Echocardiographic markers for mitral valve surgery to preserve left ventricular performance in mitral regurgitation.

BACKGROUND: The timing of mitral valve (MV) surgery to preserve left ventricular (LV) contractility in patients with mitral regurgitation (MR) has been defined by complex cardiac catheterization techniques. Whether noninvasive methods can identify patients with MR, a normal LV ejection fraction, and early LV contractile impairment is unknown. We hypothesized that echocardiographic measures would separate patients with MR and a normal LV ejection fraction into those with and without contractile dysfunction and, thus, prospectively predict the response of LV size and performance to MV surgery. METHODS AND RESULTS: We studied 27 patients with micromanometer LV pressures and radionuclide angiography to obtain a determination of LV volumes and ejection fraction and calculate chamber elastance, a measure of LV contractility, before MV surgery. Echocardiographic studies were performed before MV surgery and repeated at 3 and 12 months after surgery. Age, New York Heart Association class, LV plus maximum pressure per unit change in time, LV systolic and end-diastolic pressures, and echocardiographic posterior wall thickness and radius to wall thickness ratio did not identify preoperative LV contractile dysfunction. However, other echocardiographic measures were related to LV contractility, including LV end-diastolic dimension (r = -0.50, P <.005), LV end-systolic dimension (r = -0.60, P <.0001), and LV fractional shortening (r = 0.50, P =.005). From analysis of receiver operator characteristic curves, an LV end-systolic dimension of >/=40 mm was identified as most predictive for separating patients with MR before surgery into those with and without LV contractile dysfunction (sensitivity of 82% and specificity of 100%). The patients with MR and impaired preoperative LV contractility showed a dramatic deterioration in LV fractional shortening at 3 months after MV surgery (P =.01), which recovered to within the normal range for fractional shortening at 12 months (P =.02) from a progressive reduction in LV end-systolic dimension. This response in LV size and performance temporally differed from that in the patients with MR and normal contractility (2-way analysis of variance P <.0001). However, at 12 months after MV surgery, LV end-diastolic dimension, end-systolic dimension, and fractional shortening were normal in both groups of patients with MR. CONCLUSION: We conclude that echocardiographic measures, particularly an end-systolic dimension of >/=40 mm, may be useful for identifying patients with MR before surgery with early, occult LV contractile dysfunction in whom MV surgery may be recommended to preserve LV systolic performance.

Electrocardiographic predictors of successful ablation of tachycardia or bigeminy arising in the right ventricular outflow tract.

Among various electrocardiographic variables, the QRS duration in V2 was found to be the best discriminator of outcome in patients undergoing radiofrequency catheter ablation of the right ventricular outflow tract tachycardia and/or bigeminy. If the QRS duration is <160 ms in lead V2, the probability of successful ablation is lower than if the QRS duration is longer.

Frequency- and voltage-dependent effects of disopyramide in canine Purkinje fibers.

The voltage- and frequency-dependent blocking actions of disopyramide were assessed in canine Purkinje fibers within the framework of concentrations, membrane potentials, and heart rates which have relevance to the therapeutic actions of this drug. Vmax was used to assess the magnitude of sodium channel block. Disopyramide produced a concentration- and rate-dependent increase in the magnitude and kinetics of Vmax depression. Effects on activation time (used as an estimate of drug effect on conduction) were exactly analogous to effects on Vmax. A concentration-dependent increase in tonic block was also observed. Despite significant increases in tonic block at more depolarized potentials, rate-dependent block increased only marginally with membrane potential over the range of potentials in which propagated action potentials occur. Increases in extracellular potassium concentration accentuated drug effect on Vmax but attenuated drug effect on action potential duration. Recovery from rate-dependent block followed two exponential processes with time constants of 689 +/- 535 ms and 15.7 +/- 2.7 s. The latter component represents dissociation of drug from its binding site and the former probably represents recovery from slow inactivation. A concentration-dependent increase in the amplitude of the first component suggested that disopyramide may promote slow inactivation. There was less than 5% recovery from block during intervals equivalent to clinical diastole. Thus, depression of beats of all degrees of prematurity was similar to that of basic drive beats. Prolongation of action potential duration by therapeutic concentrations of drug following a long quiescent interval was minimal. However, profound lengthening of action potential duration occurred following washout of drug effect at a time when Vmax depression had reverted to normal, suggesting that binding of disopyramide to potassium channels may not be readily reversed. Variable effects on action potential duration may thus be attributed to a block of the window current flowing during the action potential being partially or over balanced by block of potassium channels. Purkinje fiber refractoriness was prolonged in a frequency-dependent manner. Disopyramide did not significantly alter the effective refractory period of basic beats but did increase the effective refractory period of sequential tightly coupled extra stimuli. The results can account for the antiarrhythmic actions of disopyramide during a rapid tachycardia and prevention of its initiation by programmed electrical stimulation.