Background-Catheter ablation of atrial tachycardia (AT) arising near the coronary cusps has been reported in limited numbers of patients. We investigated the electrophysiological characteristics of these ATs in 22 consecutive patients. Methods and Results-This study included 22 patients (mean ageϮSD, 53Ϯ11 years; 86% female) with ATs arising near the aortic coronary cusps who underwent successful ablation. Activation mapping was performed during tachycardia to identify the earliest activation site. All patients achieved successful ablation through either a retrograde aortic (nϭ19) or a transseptal (nϭ3) approach. The successful ablation sites were located in the noncoronary cusp (NCC) (nϭ16), including 3 near the junction between the NCC and right coronary cusp. The remaining 6 cases were ablated from the left coronary cusp (LCC) (nϭ3) or the left atrium posterior to the LCC (nϭ3). For most tachycardias, there were distinctive P-wave morphological features recorded for each cusp location. Furthermore, analysis of the electrogram morphological features recorded during tachycardia at successful ablation sites revealed an atrial/ventricular (A/V) ratio Ͼ1 in 14 of 16 NCC ATs; the remaining 2, from the NCC near the junction with the right coronary cusp, showed an A/V ratio Յ1. At ablation sites in the LCC, the A/V ratio was Ͻ1 (4 of 6 patients) or 1 (remaining 2 patients). During a follow-up duration of 30Ϯ13 months, all patients were free of arrhythmias without antiarrhythmic drugs. Conclusions-ATs surrounding the aortic coronary cusps can be safely and effectively ablated, with good long-term outcomes. In addition to the P-wave morphological features, the A/V ratio of the local electrogram recording during tachycardia facilitated the localization of successful sites. (Circ Arrhythm Electrophysiol. 2011;4:902-908.)

BackgroundEndocardial mapping for scars and abnormal electrograms forms the most essential component of ventricular tachycardia ablation. The utility of ultra‐high resolution mapping of ventricular scar was assessed using a multielectrode contact mapping system in a chronic canine infarct model.MethodsChronic infarcts were created in five anesthetized dogs by ligating the left anterior descending coronary artery. Late gadolinium‐enhanced magnetic resonance imaging (LGE MRI) was obtained 4.9 ± 0.9 months after infarction, with three‐dimensional (3D) gadolinium enhancement signal intensity maps at 1‐mm and 5‐mm depths from the endocardium. Ultra‐high resolution electroanatomical maps were created using a novel mapping system (Rhythmia Mapping System, Rhythmia Medical/Boston Scientific, Marlborough, MA, USA) Rhythmia Medical, Boston Scientific, Marlborough, MA, USA with an 8.5F catheter with mini‐basket electrode array (64 tiny electrodes, 2.5‐mm spacing, center‐to‐center).ResultsThe maps contained 7,754 ± 1,960 electrograms per animal with a mean resolution of 2.8 ± 0.6 mm. Low bipolar voltage (<2 mV) correlated closely with scar on the LGE MRI and the 3D signal intensity map (1‐mm depth). The scar areas between the MRI signal intensity map and electroanatomic map matched at 87.7% of sites. Bipolar and unipolar voltages, compared in 592 electrograms from four MRI‐defined scar types (endocardial scar, epicardial scar, mottled transmural scar, and dense transmural scar) as well as normal tissue, were significantly different. A unipolar voltage of <13 mV correlated with transmural extension of scar in MRI. Electrograms exhibiting isolated late potentials (ILPs) were manually annotated and ILP maps were created showing ILP location and timing. ILPs were identified in 203 ± 159 electrograms per dog (within low‐voltage areas) and ILP maps showed gradation in timing of ILPs at different locations in the scar.ConclusionsUltra‐high resolution contact electroanatomical mapping accurately localizes ventricular scar and abnormal myocardial tissue in this chronic canine infarct model. The high fidelity electrograms provided clear identification of the very low amplitude ILPs within the scar tissue and has the potential to quickly identify targets for ablation.

