Abstract: OBJECTIVE: The purpose of this study was to determine whether sinus rhythm activation maps could be used to detect the origin and characteristics of reentrant ventricular tachycardia in postinfarction patients. METHODS: In each of 11 post-myocardial infarction patients, unipolar electrograms were acquired at 256 virtual endocardial sites using noncontact mapping. Electrograms were marked for activation time and mapped on a three-dimensional grid. Spatial differences in sinus rhythm activation time were correlated to isthmus characteristics and to activation through the diastolic pathway during tachycardia on the basis of the presence of contiguous lines of slow conduction and block. RESULTS: Twenty tachycardia morphologies were analyzed. Fourteen sustained reentrant circuit morphologies occurred in nine patients, with dual morphologies having a shared isthmus occurring in five of nine patients. Dual morphologies were caused by changes in entrance-exit point location about a common isthmus. One transient circuit morphology of <10 beats occurred in three of nine patients also having sustained reentry. The estimated isthmus determined from sinus rhythm activation overlapped the diastolic pathway determined from tachycardia maps with 83.8% sensitivity and 89.2% specificity. The mean difference in sinus rhythm activation time across the isthmus border was larger in transient compared with sustained morphologies (32.8 +/- 9.5 ms vs. 22.8 +/- 1.8 ms), with smaller isthmus size (4.8 +/- 1.1 cm(2) vs. 10.0 +/- 1.1 cm(2); P < .05), narrower entrance-exit points (7.0 +/- 1.5 mm vs. 9.3 +/- 0.8 mm; P < .05), and greater activation time difference across them (16.3 +/- 3.5 ms vs. 10.1 +/- 1.0 ms; P < .05). CONCLUSION: In post-myocardial infarction patients, the reentry isthmus can be localized in the endocardial border zone from sinus rhythm activation maps. Nonsustained reentry occurs when isthmus size is small and entrance-exit points are narrow and more electrically discontinuous.
Abstract: INTRODUCTION: Characteristics of the 12-lead ECG during VT are used to guide initial placement of mapping catheters in endocardial ventricular tachycardia (VT) ablation. Previously constructed algorithms for guidance in human infarct-related VT are limited to patients known to have anterior or inferior infarcts only. We hypothesized that 12-lead ECG characteristics could be used to determine VT exit site in patients with all types of infarction of unknown location. METHODS AND RESULTS: From noncontact activation maps of 121 LV VT in 51 patients undergoing catheter ablation, VT exit sites were determined and correlated with ECG characteristics according to bundle branch block configuration, limb lead polarity and patterns of precordial R-wave transition. Eight ECG patterns were identified that accounted for 71% of all VT and gave a positive predictive value (PPV) > or =70% using the first two criteria. No correlation was found with patterns of R-wave transition. Using these criteria an algorithm was developed, which was then applied prospectively and blinded to a further 17 VT in 11 patients. Of the 15 VT (88%) to which the algorithm predicted an exit site location (with a PPV > or =70%), 14 VT (93%) were correctly predicted by the algorithm. CONCLUSION: This algorithm can be used to predict endocardial LV VT exit site location in patients undergoing catheter ablation of VT without knowledge of or reference to infarct location, and can be applied to patients with posterior and/or multiple sites of infarction.
Abstract: OBJECTIVES: The purpose of this study was to examine the resetting response in human ventricular tachycardia (VT) circuits with 3-dimensional mapping. BACKGROUND: In characterizing re-entry with the resetting response, inferences are made about interaction of single ventricular extrastimuli (SVE) with VT. METHODS: Non-contact mapping was used to examine the effects of SVE from 25 sites on 10 infarct-related VT circuits. RESULTS: The local temporal excitable gap (EGap) was 113.8 +/- 64.3 ms, 25.8 +/- 11.2% of VT cycle length. In 7 VT circuits there was a clear difference in the EGap at different points in the circuit. All circuits could be pre-excited over a range of SVEs, resulting in either: 1) premature activation throughout the circuit resulting in reset; 2) premature activation at entry, but subsequent interval dependent conduction slowing (IDCS) resulting in a fully compensatory return cycle; or 3) change to functional lines of block and return cycle QRS morphology. The principal determinant of whether SVE resulted in reset was the degree of IDCS within the diastolic pathway (DP) of the circuit. Resetting occurred from 9 sites (7 VT) but was absent from 15 sites despite pre-excitation of a sizeable EGap in the circuit in all cases. CONCLUSIONS: In infarct-related VT, all circuits can be pre-excited over a range of SVEs, the effect of which is dependent on the degree of IDCS within the DP or modification of functional block defining the circuit. Failure to reset does not therefore indicate the absence of an EGap or failure of entry to the circuit. The temporal and spatial properties of the EGap vary at different sites of entry to the circuit.
