Yoriko Kusano

Incidence and mechanism of interruption of reentrant ventricular tachycardia with rapid ventricular pacing.

BackgroundInformation concerning the electrophysiological characteristics of the reentrant circuit is still limited. To understand the incidence and mechanism of pacing-induced interruption of ventricular tachycardia (VT), rapid pacing was performed to entrain VT, and the local electrogram at the VT origin and the surface electrocardiogram were analyzed. Methods and ResultsAmong 25 patients, evidence of transient entrainment was confirmed in 20 patients, but the critical paced cycle length at which VT was interrupted was obtained in 13 patients when the paced cycle length was decreased in steps of 10 msec. During pacing at the critical cycle length (defined as block cycle length), changes in the local electrogram at VT origin were confirmed in all of the 13 patients; that is, 1) a change in morphology and 2) a change in the timing of activation: a sudden shortening in the stimulus to local electrogram time (third entrainment criterion by Waldo). The two changes mean that the exit is activated from a different direction (retrograde capture) because of an orthodromic block in the slow conduction zone. The QRS complex in the surface electrocardiogram showed a change in configuration from the fusion complex to the fully paced one at the same time when the exit was captured antidromically. ConclusionsBased on our observations in these patients, ventricular tachycardia interruption is very often associated with orthodromic block in the reentrant circuit at a critical cycle length of rapid pacing.

Myocardial CD36 expression and fatty acid accumulation in patients with type I and II CD36 deficiency

Long-chain fatty acids (LCFA) are one of the major cardiac energy substrates, so understanding LCFA metabolism may help in elucidating the mechanisms of various heart diseases. CD36 is a multifunctional membrane glycoprotein that acts not only as a receptor for thrombospondin, collagen and oxidized low density lipoprotein but also as a receptor for LCFA. We investigated the relationship between CD36 expression in myocardial capillary endothelial cells and myocardial LCFA uptake in patients with CD36 deficiency. We analyzed CD36 expression in blood cells from 250 patients with heart diseases by means of a flow cytometer. In 218 patients, myocardial LCFA scintigraphy was performed with123I-β-methyl-p-iodophenyl pentadecanoic acid (BMIPP). In 5 patients, myocardial capillary endothelial cells were examined immunohistochemically for CD36 expression. Eleven patients (4%) showed signs of type I CD36 deficiency (neither platelets nor monocytes expressed CD36). Twenty patients (8%) had type II CD36 deficiency (monocytes expressed CD36 but platelets did not). In all 11 patients with type I CD36 deficiency, no BMIPP accumulation was observed in the heart, but in 13 patients with type II CD36 deficiency, BMIPP accumulation in the heart was focally reduced, but there were no patients without BMIPP accumulation in the heart. Although the myocardial capillary endothelial cells from two CD36-positive patients expressed CD36, those from two patients with type I CD36 deficiency did not. In a patient with type II CD36 deficiency, some capillary endothelial cells displayed patchy CD36 expression.CD36 deficiency was documented in 31 (12%) patients with heart diseases. Because CD36 was not expressed in the myocardial capillary endothelial cells in patients with type I CD36 deficiency, type I CD36 deficiency is closely related to lack of myocardial LCFA accumulation and metabolism in the myocardium.

Frequency of presumed reentry with an excitable gap in sustained ventricular tachycardia unassociated with coronary artery disease

In sustained ventricular tachycardia (VT) unrelated to coronary artery disease, the incidence of reentry with an excitable gap was examined, and rapid pacing was performed to entrain VT in 48 episodes in 42 consecutive patients. Coronary artery disease was excluded by coronary arteriography. The underlying heart diseases were postoperative congenital heart diseases (n = 5), dilated (n = 7) or hypertrophic (n = 4) cardiomyopathy, arrhythmogenic right ventricular dysplasia (n = 6) and miscellaneous heart diseases (n = 5), as well as no demonstrable heart disease (n = 15) in which 8 patients had verapamil-responsive VT. Except for 1 patient with hypertrophic cardiomyopathy, 48 morphologically distinct monomorphic sustained VTs were induced. Twenty-five VTs showed right bundle branch block morphology and 23 left bundle branch block morphology, and VT was entrained in 84 and 96%, respectively. The overall incidence of the entrainment was 89.6% (43 of 48 monomorphic VTs), and the frequency of the ability to entrain VT ranged between 33.3 and 100% in the subgroups. The lowest frequency was found in hypertrophic cardiomyopathy. In conclusion, most inducible monomorphic sustained VT unassociated with coronary artery disease was presumed to be reentry with an excitable gap.

