Richard Wu

Pulmonary vein anatomy in patients undergoing catheter ablation of atrial fibrillation: lessons learned by use of magnetic resonance imaging.

Background—This study sought to define the technique and results of magnetic resonance imaging (MRI) of pulmonary vein (PV) anatomy before and after catheter ablation of atrial fibrillation (AF). Methods and Results—Twenty-eight patients with AF underwent ablation. Patients underwent gadolinium-enhanced MRI before and 6 weeks after their procedures. A control group of 27 patients also underwent MRI. Variant PV anatomy was observed in 38% of patients. AF patients had larger PV diameters than control subjects, but no difference was observed in the size of the PV ostia among AF patients. The PV ostia were oblong in shape with an anteroposterior dimension less than the superoinferior dimension. The left PVs had a longer “neck” than the right PVs. A detectable PV narrowing was observed in 24% of veins. The severity of stenosis was severe in 1 vein (1.4%), moderate in 1 vein (1.4%), and mild in 15 veins (21.1%). All patients were asymptomatic, and none required treatment. Conclusions—This study demonstrates that AF patient have larger PVs than control subjects and demonstrates the value of MRI in facilitating AF ablation. The benefits of preprocedural MRI of PVs include the ability to evaluate the number, size, and shape of the PVs. MRI also provides an assessment of the severity of PV stenosis.

Role of the calcium-independent transient outward current I(to1) in shaping action potential morphology and duration

The Kv4.3-encoded current (IKv4.3) has been identified as the major component of the voltage-dependent Ca2+-independent transient outward current (Ito1) in human and canine ventricular cells. Experimental evidence supports a correlation between Ito1 density and prominence of the phase 1 notch; however, the role of Ito1 in modulating action potential duration (APD) remains unclear. To help resolve this role, Markov state models of the human and canine Kv4.3- and Kv1.4-encoded currents at 35°C are developed on the basis of experimental measurements. A model of canine Ito1 is formulated as the combination of these Kv4.3 and Kv1.4 currents and is incorporated into an existing canine ventricular myocyte model. Simulations demonstrate strong coupling between L-type Ca2+ current and IKv4.3 and predict a bimodal relationship between IKv4.3 density and APD whereby perturbations in IKv4.3 density may produce either prolongation or shortening of APD, depending on baseline Ito1 current level.

Regulation of Kv4.3 Current by KChIP2 Splice Variants A Component of Native Cardiac Ito

Background—The transient outward potassium current (Ito) encoded by the Kv4 family of potassium channels is important in the repolarization of cardiac myocytes. KChIPs are a recently identified group of Ca2+-binding accessory subunits that modulate Kv4-encoded currents. KChIP2 is the only family member expressed in the heart. Methods and Results—We previously cloned 2 novel splice variants of KChIP2 from human heart, named KChIP2S and KChIP2T. The transmural distribution of KChIP2 mRNA and protein in human and canine left ventricle was examined using kinetic RT-PCR and Western blots in the same tissues. A steep gradient of mRNA with greater KChIP2 expression in the epicardium was observed. However, no gradient of immunoreactive protein was observed. Immunocytochemistry reveals KChIP2 expression in the t-tubules and the nucleus. The predominant effects of all 3 KChIP2 splice variants on hKv4.3-encoded current are to increase the density, slow the current decay in a Ca2+-dependent manner, and hasten recovery from inactivation in a splice variant–specific fashion. Conclusions—A family of KChIP2 proteins is expressed in human hearts that exhibits differential modulation of hKv4.3 current in a Ca2+-dependent fashion. The effect of KChIP2 on the biophysical properties of expressed Kv4.3 current and the absence of a gradient of protein across the ventricular wall suggest that KChIP2 is either not a requisite component of human or canine ventricular Ito or that its functional effect is being affected or additionally modified by other factors present in myocardial cells.

Electrical and structural remodeling of the failing ventricle.

Heart failure (HF) is a complex disease that presents a major public health challenge to Western society. The prevalence of HF increases with age in the elderly population, and the societal disease burden will increase with prolongation of life expectancy. HF is initially characterized by an adaptive increase of neurohumoral activation to compensate for reduction of cardiac output. This leads to a combination of neurohumoral activation and mechanical stress in the failing heart that trigger a cascade of maladaptive electrical and structural events that impair both the systolic and diastolic function of the heart.

Catheter ablation of atrial flutter and macroreentrant atrial tachycardia

Catheter ablation has evolved from an experimental technique to first-line therapy for the treatment of atrial flutter. Atrial flutter is characterized by a macroreentrant atrial tachycardia circuit. Successful ablation of atrial flutter involves (1) mapping the atrial flutter to define the conduction zones within the re-entrant circuit to determine whether the atrial flutter is isthmus-dependent, non–isthmus-dependent, or atypical; (2) interrupting the atrial flutter macroreentrant circuit with an ablation catheter by creating either focal or linear lesions within a critical zone of slow conduction that extends to anatomical borders; and (3) terminating the tachycardia and demonstrating conduction block within the atrial flutter circuit after ablation. This update discusses the classification schemes of atrial flutter and macroreentrant atrial tachycardias, reviews the technique of radiofrequency catheter ablation, and highlights recent ablation approaches for atrial flutters and macroreentrant atrial tachycardias.

Not Just Another Notch

A 21-year-old woman without prior cardiac history presented to the emergency department with palpitations. On telemetry she was noted to have a paroxysmal supraventricular tachycardia with no discernible P waves. She was given 6 mg of intravenous adenosine with prompt conversion to normal sinus rhythm. Thirty minutes after termination of her arrhythmia, she was found to have the following ECG (Figure). What findings are present on this ECG? What conditions are associated with the findings present on this ECG? Please turn the page to read the diagnosis. The ECG shows sinus tachycardia at 128 bpm with right-axis deviation at 95° and incomplete right bundle-branch block. In leads III and aVF, a fragmented QRS complex is prominent (Figure 1). The ECG is an …