Nipon Chattipakorn

Restitution dynamics during pacing and arrhythmias in isolated pig hearts.

Introduction: The dependence of action potential duration (APD) on the preceding diastolic interval (DI), i.e., restitution, has been purported to predict the development of alternans and reentrant arrhythmias. However, restitution depends on the history of activation (i.e., memory), and its relevance to arrhythmia induction and maintenance is unknown.

Prediction of Defibrillation Outcome by Epicardial Activation Patterns Following Shocks Near the Defibrillation Threshold

Activation Patterns and Defibrillation Outcome. Introduction: Ventricular defibrillation is probabilistic and shock strength dependent. We investigated the relationship between defibrillation outcome and postshock activation patterns for shocks of the same strength (‐50% probability of success for defibrillation [ED50] to yield an equal number of successful and failed shocks).

Relationship between oversizing of self-expanding stents and late loss index in carotid stenting

Stenting of the internal carotid artery is facilitated by stenting across the carotid bifurcation and sizing the diameter of a self-expanding stent to the large common carotid segment. This usually results in marked oversizing of the self-expanding stent in the internal carotid segment. This study was done to determine the relationship between stent oversizing and late luminal loss index after stenting of the internal carotid artery. Between September 1995 and March 1997, there were 165 patients (189 vessels) who underwent successful carotid stenting with self-expanding stents. Fifty-nine patients (63 vessels) had six-month follow-up carotid angiograms and on-line quantitative angiographic analysis. The mean reference diameter of the internal carotid arteries was 4.93+/-1.31 mm. Nominal stent size was 5 mm in 4 patients, 6 mm in 6 patients, 8 mm in 106 patients, 10 mm in 77 patients, and 12 mm in 1 patient. The average stent/patient was 1.03+/-0.16. There were three patients who had more than 50% diameter renarrowing at follow-up. The mean late loss index was 0.25+/-0.41. By linear regression analysis, there was no clear linear relationship between stent oversizing and late loss index after stenting (correlation coefficient = -0.21, P = 0.09). When analysis of variance with linear contrast was used to analyze six groups of different stent/artery ratios (from 1.4 to > or = 2), late loss indexes are significantly lower in the groups of high stent/artery ratio than the groups of low stent/artery ratio (P = 0.01). The process of oversizing of self-expanding stents deployed in the internal carotid artery does not appear to be associated with late restenosis and high stent/artery ratio seems to be associated with low late loss index.

Influence of Postshock Epicardial Activation Patterns on Initiation of Ventricular Fibrillation by Upper Limit of Vulnerability Shocks

BACKGROUNDnShocks of identical strength and timing sometimes induce ventricular fibrillation (VFI) and other times do not (NoVFI). To investigate this probabilistic behavior, a shock strength near the upper limit of vulnerability, ULV(50), was delivered to yield equal numbers of VFI and NoVFI episodes.nnnMETHODS AND RESULTSnIn 6 pigs, a 504-electrode sock was pulled over the ventricles. ULV(50) was determined by scanning the T wave. S(1) pacing was from the right ventricular apex. Ten S(2) shocks of approximate ULV(50) strength were delivered at the same S(1)-S(2) coupling interval. Intercycle interval (ICI) and wave front conduction time (WCT) were determined for the first 5 postshock cycles. ICI and the WCT of cycle 1 were not different for VFI versus NoVFI episodes (P=0.3). Beginning at cycle 2, ICI was shorter and WCT was longer for VFI than NoVFI episodes (P<0.05).nnnCONCLUSIONSnThe first cycle after shocks of the same strength (ULV(50)) delivered at the same time has the same activation pattern regardless of shock outcome. During successive cycles, however, a progressive decrease in ICI and increase in WCT occur during VFI but not NoVFI episodes. These findings suggest shock outcome is (1) deterministic but exquisitely sensitive to differences in electrophysiological state at the time of the shock that are too small to detect or (2) probabilistic and not determined until after the first postshock cycle.

Delayed Afterdepolarization Inhibitor: A Potential Pharmacologic Intervention to Improve Defibrillation Efficacy

DAD Inhibitor Improves Defibrillation. Introduction: Electrical and optical mapping studies of defibrillation have demonstrated that following shocks of strength near the defibrillation threshold (DFT), the first several postshock cycles always arise focally. No immediate postshock reentry was observed. Delayed afterdepolarizations (DADs) have been suggested as a possible cause of this rapid repetitive postshock activity. The aim of this study was to test the hypothesis that DFT is decreased by application of a DAD inhibitor.

Left ventricular apex ablation decreases the upper limit of vulnerability.