Abstract: HYPOTHESIS: Endocardial catheter ablation of ventricular tachycardia (VT) may fail if originating from epicardial or intramural locations. We hypothesized that mapping could be achieved using an angioplasty guidewire in the coronary circulation, to guide trans-coronary ablation. METHODS AND RESULTS: Six patients (2 male), 64 +/- 14 years and previously unsuccessful endocardial VT ablation were studied. Using ECG and existing endocardial mapping data, a coronary artery supplying the predicted VT origin was selected. A 0.014-in angioplasty guidewire was advanced into branches of the artery and connected to an amplifier to record unipolar signals against an indifferent electrode within the inferior vena cava. An uninflated angioplasty balloon was advanced over the wire such that only the distal 5 mm was used for mapping. One VT per patient was mapped (CL 348 +/- 102.1 ms). Diastolic potentials were recorded from all (77.7 +/- 43.8 ms pre-QRS onset) and concealed entrainment demonstrated in 3. Pacemapping during sinus rhythm was used in the remainder due to failure of entrainment (n = 2) or degeneration to VF (n = 1). Following branch identification, cold saline injection causing VT termination was used for further confirmation. Five VTs were ablated using intra-coronary ethanol injection via the central lumen of the inflated over the wire balloon. The other was ablated using radiofrequency energy in a coronary vein adjacent to the target artery, which was too small for an angioplasty balloon. No complications or recurrence of ablated VT was seen over 19 +/- 17 months of follow up. CONCLUSIONS: Intracoronary guidewire mapping is a novel method of electrophysiological epicardial mapping to help guide trans-coronary VT ablation.
Abstract: OBJECTIVES: This study assessed the effects of carbenoxolone on human myocardial conduction and refractoriness. BACKGROUND: Carbenoxolone, an antipeptic ulcer drug, has been shown to reduce gap junctional coupling without affecting cellular ion channels. Gap junctions (GJ) are considered to be determinants of cardiac action potential propagation. The effects of GJ uncoupling in the human heart are unknown. METHODS: Right atrial (RA) and ventricular (RV) activation mapping (Carto, Biosense Webster Inc., Diamond Bar, California) was performed during sinus rhythm. Right atrial and RV wavefront propagation velocity (WPV), specifically in the direction of propagation, was determined from these maps using a triangulation method. Refractoriness at multiple RA and RV sites, sinus rhythm cycle length, and AH, PR, QRS, and QT intervals were measured. The protocol was repeated 1 h after oral administration of 100 mg of carbenoxolone. RESULTS: In 11 patients, WPV was reduced from 79.6 +/- 13.3 cm/s to 57.2 +/- 9.1 cm/s (-27.1 +/- 12.8%, p < 0.001) in RA and from 98.7 +/- 19.8 cm/s to 76.5 +/- 21.7 cm/s (-22.7 +/- 14.1%, p < 0.01) in RV after carbenoxolone. Conduction slowing was more marked in 6 older patients with ischemic heart disease compared with younger subjects with normal hearts (RA -35.1 +/- 5.5% vs. -17.5 +/- 12.7%, p = 0.03; RV -33.8 +/- 5.1% vs. -9.3 +/- 7.7%, p < 0.001). Refractoriness and electrocardiogram parameters remained unchanged. CONCLUSIONS: Carbenoxolone causes a 27% reduction in human RA WPV and 23% in the RV without affecting refractoriness. The slowing of myocardial conduction by carbenoxolone demonstrates the significance of GJ in regulating human myocardial conduction and provides a tool for investigating the effects of GJ uncoupling on human arrhythmogenesis.
