Keiichi Ashikaga

Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-sensitive idiopathic left ventricular tachycardia

OBJECTIVES We characterized pharmacologically the slow conduction zone of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) with regard to the late diastolic potential (LDP). BACKGROUND We showed that the slow conduction zone of ILVT could be divided into two components by LDP; that is, the distal component with a tachycardia-dependent conduction delay property and the proximal one without it. METHODS Electrophysiologic studies were performed in eight consecutive patients. The LDP was recorded during left ventricular (LV) mapping during ILVT. Entrainment was performed from the right ventricular outflow tract while recording LDP. The effects of lidocaine (1 mg/kg body weight) and verapamil (0.5 or 1.0 mg) were examined during entrainment. RESULTS The LDPs preceding the Purkinje potential (PP) were serially recorded from the upper third to the middle of the LV septum along the narrow longitudinal line. The ventricular tachycardia (VT) cycle length increased after lidocaine (p < 0.05), and further after verapamil (p < 0.05). The increments in the VT cycle length after administration of the drugs strongly correlated with those in LDP-PP (r > 0.9 for both drugs). The interval from the ventricular potential to LDP was unchanged after administration of the drugs. In one patient, verapamil terminated VT by local conduction block between LDP and PP. The LDP-PP measured during entrainment increased after lidocaine, and further after verapamil, whereas the interval from the stimulus to LDP remained unchanged. CONCLUSIONS The component distal to LDP is mainly calcium channel-dependent and partly depressed sodium channel-dependent. The proximal component is considered to be sodium channel-dependent (normal).

Mechanism of ST elevation and ventricular arrhythmias in an experimental Brugada syndrome model.

Background—Although phase 2 reentry is said to be responsible for initiation of ventricular tachycardia (VT) in Brugada syndrome, information about the activation sequence during VT is limited. Methods and Results—We developed an experimental Brugada syndrome model using a canine isolated right ventricular preparation cross-circulated with arterial blood of a supporter dog and examined the VT mechanism. Two plaque electrodes (35×30 mm) containing 96 bipolar electrodes were attached to the endocardium and epicardium. Saddleback and coved types of ST elevation in transmural ECG were induced by pilsicainide, a pure sodium channel blocker, and pinacidil, a KATP channel opener. Eighteen polymorphic VT episodes were recorded in 9 of the 12 preparations associated with ST elevation. Fourteen episodes spontaneously developed in 5 preparations after an extrasystole during basic drive pacing. Analysis of local recovery times revealed increased dispersion especially in epicardium, and the extrasystole originated from a site with a short recovery time, suggesting that phase 2 reentry was its mechanism. The other 4 VTs in 4 preparations were induced by premature stimulation. Analysis of the activation sequences during VT revealed reentry between epicardium and endocardium or reentry around an arc of a functional block confined to epicardium or endocardium with bystander activation of the other. Conclusions—Electrical heterogeneity in the recovery phase was induced in this experimental Brugada syndrome model, which can be a substrate for the development of phase 2 reentry and the subsequent reentry around an arc of the functional block, resulting in sustained VT.

Late Restenosis Following Sirolimus-Eluting Stent Implantation

OBJECTIVES This serial angiographic study evaluated the incidence and predictors of late restenosis after sirolimus-eluting stent (SES) implantation. BACKGROUND Previous studies showed late restenosis (i.e., late catch-up phenomenon) after implantation of 7-hexanoyltaxol-eluting stents and nonpolymeric, paclitaxel-eluting stents. METHODS Between August 2004 and December 2006, SES implantation was performed in 1,393 patients with 2,008 lesions, in whom 8-month and 2-year follow-up coronary angiography were planned. RESULTS Of 2,008 lesions, 1,659 (83%) underwent 8-month follow-up angiography (8.3 ± 2.2 months). Restenosis was observed in 122 lesions (7.4%). Coronary angiography 2 years (1.9 ± 0.4 years) after SES deployment was performed in 1,168 lesions (74% of lesions without restenosis at 8-month follow-up angiography). Late restenosis was observed in 83 lesions (7.1%). There was significant decrease in minimum luminal diameter (MLD) between 8-month and 2-year follow-up (2.56 ± 0.56 mm vs. 2.35 ± 0.71 mm, p < 0.001). Multivariate analysis showed in-stent restenosis before SES implantation and MLD at 8-month follow-up as independent predictors of late restenosis. CONCLUSIONS Between 8-month and 2-year follow-up after SES implantation, MLD decreases, which results in late restenosis in some lesions. In-stent restenosis before SES implantation and MLD at 8-month follow-up are independent predictors of late restenosis.

V-H-A Pattern as a criterion for the differential diagnosis of atypical AV nodal reentrant tachycardia from AV reciprocating tachycardia.

