Jim Pouliopoulos

Cooled Needle Catheter Ablation Creates Deeper and Wider Lesions Than Irrigated Tip Catheter Ablation

Objectives: To design and test a catheter that could create deeper ablation lesions.

Intramyocardial Adiposity After Myocardial Infarction New Implications of a Substrate for Ventricular Tachycardia

Background— Collagen has been attributed as the principal structural substrate of ventricular tachycardia (VT) after myocardial infarction (MI), even though adiposity of myocardium after MI is well recognized histologically. We investigated the effects of intramyocardial adiposity compared with collagen on electrophysiological properties, connexin43 expression, and VT induction after MI. Methods and Results— Simultaneous left ventricular plunge-needle, noncontact mapping was performed in sheep without MI (MI−; n=5), with MI and inducible VT (MI+VT+; n=7), and with MI and no inducible VT (MI+VT−; n=8). Histological intramyocardial quantity of adipose and collagen and degree of discontinuity were coregistered with electrophysiological parameters (MI+; 290 specimens). Additional assessment of connexin43 expression was performed. Left ventricular scar contained a body mass–independent abundance of adipocytes (adipose:collagen=0.8). Increased adipose density and discontinuity contributed to a greater inverse correlation (r) with conduction velocity (r for adipose=0.39, r for discontinuity=0.45, r for collagen=0.26) and electrogram amplitude (r for adipose=0.73, r for contiguity=0.77, r for collagen=0.68) compared with collagen. Collagen density was similar between the MI+ groups (P>0.29). However, the MI+VT+ group demonstrated a significant (all P⩽0.01) increase in adipose (8%) and discontinuity (qualitative) and decrease in conduction velocity (13%) and electrogram amplitude (21%) at MI borders compared with the MI+VT− group. In scar, myocytes adjacent to fibrofatty interfaces demonstrated increased connexin43 lateralization. A gradient increase in adipose was observed at sites that supported preferential presystolic VT activation and exhibited attenuation of excitation wavelength (P<0.001). Conclusions— Intramyocardial adiposity, in association with myocardial discontinuity within left ventricular scar borders, is a significant factor associated with altered electrophysiological properties, aberrant connexin43 expression, and increased propensity for VT after MI.Background— Collagen has been attributed as the principal structural substrate of ventricular tachycardia (VT) after myocardial infarction (MI), even though adiposity of myocardium after MI is well recognized histologically. We investigated the effects of intramyocardial adiposity compared with collagen on electrophysiological properties, connexin43 expression, and VT induction after MI. Methods and Results— Simultaneous left ventricular plunge-needle, noncontact mapping was performed in sheep without MI (MI−; n=5), with MI and inducible VT (MI+VT+; n=7), and with MI and no inducible VT (MI+VT−; n=8). Histological intramyocardial quantity of adipose and collagen and degree of discontinuity were coregistered with electrophysiological parameters (MI+; 290 specimens). Additional assessment of connexin43 expression was performed. Left ventricular scar contained a body mass–independent abundance of adipocytes (adipose:collagen=0.8). Increased adipose density and discontinuity contributed to a greater inverse correlation ( r ) with conduction velocity ( r for adipose=0.39, r for discontinuity=0.45, r for collagen=0.26) and electrogram amplitude ( r for adipose=0.73, r for contiguity=0.77, r for collagen=0.68) compared with collagen. Collagen density was similar between the MI+ groups ( P >0.29). However, the MI+VT+ group demonstrated a significant (all P ≤0.01) increase in adipose (8%) and discontinuity (qualitative) and decrease in conduction velocity (13%) and electrogram amplitude (21%) at MI borders compared with the MI+VT− group. In scar, myocytes adjacent to fibrofatty interfaces demonstrated increased connexin43 lateralization. A gradient increase in adipose was observed at sites that supported preferential presystolic VT activation and exhibited attenuation of excitation wavelength ( P <0.001). Conclusions— Intramyocardial adiposity, in association with myocardial discontinuity within left ventricular scar borders, is a significant factor associated with altered electrophysiological properties, aberrant connexin43 expression, and increased propensity for VT after MI. # Clinical Perspective {#article-title-48}

Bipolar Ablation of the Interventricular Septum is More Efficient at Creating a Transmural Line than Sequential Unipolar Ablation

Introduction: Post infarct ventricular tachycardia (VT) often involves the interventricular septum (IVS) and requires transmural septal ablation. The purpose of this study was to compare the efficacy of bipolar ablation (BIA) versus sequential unipolar ablation (SUA) in creating a transmural ablation line along the IVS scar border.

