If color Doppler imaging is to continue to evolve into a reliable clinical method to noninvasively evaluate regurgitant lesions, then its grading methods must be quantitated and calibrated under extreme hemodynamic conditions. A left heart pulse duplicator was used to provide a completely controllable system to study aortic incompetence jet morphologies as a function of hemodynamic extremes. The system was first used to calibrate the limits of resolution of color Doppler imaging. Next, to define which jet features reliably predict the defect size or the regurgitant fraction and which are primarily influenced by instantaneous hemodynamic variables, we measured the jets' maximal length, width, proximal width, and temporal pattern of color variance during independent variations in the heart rate, cardiac output, and pressure gradient across the incompetent valve. The proximal jet width (immediately below the valve plane) was the only reliable independent predictor of both the defect size and the regurgitant fraction. Jet depth accurately predicted peak velocity (quantitated by laser Doppler velocimetry); it reliably predicted the severity of incompetence only at a known pressure gradient across the valve. Large defects (5 mm) produced jets with maximal color variance in early diastole, whereas small defects produced pandiastolic variance. Circulation 75, No. 4, 837-846, 1987. QUANTIFICATION of native and prosthetic valvular incompetence has traditionally relied upon contrast angiography. Besides

P atients with atrial fibrillation (AF) may require electric cardioversion, either because of intolerable symptoms related to AF or as part of a rhythm control strategy. See Editorial by KotechaElectric cardioversion using a biphasic waveform has a procedural success rate of 86% to 94%, sometimes requiring multiple shocks.1-3 The success of electric cardioversion depends on the duration of AF, transthoracic impedance, delivered energy, and the type of electric shock used.1 Pharmacological cardioversion using antiarrhythmic drugs (AADs) has a lower success rate and may take a few hours to days to achieve sinus rhythm.Magnesium (Mg) is an abundant mineral in the body, present in bone, the heart, and the central nervous system. In the heart, Mg modulates potassium (slow-activating delayed rectifier K channel, I Ks ) and calcium channels (L-type) in both the atria and the ventricles. 4,5 Mg has been shown to have membrane-stabilizing properties within the atrium. 4 This membrane-stabilizing property may be particularly helpful in rhythm control of AF. Data from the Framingham offspring and Atherosclerosis Risk in Communities (ARIC) prospective cohorts have linked low serum Mg levels to AF. 6,7 Studies on pharmacological cardioversion have shown increased success of cardioversion when Mg is used along with an AAD. 8,9 A recent study on electric cardioversion showed that the infusion of a K-Mg electrolyte solution was successful in facilitating electric cardioversion of AF.3 On the basis of data suggesting an association of low Mg levels with the incidence of AF and the membrane-stabilizing property of Mg in the atrium with the modulation of I K+ and I Ca2+ currents, we postulated that administration of Mg alone would be useful in increasing the success of cardioversion. The purpose of this study was to investigate the benefit of intravenous © 2016 American Heart Association, Inc. Circ Arrhythm Electrophysiol

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The effect of administration of pirmenol, an extensively metabolized and plasma protein-bound antiarrhythmic agent, was evaluated in ten patients on chronic warfarin therapy. After a 3-week baseline period and 7 days of placebo administration, patients received 150 mg of oral pirmenol every 12 hours for 14 days. Prothrombin time was determined during the baseline and placebo periods, during pirmenol administration, and 14 days after the last pirmenol dose (washout). There was no significant difference between mean baseline, placebo, pirmenol, and washout prothrombin times. Coadministration of pirmenol does not appear to affect the anticoagulant activity of warfarin.