Background: During ventricular extrastimulation, His bundle potential (H) following ventricular (V) and followed by atrial potentials (A), i.e., V‐H‐A, is observed in the His bundle electrogram when ventriculo‐atrial (VA) conduction occurs via the normal conduction system. We examined the diagnostic value of V‐H‐A for atypical form of atrioventricular nodal reentrant tachycardia (AVNRT), which showed the earliest atrial activation site at the posterior paraseptal region during the tachycardia.

Presence of older thrombus in patients with late and very late drug-eluting stent thrombosis

BACKGROUND Although drug-eluting stents (DES) have considerably reduced the incidence of in-stent restenosis, late and very late stent thrombosis (ST) after DES implantation have emerged as major safety concerns. We morphologically investigated the age of DES thrombi aspirated during percutaneous coronary intervention (PCI) from patients with either late or very late ST that resulted in acute myocardial infarction (AMI). METHODS AND RESULTS We obtained DES thrombi during PCI from 16 consecutive patients with ST (late and very late ST, n=4 and n=12, respectively), who presented with AMI within 24 h of the onset of anginal symptoms. Thrombi were morphologically classified as fresh, lytic, and organized. Fresh thrombus was identified in 5 (31%) of the 16 patients and lytic thrombus was found in 3 (19%). Organized thrombus was notably found in 8 (50%) patients, of whom 5 (31%) had only the organized type and 3 (19%) had both fresh and organized thrombi. The frequency of fresh thrombus tended to be higher in patients with stent failure such as stent malapposition and fracture, but the difference did not reach significance (p=0.06). CONCLUSIONS Although the study group is small, about two-thirds of DES thrombi in late and very late ST were days or weeks old. These findings suggest an important discrepancy between the time of onset of the intra-stent thrombotic process and the occurrence of acute clinical symptoms, and provide further information about another potential mechanism of DES thrombosis.

The Course of Ischemic Mitral Regurgitation in Acute Myocardial Infarction After Primary Percutaneous Coronary Intervention From Emergency Room to Long-Term Follow-Up

Background—Previously published evidence on ischemic mitral regurgitation (IMR) and its adverse prognosis after myocardial infarction has been based on the severity of IMR in the subacute or chronic period of myocardial infarction. However, the state of IMR can vary from the early stage to the chronic stage as a result of various responses of myocardium after primary percutaneous coronary intervention (PCI). Methods and Results—Standard echocardiography was serially performed in 546 consecutive patients with first-onset acute myocardial infarction (1) immediately after their arrival (pre-PCI), (2) before discharge (early post-PCI), and (3) 6 to 8 months after PCI (late post-PCI). The course of IMR after primary PCI and the prognostic impact of the IMR in each phase were investigated. IMR was found in 193/546 (35%) patients at the emergency room. In the acute phase after PCI, IMR improved in 63 patients. IMR worsened in 78 patients despite successful PCI. Shorter onset-to-reperfusion time and nontotal occlusion before PCI were the independent predictors of early improvement of IMR. In the chronic phase, IMR improved in 79 patients and worsened in 36 patients. Lower peak creatine kinase–myocardial band was an independent predictor of late improvement of IMR. IMR before PCI worsened 30-day prognosis (P=0.02), and persistent IMR in the chronic phase worsened long-term prognosis (P=0.04) after primary PCI. Conclusions—Degrees of IMR changed in the early and chronic phase after primary PCI for acute myocardial infarction. IMR on arrival and persistent IMR in the chronic phase worsened short-term and long-term prognosis after acute myocardial infarction, respectively.

Radiofrequency Catheter Ablation with the Use of a Noncontact Mapping System for Ventricular Tachycardia Originating from the Aortic Sinus Cusp —A Case Report—

Here we present a 15‐year old female in whom an idiopathic ventricular tachycardia (VT) originating from the left aortic sinus cusp was eliminated by radiofrequency catheter ablation (RFCA) under navigation using a noncontact mapping system (NCM). The dynamic activation map constructed with the NCM clearly identified a VT focus in the left aortic sinus cusp, from which the activation spread out to the entire left ventricle. At that site, the virtual unipolar electrogram recorded with the NCM was the same as the contact unipolar electrogram in terms of morphology and timing, a pre‐systolic potential preceding the QRS complex by 40 msec was recorded by contact bipolar electrogram and rapid pacing during sinus rhythm resulted in a perfect pace match. RFCA at that site eliminated the VT and the patient has had no recurrence during 10 months of follow‐up.