Comparison of Electroanatomic Contact and Noncontact Mapping of Ventricular Scar in a Postinfarct Ovine Model With Intramural Needle Electrode Recording and Histological Validation

Background—Substrate-based ablation is useful for nonhemodynamically tolerated postinfarct ventricular tachycardia. We assessed the accuracy of the CARTO contact and EnSite noncontact systems at identifying scar in a chronic ovine model with intramural plunge needle electrode recording and histological validation. Methods and Results—Scar mapping was performed on 8 male sheep with previous percutaneous-induced myocardial infarction. Up to 20 plunge needles were inserted into the left ventricle of each animal in areas of dense scar, scar border, and normal myocardium. A simultaneous CARTO map and EnSite geometry were acquired using a single catheter, and needle electrode locations were registered. A dynamic substrate map was constructed using ratiometric 50% peak negative voltage. The scar percentage around each needle location was quantified histologically. Analysis was performed on 152 plunge needles and corresponding histological blocks. Spearman correlation with histology was 0.690 (P<0.001) for needle electrode peak-to-peak voltage (PPV), 0.362 (P<0.001) and 0.492 (P<0.001) for CARTO bipolar and unipolar PPV, and 0.381 (P<0.001) for EnSite dynamic substrate map (≤40 mm from array). The area under the receiver operator characteristics curve (<50% and ≥50% scar) was 0.896 for needle electrode PPV, 0.726 and 0.697 for CARTO bipolar and unipolar PPV, and 0.703 for EnSite dynamic substrate map (≤40 mm from array). Conclusions—Both the CARTO contact and EnSite noncontact systems were moderately accurate in identifying postinfarct scar when compared with intramural electrodes and confirmed with histology. The EnSite dynamic substrate map was comparable to the CARTO contact bipolar PPV when points >40 mm from the array were excluded.

Protection of the coronary arteries during epicardial radiofrequency ablation with intracoronary chilled saline irrigation: Assessment in an in vitro model.

Introduction: The coronary arteries can be damaged during epicardial radiofrequency ablation (RFA) procedures. We hypothesized that intracoronary irrigation with chilled saline may be a useful technique for minimizing heat‐induced damage to the coronary artery endothelium during this procedure.

Role of adipose tissue in the pathogenesis of cardiac arrhythmias

Epicardial adipose tissue is present in normal healthy individuals. It is a unique fat depot that, under physiologic conditions, plays a cardioprotective role. However, excess epicardial adipose tissue has been shown to be associated with prevalence and severity of atrial fibrillation. In arrhythmogenic right ventricular cardiomyopathy and myotonic dystrophy, fibrofatty infiltration of the myocardium is associated with ventricular arrhythmias. In the ovine model of ischemic cardiomyopathy, the presence of intramyocardial adipose or lipomatous metaplasia has been associated with increased propensity to ventricular tachycardia. These observations suggest a role of adipose tissue in the pathogenesis of cardiac arrhythmias. In this article, we review the role of cardiac adipose tissue in various cardiac arrhythmias and discuss the possible pathophysiologic mechanisms.

Evolution of Ventricular Tachycardia and Its Electrophysiological Substrate Early After Myocardial Infarction: An Ovine Model

Background— Sudden arrhythmic death after myocardial infarction (MI) is most frequent in the first month. Early programmed ventricular stimulation (within 1 week) post-MI has been able to identify long-term ventricular tachycardia (VT) occurrence. We aimed to determine the timing of development and stabilization of VT circuits after MI and how the evolution of the underlying substrate differs with VT inducibility. Methods and Results— MIs were induced in 36 sheep. The 21 survivors underwent serial electroanatomic mapping and programmed ventricular stimulation. Animals were classified as VTpos (inducible VT) or VTneg (noninducible VT) at day 8. Forty-three percent of MI survivors were VTpos on day 8 (9/21), and all remained inducible on day 100 with 1.5 (1.0–2.0) and 1.0 (1.0–2.0) morphologies per animal on days 8 and 100, respectively. Twelve-lead electrocardiogram matched in 15 of 19 VTs between days 8 and 100. The earliest presystolic ventricular activations during VT circuits were in similar locations at the 2 time points. The 12 VTneg animals remained noninducible on day 100. There was no difference in voltage or velocity substrate with time or inducibility. The area with fractionated signals increased with time and VT inducibility. VTpos animals had more linear regions of slowed conduction forming conducting channels. Conclusions— The inducibility and earliest presystolic endocardial activation sites of VT as well as voltage and velocity substrate on day 8 predicted those on day 100 postinfarct, indicating early formation and stabilization of the arrhythmogenic substrate. VT inducibility was influenced by the distribution of conducting channels and increased complex fractionated signals.

