Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart.

Pogwizd, Steven M.; Hoyt, Robert; Saffitz, Jeffrey E.; Corr, Peter B.; Cox, James L.; Cain, Michael E.

doi:10.1161/01.cir.86.6.1872

Cited by 230 publications

(175 citation statements)

References 26 publications

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“…Reentry circuit isthmuses can be bordered by unexcitable scars that create conduction block. 5,6 Our study shows that VT reentry circuit isthmuses can be identified from delineation of electrically unexcitable scar defined by a high pacing threshold. RF ablation in these regions abolished inducible VT in 10 of 14 patients and abolished or markedly reduced spontaneous VT during follow-up.…”

Section: Discussionmentioning

confidence: 79%

“…3,4 In human hearts explanted many years after the infarction, extensive fibrosis creating areas of fixed conduction block is often present. 5,6 These observations suggest that reentry circuit isthmuses can potentially be defined during sinus rhythm by delineating the areas of dense, fibrous scar. How best to accomplish this task with catheter mapping has not been established.…”

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confidence: 99%

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Electrically Unexcitable Scar Mapping Based on Pacing Threshold for Identification of the Reentry Circuit Isthmus

et al. 2002

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Background-We hypothesized that delineating electrically unexcitable scar (EUS) within low-voltage infarct regions will locate reentry circuit isthmuses by defining their borders. The pacing threshold and electrogram amplitude that best determines EUS is unknown. Methods and Results-The change in dimension of the virtual electrode was estimated in 11 patients and observed to increase by 4.4Ϯ2.5 mm as stimulus strength increases from threshold (2.9Ϯ1.8 mA) to 10 mA. EUS was defined as a threshold Ͼ10 mA. In 14 consecutive patients, mapping and ablation of ventricular tachycardia (VT) were performed using an electroanatomic mapping system. During sinus rhythm, unipolar pacing was performed at sites with bipolar electrogram amplitude Ͻ1.5 mV. EUS regions were marked on the maps. Reentry circuit isthmuses were identified by entrainment mapping or pace mapping, and ablation was performed. EUS was identified in the infarct in all 14 patients (11.8Ϯ13.9 cm 2 ). All 20 VT circuit isthmuses identified were adjacent to EUS. Although electrogram amplitude correlated with pacing threshold (rϭ0.64, PϽ0.0001), many isthmuses had very low-amplitude electrograms, and EUS could not be identified from electrogram amplitude alone. RF ablation lines connecting selected EUS regions abolished all inducible VTs in 10 patients (71%); spontaneous VT was markedly reduced during follow-up (from 142Ϯ360 to 0.9Ϯ2.0 episodes per month, Pϭ0.002). Conclusions-This

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Section: Discussionmentioning

confidence: 79%

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confidence: 99%

Electrically Unexcitable Scar Mapping Based on Pacing Threshold for Identification of the Reentry Circuit Isthmus

et al. 2002

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“…10,[12][13][14] The abnormal variability in impulse velocity and potential substrate for reentrant circuits may be facilitated in hearts undergoing progressive dilation in which there is dynamic imbalance between distending forces and the stretch-resistant extracellular collagen scaffold during postinfarction LV remodeling. This propensity may be amplified by elevated plasma levels of adrenergic neurohormones after infarction.…”

Section: Discussionmentioning

confidence: 99%

“…6 -8 Although ventricular arrhythmias are common in patients with LV dysfunction and congestive heart failure, 9,10 the relation between LV remodeling and ventricular arrhythmias after acute myocardial infarction has not been explored systematically. 11 Ventricular tachycardia is believed to be due to anisotropic reentry, consequent on slowed impulse propagation velocities through myocardium partially replaced by fibrosis, 10,[12][13][14] which typifies postinfarction remodeling myocardium. In addition, activation of plasma neurohormones after infarction 15 provides a potential electrophysiological substrate for triggering ventricular arrhythmias.…”

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confidence: 99%

Left Ventricular Remodeling and Ventricular Arrhythmias After Myocardial Infarction

et al. 2003

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Background-The relation between left ventricular (LV) remodeling and ventricular arrhythmias after myocardial infarction is poorly documented. We investigated the relations between LV size, hypertrophy, and function and ventricular arrhythmias in 263 patients from the Survival and Ventricular Enlargement (SAVE) study, using quantitative 2D echocardiography and ambulatory ECG monitoring after myocardial infarction. Methods and Results-Transthoracic 2D echocardiograms and arrhythmia monitoring were performed at baseline (mean, 11 days) and 1 and 2 years after infarction. LV size, short-axis muscle (mass) area (LVMA), and function were quantified from 2D echocardiograms. The prevalence of ventricular tachycardia (VT) and frequent ventricular ectopy (premature ventricular contractions [PVCs] Ͼ10/h) was assessed from ambulatory ECG. VT and PVCs Ͼ10/h occurred in 20% and 29% of patients at baseline, in 22% and 35% at 1 year and 23% and 39% at 2 years, respectively. VT and PVCs Ͼ10/h at baseline and 1 and 2 years were significantly related to LV size, LVMA, and function. Furthermore, changes in LV size and function from baseline to 2 years predicted both VT and PVCs Ͼ10/h. The study was underpowered to detect treatment effect of ACE inhibitors and ␤-adrenergic receptor blockers but did not alter the relations between ventricular arrhythmias, LV size, and function. Conclusions-Quantitative echocardiographic assessment of LV size, LVMA, and function and changes in these measurements over time predict ventricular arrhythmias after infarction. Altered LV architecture and function during postinfarction LV remodeling provide an important substrate for triggering high-grade ventricular arrhythmias.

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“…15 Myocardial scar-based reentry accounts for only half of the mechanisms of ventricular arrhythmias in patients with nonischemic cardiomyopathy, with the rest having focal initiation of ventricular tachycardia from triggered activity with early afterdepolarizations and delayed afterdepolarizations. 16 Irrespective of the HF cause, patients with advanced HF (stage D) have a different distribution of arrhythmias that may be triggered primarily by pump failure. One series showed that 62% of such patients had severe bradycardia or electromechanical dissociation as the underlying cause for their SCD and only 38% had ventricular tachycardia/ventricular fibrillation.…”

Section: Pathophysiologymentioning

confidence: 99%

Sudden Cardiac Death in Heart Failure

Klein¹,

Hsia²

2014

Cardiology Clinics

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Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart.

Abstract: Both intramural reentry and a focal mechanism underlie sustained VT in patients with healed myocardial infarction.

Cited by 230 publications

References 26 publications

Electrically Unexcitable Scar Mapping Based on Pacing Threshold for Identification of the Reentry Circuit Isthmus

Electrically Unexcitable Scar Mapping Based on Pacing Threshold for Identification of the Reentry Circuit Isthmus

Left Ventricular Remodeling and Ventricular Arrhythmias After Myocardial Infarction

Sudden Cardiac Death in Heart Failure

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