndrome (BrS) are rare though potentially lethal. METHODS AND RESULTS: We studied 22 men with BrS and ES, defined as ≥3 episodes/d of ventricular fibrillation (VF) and compared their characteristics with those of 110 age-matched, control men with BrS without ES. BrS was diagnosed by a spontaneous or drug-induced type 1 pattern on the ECG in the absence of structural heart disease. Early repolarization (ER) was diagnosed by J waves, ie, >0.1 mV notches or slurs of the terminal portion of the QRS complex. The BrS ECG pattern was provoked with pilsicainide. A spontaneous type I ECG pattern, J waves, and horizontal/descending ST elevation were found, respectively, in 77%, 36%, and 88% of patients with ES, versus 28% (P<0.0001), 9% (P=0.003), and 60% (P=0.06) of controls. The J-wave amplitude was significantly higher in patients with than without ES (P=0.03). VF occurred during undisturbed sinus rhythm in 14 of 19 patients (74%), and ES were controlled by isoproterenol administration. All patients with ES received an implantable cardioverter defibrillator and over a 6.0±5.4 years follow-up, the prognosis of patients with ES was significantly worse than that of patients without ES. Bepridil was effective in preventing VF in 6 patients. CONCLUSIONS: A high prevalence of ER was found in a subgroup of patients with BrS associated with ES. ES appeared to be suppressed by isoproterenol or quinidine, whereas bepridil and quinidine were effective in the long-term prevention of VF in the highest-risk patients.