Septal Activation in Patients with LBBB and Heart Failure. Introduction: Little is known about the septal activation pattern in patients with heart failure and left bundle branch block (LBBB‐HF). Methods and Results: The right ventricular (RV) and left ventricular (LV) activation patterns of 12 patients (mean age 67 ± 11 years) with LBBB‐HF and 5 patients (mean age 45 ± 14) with normal hearts were studied during sinus rhythm using a three‐dimensional mapping system. The etiology of HF was myocardial infarction (n = 4) or idiopathic dilated cardiomyopathy (n = 8). In patients with LBBB‐HF, endocardial activation usually started before the onset of the surface QRS complex on the RV free wall. Latest RV activation occurred in the basal region, and total RV activation time was longer than in patients with normal hearts. In patients with LBBB‐HF, the left septum was activated via slowly conducting LBB or via right‐to‐left transseptal conduction. In both patients with LBBB‐HF and those with normal hearts, latest LV activation occurred either in the posterior or posterolateral‐basal region. Conduction velocity was slower in the peri‐scar region, in patients with previous myocardial infarct and globally slow, in patients with idiopathic dilated cardiomyopathy. Conclusion: The two types of left septal activation observed in patients with LBBB‐HF may have consequences for biventricular hemodynamic performance. Conduction slowing along the LV, regionally or globally, suggests a contribution outside the specific conduction system in the ECG pattern of LBBB. (J Cardiovasc Electrophysiol, Vol. 14, pp. 135‐141, February 2003)

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Background-The aim of this study was to determine the biatrial activation pattern in isthmus-dependent atrial flutter (AFL) to understand the functional interatrial connections and the activation pattern of the left atrium (LA). Methods and Results-Biatrial activation was performed, using an electroanatomic mapping system, in 10 patients undergoing right atrial isthmus ablation for counterclockwise (nϭ7) or clockwise (nϭ3) AFL. The AFL circuit was peritricuspid and propagated slowly (0.5Ϯ0.2 m/s) through the isthmus. LA was activated by two wave fronts, with discrete breakthroughs in the superior, mid, or inferior atrial septum. The activation of LA overlapped 50Ϯ16% of the AFL cycle length. In counterclockwise AFL, at least one breakthrough was located in the inferior atrial septum. LA activation began immediately after the exit of the flutter wave from the isthmus and was directed inferosuperiorly in all patients, being synchronous with the atrial septal activation. The septal breakthroughs in patients with clockwise AFL were variably located. The direction of LA activation was superoinferior in 2 and inferosuperior in 1 patient. Conclusions-The circuit of isthmus-dependent AFL was entirely in the right atrium. LA activation was a bystander and followed trans-septal conduction across the inferior coronary sinus-LA connection, Bachmann's bundle, and/or fossa ovalis. (Circulation. 2001;104:2545-2550.)

Objectives: Electrical remodeling in cardiac hypertrophy often involves the downregulation of K + currents, including β-adrenergic (β-A)-sensitive I Ks . Temporal patterns of ion-channel downregulation are poorly resolved. In dogs with complete atrioventricular block (AVB), we examined (1) the time course of molecular alterations underlying I Ks downregulation from acute to chronic hypertrophy; and (2) concomitant changing responses of repolarization to β-adrenergic receptor (β-AR) stimulation. Methods and Results: Serial left-ventricular (LV) biopsies were collected from anesthetized dogs during sinus rhythm (SR; control) and at 3, 7 and 30 days of AVB. KCNQ1 mRNA and protein decreased within 3 days (protein expression 58 ± 10% of control), remaining low thereafter. β1-AR mRNA and protein decreased more gradually to 53 ± 8% at 7 days. In chronic-AVB LV myocytes, I Ks -tail density was reduced: 1.4 ± 0.3 pA/pF versus 2.6 ± 0.4 pA/pF in controls. β-A enhancement of I Ks was reduced. Isoproterenol shortened action-potential duration in control cells, while causing heterogeneous repolarization responses in chronic AVB. β-A early afterdepolarizations were induced in 4 of 13 chronic-AVB cells, but not in controls. In intact conscious dogs, isoproterenol shortened QT c at SR (by −8 ± 3% from 295 ms), left it unaltered at 3 days AVB (+1 ± 3% from 325 ms) and prolonged QT c at 30 days (+ 6 ± 3% from 365 ms). Conclusions: Profound decrease of KCNQ1 occurs within days after AVB induction and is followed by a more gradual decrease of β1-AR expression. Downregulation and blunted β-A activation of I Ks contribute to the loss of β-A-induced shortening of ventricular repolarization, favoring proarrhythmia. Provocation testing with isoproterenol identifies repolarization instability based on acquired channelopathy.

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