Beneficial effect of dual-chamber pacing for a left mid-ventricular obstruction with apical aneurysm.

Sustained ventricular tachycardia (VT) developed in a 63-year-old woman. The 2-dimensional echocardiogram revealed left mid-ventricular obstructive hypertrophy and a discrete apical chamber. A continuous wave Doppler signal across the mid-ventricular narrowing exhibited early systolic ejection flow and diastolic paradoxical jet flow from the apex to the basal chamber, implying a significant systolic and diastolic intraventricular gradient with a high apical pressure. The left ventriculogram confirmed a mid-ventricular obstruction with an apical aneurysm. Invasive assessment of intraventricular pressure showed a peak-to-peak gradient greater than 100 mmHg. Treatment with antiarrhythmic agents could not prevent the VT, but dual-chamber pacing reduced the intraventricular pressure gradient and suppressed the VT completely. Continuous wave Doppler showed that the early systolic ejection flow from the apex had disappeared, that there was isovolumetric relaxation flow toward the apex and that there was attenuation of the diastolic paradoxical jet flow toward the basal chamber. Such findings by continuous wave Doppler can be useful in pacing therapy for evaluating changes in the severity of mid-ventricular obstruction.

Ca2+ overload evokes a transient outward current in guinea-pig ventricular myocytes.

There are 2 types of transient outward currents (Ito) in the hearts of various mammals: a 4-aminopyridine (4-AP) sensitive K+ current and a 4-AP resistant Ca2+ activated current, carried by Cl-, (referred to as I(to1) and I(to2), respectively). However, the I(to) has been considered to be absent in guinea-pig ventricular myocytes and so this study tested the hypothesis that I(to1) is generally absent in guinea-pig ventricular myocytes, but I(to2) appears under the condition of Ca2+ overload. Membrane currents were recorded by the whole-cell patch-clamp technique and Ca2+ overload was achieved by adding internal, and eliminating external, Na+ with subsequent enhancement of Ca2+ influx via the Na+-Ca2+ exchange. Under physiological conditions, I(to) could not be elicited by 300 ms-test pulse from -70 mV to 0 mV (n=32). However, under Ca2+ overload, a biphasic current resulting from the overlap of the L-type Ca2+ channel current and Ito was elicited (n=38). This I(to) was resistant to 4-AP (3 mmol/L, n=30) but sensitive to both anthrancene-9-carboxylic acid (9-AC, 3 mmol/L, n=8) and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (100 micromol/L, n=3). Replacing K+ with Cs+ on both sides of the membrane failed to abolish I(to) (n=38). I(to) disappeared by lowering the external Cl- (n=3). The amplitude of I(to) was dependent on that of the L-type Ca2+ channel current (n=4). Because Ca2+ release from the sarcoplasmic reticulum was prevented by caffeine (5 mmol/L), I(to) was negligible (n=6). These results suggest that I(to1) is absent, but Ca2+ overload evokes I(to2) in guinea-pig ventricular myocytes.