Impaired Longitudinal Conduction in Crista Terminalis is Necessary for Sustenance of Experimental Atrial Flutter

Sustained atrial flutter (AFL) can be induced by creating a lesion between the vena cava in dogs. In previous studies on this model, the crista terminalis (CT) was often injured, and thus, role of CT in sustained reentry was not well understood. We hypothesized that impaired longitudinal conduction in CT is necessary for sustained AFL. In 16 anesthetized, open‐chest dogs, linear radiofrequency ablation of the intercaval region was performed without interrupting CT. Intra‐atrial conduction times (IAT) along CT were measured using a plaque electrode (25 × 35 mm) containing 30 bipolar electrodes before and after additional ablation of CT (group A, n = 10) or the pectinate muscle (PM) region (group B, n = 6). In group A, IAT along CT was 27 ± 5 ms at baseline and was increased to 43 ± 3 ms after ablation of CT (P < 0.001). In group B, IAT along CT was 28 ± 4 ms at baseline and 27 ± 3 ms after ablation of PM (P = NS). Sustained AFL lasting >20 minutes was induced in 10/10 dogs in group A only after additional ablation of CT, and in 0/6 dogs in group B (P < 0.001). The cycle lengths of AFL after ablation of the intercaval region and additional ablation of CT were 119 ± 14 and 140 ± 14 ms, respectively (P < 0.01). There was a significant positive correlation between the cycle length of AFL and IAT along CT (r2= 0.63, P < 0.001). These results indicate that longitudinal conduction property in CT and not in PM strongly affects sustenance of AFL in this model. (PACE 2003; 26:2008–2015)

An Alternative Approach for Radiofrequency Catheter Ablation for Intra-atrial Reentrant Tachycardia Associated with Open-Heart Surgery

We present case reports of 2 patients with scar‐related intra‐atrial reentrant tachycardia (IART) associated with previous open‐heart surgeries, in which standard ablation strategies failed to eliminate atrial tachycardia (AT). The strategies targeted a narrow conducting channel between the right atrial scars or between the scar and inferior vena cava. In these patients, an alternative approach to transect another narrow conducting pathway between the scar and crista terminalis (CT), which was revealed by a noncontact mapping system, successfully terminated and eliminated the IART. Both the cases were free of recurrent AT at the 24‐and 25‐month follow up visits, respectively. Transection of the corridor between the CT and the incision scar appears to be an effective technique for eliminating scar‐related IART and can be considered as a second‐line procedure for radiofrequency catheter ablation to eliminate IART.

Echocardiographic and pathologic findings of wild-type transthyretin senile systemic amyloidosis developed in early 50s

A 63-year-old male with heart failure was admitted to our hospital. He had past medical history of bilateral carpal tunnel syndrome (CTS) in his early 50s. Cardiomegaly had been detected 6 years ago, and echocardiography revealed diffuse left ventricular (LV) hypertrophy. The patient had been observed by a family doctor until he gradually developed exertional dyspnea. He had no family history of cardiovascular diseases. Electrocardiogram showed complete left bundle branch block with atrial fibrillation. The same findings had been described in his past medical records in his early 50s. Echocardiography revealed increased LV wall thickness (interventricular septum 13.3 mm, posterior wall thickness 15.9 mm) with granular sparkling in the ventricular septum (Fig. 1). LV systolic function was diffusely reduced (ejection fraction 30–35%). Doppler echocardiography suggested diastolic dysfunction, as supported by an E-wave deceleration time of 242.0 ms and an E/e′ of 22.7 (E = 0.7 m/s, e′= 0.03 m/s). The right ventricle was enlarged, and mild tricuspid regurgitation was presented (estimated right ventricular pressure was 44 mmHg). A relative apical longitudinal strain was 1.7 with apical sparing. Serum laboratory testing showed amyloid A protein positive and BNP elevation (227.4 pg/mL). A technetium diphosphno-propanodicarboxylic acid (Tc-DPD) scintigram was also positive for myocardial uptake. We suspected this patient had cardiac amyloidosis. Bence-Jones protein and M-protein were negative. Endomyocardial biopsy confirmed transthyretin (TTR)-type cardiac amyloidosis (Fig. 1). In the biopsy specimen, Congo red staining revealed yellow–green birefringence of the deposits observed by polarizing microscope, and the deposits showed positive immunostaining for TTR. A hereditary form of TTR-derived amyloidosis was excluded by genetic analysis, and we made a diagnosis of wild-type TTR senile systemic amyloidosis (SSA). Conventional heart failure therapy (angiotensin-converting enzyme inhibitor, β-blocker, diuretics, and cardiac resynchronization therapy) was effective, and his heart failure condition is stable with oral medications. SSA is a form of amyloidosis associated with aging, and characterized by the deposition of amyloid fibrils derived from wild-type transthyretin (TTR) [1]. The diagnosis of SSA has become easier in recent years with advances in cardiac imaging (echocardiography, radioisotope, and magnetic resonance imaging) and more widespread use of genetic analysis [2,3]. Recent studies have indicated much younger SSA patients, with an onset around 50 years [4]. The present case had developed CTS in his early 50s, and then cardiomegaly was pointed out in his middle 50s, followed by progressive congestive heart failure in his 60s. This case sends us an educational message that SSA can progress even in the relatively young ages, hidden behind the asymptomatic diffuse LV hypertrophy.