Successful Radiofrequency Catheter Ablation for Macroreentrant Ventricular Tachycardias in a Patient with Tetralogy of Fallot After Corrective Surgery

CHINUSHI, M., et al.: Successful Radiofrequency Catheter Ablation for Macroreentrant Ventricular Tachycardias in a Patient with Tetralogy of Fallot After Corrective Surgery. Radiofrequency (RF) catheter ablation was applied to two macroreentrant ventricular tachycardias (VTs) documented after corrective operation for tetralogy of Fallot. The activation wavefront of VT with a right bundle branch block pattern was found to revolve in a clockwise manner around a presumed myotomy scar in the right ventricle, and VT with a left bundle branch block pattern revolved around the same anatomical obstacle in a counterclockwise manner. In both VTs, the biggest conduction delay was confirmed at the right ventricular outflow tract. RF applications to the slow conduction area terminated each VT within a few seconds but were insufficient to cure the VTs. RF lesions were then applied to the, slow conduction area in a line to intersect the macroreentrant circuit, and both VTs became noninducible.

Catheter ablation with radiofrequency current of ventricular tachycardia originating from the right ventricle

Catheter ablation of ventricular tachycardia (VT) with radiofrequency current would be safer than the conventional ablation with direct current shocks. Seven patients who had eight morphologically distinct symptomatic monomorphic VTs underwent catheter ablation with radiofrequency current. The mean age +/- SD was 52 +/- 16 years, and the mean cycle length of the clinical VT was 298 +/- 36 milliseconds. Sustained VT was induced by programmed stimulation with or without isoproterenol in four patients and developed during the infusion of isoproterenol alone in two patients. Of these, four VTs were entrained with rapid pacing. The ablation was attempted at the site of earliest activation through the distal electrode and the external patch electrode on the back during VT in seven episodes in six patients. In the other patient it was applied during sinus rhythm. Energy was 40 to 50 W in the first case and 30 to 40 W in the others, and was given for 30 seconds. All VTs were terminated within 6 seconds, 3.6 +/- 0.8 seconds after the application of the radiofrequency current. Additional current was given to one to four predetermined sites by mapping. The mean number of applications was 4.0 +/- 1.3 sites. Except in the first patient, VT was eliminated successfully and VT was not induced by programmed stimulation, by the administration of isoproterenol, or by treadmill exercise testing. VT did not recur during the follow-up period of 6.8 +/- 1.1 months.

Alternation of QRS Morphology and Effect of Radiofrequency Ablation in Idiopathic Ventricular Tachycardia

We performed electrophysiological studies in 13 patients with idiopathic VT and attempted radiofrequency (RF) catheter ablation in 4 of them.Results: VT was induced by programmed stimulation in all patients and the mean cycle length was 363 ± 58 msec. In 8 of 13 patients (62%), alternation of either the cycle length and/or morphology of VT was observed. Transient entrainment was achieved in all patients by rapid pacing from the right ventricular outflow tract so reentry was considered the underlying mechanism of VT. The site of earliest activation (EAS) during VT was located at the apicoposterior portion of the left ventricular septum and used as the target site for RF catheter ablation. Spikelike presystolic activity was detected 20–40 msec prior to the large deflection of the local electrogram in four patients. VT was terminated by a few seconds of RF current in all four patients, but subsequently new VTs with a slightly different morphology were induced in three of them and re‐mapping showed a shift of the EAS. After additional RF ablation at the new EAS, VT was no longer induced. No complication was noted and VT did not recur during a follow‐up period for a mean of 9.3 ± 5.2 months.Conclusion: RF catheter ablation seems useful and safe for idiopathic VT. The alternation of QRS morphology and the findings at the time of catheter ablation suggest that an alternative pathway or multiple exits may be present in some patients with idiopathic VT, because the change in VT morphology was associated with a shift of the EAS.