Abstract: OBJECTIVES: The purpose of this study was to assess the long-term effects of ablation of infarct-related ventricular tachycardia (VT) and the subsequent requirement for implantable cardioverter-defibrillator (ICD) therapy. BACKGROUND: The long-term consequences after initially successful catheter ablation of infarct-related VT remain unclear. METHODS: Forty patients who presented with infarct-related VT were studied using noncontact mapping to guide ablation. RESULTS: One hundred forty VTs were mapped using the noncontact mapping system, including 36 (25.7%) clinical VTs. An endocardial exit site was determined in 100% of VT circuits, diastolic endocardial activity in 77 VTs (55%), and complete circuits in 24 VTs (17.1%). Eighty-one VTs (57.9%) were targeted for ablation, of which 67 (82.7% of targeted) were successfully ablated, including 27 clinical VTs (75% of clinical). Documented recurrence of an ablated VT occurred in 7.5% of patients over 36.3 +/- 21.0 months of follow-up. Episodes of new or recurrent, nontargeted VT or ventricular fibrillation (VF) occurred in 37.5% and VT recurrence without documentation of cycle length in 5%. In patients with ICDs, mean shock frequency was reduced from 6.8 +/- 7.3 per month in the year prior to ablation to 0.05 +/- 0.12 per month after ablation, over 24.7 +/- 18.9 months of follow-up (P < .0001). CONCLUSIONS: In patients with infarct-related VT, noncontact mapping-guided VT ablation is associated with a high procedural success rate, and VT recurrence necessitating ICD therapy delivery is significantly reduced. However, only 42.5% of patients remain free from VT/VF 3 years after ablation. Catheter ablation for infarct-related VT is indicated as an adjunctive therapy in patients with symptomatic VT but cannot substitute for ICDs and antiarrhythmic drugs.
Abstract: BACKGROUND: The mechanisms by which ventricular fibrillation (VF) is initiated in the infarcted human heart have not been defined. METHODS AND RESULTS: Left ventricular noncontact mapping of 8 episodes of pacing-induced VF in 6 patients (age 64.8+/-7.9 years, with previous myocardial infraction and left ventricular ejection fraction of 36+/-4%) undergoing ventricular tachycardia (VT) ablation revealed a consistent mechanism of VF induction. Whether during VT or sinus rhythm, the first of a train of paced extrastimuli to capture the LV produced an arc or arcs of functional block at regions bordering scar. With subsequent extrastimuli, the arcs elongated to circumscribe an enlarging area of increasingly late activation, with reentry through part of this functional (unidirectional) block leading to wavefront fragmentation and VF. These regions had longer fibrillation intervals (263+/-63 ms) than remote LV regions (209+/-23.4 ms; P<0.0001), implying longer refractory periods, and in 6 of the 8 VF episodes, these regions correlated with VT exit sites. In each of the 2 patients with 2 episodes of VF, both episodes formed arcs of functional block in the same location, despite pacing from different sites. CONCLUSIONS: Pacing-induced VF in the infarcted human heart is initiated by the development of functional lines of block dictated by the properties of a particular region of myocardium characterized by longer refractory periods, at or near VT circuit exit sites. Identification of these characteristic properties may help stratify risk of arrhythmic death and explain the potential for VT ablation to modify risk of VF in the infarcted heart.
Abstract: Noncontact mapping identified the endocardial origins of four distinct atrial tachycardias in a young patient with drug refractory palpitations and effected successful ablation with no recurrence of symptoms in 5 months of follow-up.
Abstract: The use of the antiplatelet agents abciximab and clopidogrel is now accepted therapy in percutaneous coronary intervention. We present a case in which these agents were used in a patient with idiopathic thrombocytopaenic purpura and a platelet count of 40x10(9)/l undergoing primary multivessel coronary stenting. This case shows that unstable coronary syndromes can occur in patients with thrombocytopaenia and that antiplatelet agents may be used safely in this context.