PurposeIron deposition has been shown to occur following myocardial infarction (MI). We investigated whether such focal iron deposition within chronic MI lead to electrical anomalies.MethodsTwo groups of dogs (ex-vivo (n = 12) and in-vivo (n = 10)) were studied at 16 weeks post MI. Hearts of animals from ex-vivo group were explanted and sectioned into infarcted and non-infarcted segments. Impedance spectroscopy was used to derive electrical permittivity () and conductivity (). Mass spectrometry was used to classify and characterize tissue sections with (IRON+) and without (IRON-) iron. Animals from in-vivo group underwent cardiac magnetic resonance imaging (CMR) for estimation of scar volume (late-gadolinium enhancement, LGE) and iron deposition (T2*) relative to left-ventricular volume. 24-hour electrocardiogram recordings were obtained and used to examine Heart Rate (HR), QT interval (QT), QT corrected for HR (QTc) and QTc dispersion (QTcd). In a fraction of these animals (n = 5), ultra-high resolution electroanatomical mapping (EAM) was performed, co-registered with LGE and T2* CMR and were used to characterize the spatial locations of isolated late potentials (ILPs).ResultsCompared to IRON- sections, IRON+ sections had higher, but no difference in. A linear relationship was found between iron content and (p<0.001), but not (p = 0.34). Among two groups of animals (Iron (<1.5%) and Iron (>1.5%)) with similar scar volumes (7.28%±1.02% (Iron (<1.5%)) vs 8.35%±2.98% (Iron (>1.5%)), p = 0.51) but markedly different iron volumes (1.12%±0.64% (Iron (<1.5%)) vs 2.47%±0.64% (Iron (>1.5%)), p = 0.02), QT and QTc were elevated and QTcd was decreased in the group with the higher iron volume during the day, night and 24-hour period (p<0.05). EAMs co-registered with CMR images showed a greater tendency for ILPs to emerge from scar regions with iron versus without iron.ConclusionThe electrical behavior of infarcted hearts with iron appears to be different from those without iron. Iron within infarcted zones may evolve as an arrhythmogenic substrate in the post MI period.

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Immune factors are involved in modulating neointimal response to arterial wall injury, but the role of individual immune effectors in this response remains unclear. Using a carotid cuff injury model in mice, we tested the role of immunoglobulin isotypes in modulating intimal thickening by using adoptive transfer of splenocytes from WT mice, or the direct administration of IgG or IgM into immune-deficient Rag-1-/- [Rag-1 knockout (Rag-1KO)] mice. The direct role of complement was also tested by depletion of complement. Splenocytes from WT mice were isolated and adoptively transferred to Rag-1KO mice subjected to carotid cuff arterial injury. Transfer of splenocytes to Rag-1KO mice resulted in increased serum IgM and IgG within 48 h and were comparable to WT levels by 21 days after injury. Splenocyte transfer in Rag-1KO decreased intimal area by 40% compared with Rag-1KO mice without cell transfer. To further differentiate the relative contribution of IgM or IgG in reducing intimal thickening, additional groups of Rag-1KO mice were subjected to injury and given intravenous injections of pooled mouse IgG or IgM. Both IgG and IgM treatment significantly reduced intimal thickening compared with untreated Rag-1KO mice. Immunoglobulin treatments modified serum complement C3 profile and decreased C3 presence in injured arteries. Depletion of C3 using cobra venom factor in Rag-1KO mice significantly decreased intimal thickening. Our results identify the direct role of natural IgG and IgM, and complement in the modulation of neointimal response to arterial injury.

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The routine use of DES in acute myocardial infarction is associated with reduced rates of MACE at 12 months vs BMS, despite a higher rate of complex procedures in the DES treated patients. In addition to its anti-restenosis effect, the improved outcome of patients treated with DES may be linked to a more complete revascularization in association with prolonged clopidogrel therapy.