Abnormal fatty acid metabolism in patients with coronary vasospasm

Although various noninvasive methods have been used to detect vasospasm, none of them are sensitive enough for patients with sporadic attacks. Since abnormal fatty acid metabolism is observed in ischemic myocardium,123I-β-methyl-p-iodophenyl pentadecanoic acid (BMIPP), a radiolabeled fatty acid analog, has recently been proposed as a useful tracer for detecting myocardial damage. The aim of this study was to clarify the clinical implications of decreased myocardial BMIPP uptake in patients with vasospastic angina. We evaluated 53 patients with vasospastic angina (32 with clinically documented vasospasm [Group-A] and 21 with vasospasm induced by ergonovine provocation [Group-B]) and 27 control subjects, 20 in Group-A were re-evaluated 6 months after medical treatment. The territorial regions of vasospasm-induced coronary artery, the wall motion by left ventriculography, and BMIPP uptake were compared. Vasospasm was induced in multiple coronary arteries in 29 (55%) patients. Reduced wall motion and decreased BMIPP uptake were observed in 19 (36%) patients and 47 (89%) patients, respectively. The sensitivity and specificity of determination of vasospasm-induced coronary arteries with BMIPP scintigraphy were 71% (69/97 coronary arteries) and 88% (126/143), respectively. Vasospasm was re-induced by ergonovine provocation in 8 patients (Group-I) and not re-induced in 12 (Group-II) after treatment. In Group-I, improvement of decreased BMIPP uptake was lower than in Group-II (19 ± 11 vs. 59 ± 22%, mean ± SD, p < 0.001). The regions in which vasospasm was re-provoked exhibited decreased BMIPP uptake.Abnormal fatty acid metabolism was more often observed than wall motion abnormality in the vasospastic region in patients with vasospastic angina. BMIPP scintigraphy is a highly accurate and non-invasive technique for determining the presence and location of vasospasm.

Entrainment of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Tachycardia

In two patients with arrhythrnogenic right ventricular dysplasia (ARVDJ, sustained ventricular tachycardia (VT) was induced by programmed stimulations during serial drug testings. One patient had five and the other had two VT morphologies, and the sites of origin were determined by endocardial catheter mappings. When overdrive pacing was performed, constant fusion in the QflS complex was observed in the two patients. Constant fusion of a different degree was also observed at different paced cycle lengths. Both patients had dilated right ventricles and wall‐motion abnormality, and the diagnosis of ARVD was further confirmed by the specimen resected at the site of origin of VT. Therefore, VT in ARVD can be entrained and reentry is the most likely mechanism of such VT.

Successful radiofrequency current catheter ablation of sustained ventricular tachycardia.

We performed radiofrequency current catheter ablation in two patients with nonischemic sustained ventricular tachycardia (VT). In one patient, two morphologically distinct VTs were induced by electrical stimulation. One showed right bundle branch block pattern and the other left bundle branch block pattern. The earliest site of activation during each VT was determined at the septum of the right ventricle. However, these two sites were close to the His‐bundle elecfrogram recording area. In the other patient, a VT with a left bundle branch block pattern occurred spontaneously after the administration of isoproterenol. The earliest site of activation during VT was determined at the outflow tract of the right ventricle. During tachycardia, radiofrequency current ablation (40 W ± 30 sec) was delivered to the earliest site of activation, A few seconds after fulguration, each VT was terminated and additional radio‐frequency currents were given near these sites. After the ablation, VT could not be induced by the electrical stimulations, nor did it recur. No side effects were observed and the atrioventricular conduction remained intact. We feel that nonischemic VTs could possibly be treated by using radiofrequency current catheter ablation.

Successful Slow Pathway Ablation in a Patient with Atrioventricular Nodal Reentrant Tachycardia Having a Proximal Common Pathway

Radiofrequency catheter ablation was attempted in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). AVNRT was easily inducible but an intermittent loss of the atrial activation was observed during AVNRT suggesting the presence of a proximal common pathway. During sinus rhythm, a relatively delayed activation that was compatible with a slow potential, was recorded anterior to the ostium of coronary sinus, and radiofrequency catheter ablation application (20 watts) to the site induced junction tachycardia. After an additional radiofrequency catheter ablation application to close the site, AVNRT became noninducible without deterioration of atrioventricular conduction through a fast pathway. This is the first case in which radiofrequency catheter ablation application to the slow potential recording site has been successful, even in AVNRT having a proximal common pathway.