Five seconds of 50–60 W radio frequency atrial ablations were transmural and safe: an in vitro mechanistic assessment and force-controlled in vivo validation

Aims Longer procedural time is associated with complications in radiofrequency atrial fibrillation ablation. We sought to reduce ablation time and thereby potentially reduce complications. The aim was to compare the dimensions and complications of 40 W/30 s setting to that of high-power ablations (50-80 W) for 5 s in the in vitro and in vivo models. Methods and results In vitro ablations-40 W/30 s were compared with 40-80 W powers for 5 s. In vivo ablations-40 W/30 s were compared with 50-80 W powers for 5 s. All in vivo ablations were performed with 10 g contact force and 30 mL/min irrigation rate. Steam pops and depth of lung lesions identified post-mortem were noted as complications. A total of 72 lesions on the non-trabeculated part of right atrium were performed in 10 Ovine. All in vitro ablations except for the 40 W/5 s setting achieved the critical lesion depth of 2 mm. For in vivo ablations, all lesions were transmural, and the lesion depths for the settings of 40 W/30 s, 50 W/5 s, 60 W/5 s, 70 W/5 s, and 80 W/5 s were 2.2 ± 0.5, 2.3 ± 0.5, 2.1 ± 0.4, 2.0 ± 0.3, and 2.3 ± 0.7 mm, respectively. The lesion depths of short-duration ablations were similar to that of the conventional ablation. Steam pops occurred in the ablation settings of 40 W/30 s and 80 W/5 s in 8 and 11% of ablations, respectively. Complications were absent in short-duration ablations of 50 and 60 W. Conclusion High-power, short-duration atrial ablation was as safe and effective as the conventional ablation. Compared with the conventional 40 W/30 s setting, 50 and 60 W ablation for 5 s achieved transmurality and had fewer complications.

Evaluation of lesion and thermodynamic characteristics of Symplicity and EnligHTN renal denervation systems in a phantom renal artery model.

AIMS Radiofrequency renal artery denervation has been used effectively to treat resistant hypertension. However, comparison of lesion and thermodynamic characteristics for different systems has not been previously described. We aimed to assess spatiotemporal lesion growth and ablation characteristics of Symplicity and EnligHTN systems. METHODS AND RESULTS A total of 39 ablations were performed in a phantom renal artery model using Symplicity (n=17) and EnligHTN (n=22) systems. The phantom model consisted of a hollowed gel block surrounding a thermochromic liquid crystal (TLC) film, exhibiting temperature sensitivity of 50-78°C. Flow was simulated using 37°C normal saline with impedance equal to blood. Radiofrequency ablations with each system were delivered with direct electrode tip contact to the TLC. Lesion size was interpreted from the TLC as the maximum dimensions of the 51°C isotherm. Mean lesion depth was 3.82 mm±0.04 versus 3.44 mm±0.03 (p<0.001) for Symplicity and EnligHTN, respectively. Mean width was 7.17 mm±0.08 versus 6.23 mm±0.07 (p<0.001), respectively. With EnligHTN, steady state temperature was achieved 20 sec earlier, and was 15°C higher than Symplicity. CONCLUSIONS In this phantom model, Symplicity formed larger lesions compared to EnligHTN with lower catheter-tip temperature. The clinical significance of our findings needs to be explored further.

Simultaneous biventricular noncontact mapping and ablation of septal ventricular tachycardia in a chronic ovine infarct model.

Background—We assessed a novel simultaneous biventricular mapping and ablation approach for septal ventricular tachycardia (VT) in a chronic ovine infarct model. Methods and Results—In 8 sheep with inducible VT, mapping and ablation were performed 9±3 months after percutaneously induced myocardial infarction, with left ventricular ejection fraction 23±8%. Scar was identified by EnSite Dynamic Substrate Mapping plus CARTO voltage mapping. Thirty VT episodes (cycle length, 235±42 ms) were mapped with simultaneous analyses using EnSite arrays deployed in both the left ventricle and the right ventricle. Short ablation lines were created perpendicular to the breakout pathway along the scar border in the ventricle with earliest activity. If septal VT was still inducible, this line was extended before ablation in the second chamber. The end point of noninducibility of VT was achieved in all animals. The mean difference in delay in noncontact breakout timing between the ventricles was shorter for VT with (n=18) than without (n=12) septal breakout (32±7.8 ms, P<0.001). In 5 of 6 animals, after ablation in one ventricle, septal VT was still inducible with a common breakout site in the second ventricle. After septal ablation in the second ventricle, VT was no longer inducible. In the 6 animals in which septal VT had been ablated, transmural septal ablation was identified at the scar border, with overlapping left ventricular and right ventricular ablation lesions present in 5 of 6 (septal thickness 8 to 17 mm) and left ventricular endocardial ablation being transmural in 1 of 6 (6 mm). Conclusions—Biventricular scar and VT activation mapping correctly localizes septal VT pathways, directing ablation from one or both septal endocardial aspects. Creation of a transmural septal lesion at the scar border interrupting VT exit points is highly effective at ablating septal VT.