BACKGROUNDnAfter shocks with an approximately 50% probability of success for the upper limit of vulnerability (ULV(50)) of strength, the first few activations appear focally on the epicardium at almost the same site at the left ventricular (LV) apex in both successful and failed induction of ventricular fibrillation (VF). We tested the hypothesis that subendocardial ablation at this early site would decrease the shock strength required for the ULV(50).nnnMETHODS AND RESULTSnTen S1 stimuli were delivered from the right ventricular apex at a 300-ms coupling interval in 5 pigs. Biphasic shocks were delivered from right ventricular-superior vena cava electrodes after the last S1 stimulus. The ULV(50) was determined using an up/down protocol with T-wave scanning. Radiofrequency ablation was performed endocardially at the apical LV. The ULV(50) was determined again 30 minutes after ablation. To determine the importance of the ablation region, this protocol was repeated in another 5 pigs with ablation at the LV base. Delivered voltage (401+/-60 versus 323+/-50 V) and energy (11+/-3 versus 7+/-2 J) for the ULV(50) were significantly decreased after LV apex ablation by 19% and 34%, respectively. However, no difference existed in ULV(50) before and after LV base ablation. Lesions at both the LV apex and base were subendocardial and ranged from 0.8 to 1.1 cm in diameter.nnnCONCLUSIONSnSubendocardial ablation at the apical LV markedly decreases ULV(50), which suggests that the activation originating from this postshock early site is responsible for VF initiation and that interventions to electrically silence this site can influence the outcome of VF induction by ULV shocks.

Pacing After Shocks Stronger Than the Upper Limit of Vulnerability Impact on Fibrillation Induction

BACKGROUNDnAfter upper-limit-of-vulnerability (ULV) shocks of the same strength and coupling interval (CI) during the T wave, (1) the epicardial activation pattern (EAP) for the first postshock cycle is indistinguishable between shocks that do (VF) and do not (NoVF) induce ventricular fibrillation (VF) and (2) >/=3 cycles in rapid succession always occur during VF but not during NoVF episodes. To study the role of these rapid cycles, rapid pacing was performed after a shock stronger than the ULV that by itself did not induce rapid cycles and VF.nnnMETHODS AND RESULTSnA 504-electrode sock was sutured to the heart in 6 pigs to map EAPs. The S2 shock strength and S1-S2 CI at the ULV were determined by T-wave scanning with an up/down protocol. Ten shocks 50 to 100 V above the ULV (aULV) were delivered at the same S1-S2 CI to confirm that VF was not induced. Then, the postshock interval after aULV shocks was scanned with an S3 pacing stimulus from the LV apex until the shortest S2-S3 CI that captured was reached. This was repeated for S4, S5, etc, until VF was induced. To induce VF, 3 pacing stimuli (S3-S5) with progressively shorter CIs were required; S3 or S3, S4 never induced VF. After cycle S5, which induced VF, 2 EAP types occurred: focal (74%) and reentrant (26%).nnnCONCLUSIONSnAt least 3 cycles with short CIs are necessary for VF induction after aULV shocks. Cycles S3-S4 may create the substrate for cycle S5 to initiate VF.

Reduction in Atrial Defibrillation Threshold by a Single Linear Ablation Lesion

Single Lesion Lowers ADFT. Introduction: This study investigated a hybrid approach to reduce the atrial defibrillation threshold (ADFT) by determining the effect of a single linear radiofrequency ablation (RFA) lesion on both the ADFT and activation patterns during atrial fibrillation (AF).

Pacing following shocks stronger than the defibrillation threshold: impact on defibrillation outcome.

VF Induction After Defibrillation Shocks. Introduction: A recent study of shocks near defibrillation threshold (DFT) strength demonstrated that at least three rapid cycles always occur after failed shocks but not after successful shocks, suggestion that the number and rapidity of postshock cycles are important in determining defibrillation success. To test this hypothesis, rapid pacing was performed following a shock stronger than the DFT that by itself did not induce rapid cycles and ventricular fibrillation (VF).

The vortex at the apex of the left ventricle: a new twist to the story of the electrical induction of rotors?

Ventricular fibrillation (VF) is the major cause of sudden cardiac death.1 Even though electrical defibrillation is the only effective clinical treatment for this lethal arrhythmia and its mechanism has been extensively investigated,2-7 how the shock succeeds or fails to terminate VF is not completely understood.8 Although it has been known for more than a century that a shock can initiate as well as terminate VF, it was not until the past few decades that it was hypothesized that the two events share the same mechanism.2,9-12 This hypothesis is known as the upper limit of vulnerability (ULV) hypothesis because it proposes that the mechanism of VF initiation by a shock during the vulnerable period of regular rhythm is the same as the mechanism of defibrillation failure by a shock of the same strength during VF. Although it is still debated, a number of investigators have used this hypothesis to study the effect of the shock on VF induction and to extrapolate the findings to defibrillation mechanisms.6,13,14 Electrical mapping studies that allow the investigator to record local activations from hundreds of sites on or in the heart simultaneously have compared activations occurring after defibrillation to those occurring after VF induction and have found that there is similarity of the activation pattern following defibrillation and VF induction shocks, thus providing supporting evidence that they share a similar mechanism.7,13,15