1.Citrate lyase, an acetyl enzyme which catalyzes the cleavage of citrate in two consecutive steps, the acyl exchange and acyl lyase reactions, on deacetylation yields inactivated enzyme. On treatment with iodoacetate, this is irreversibly converted to another inactivated lyase.2. Both inactivated lyase species are catalytically active in the presence of certain acyl-CoA derivatives such as acetyl-CoA or citryl-CoA. 3s-Citryl-CoA is cleaved stereospecifically to acetylCoA and oxaloacetate in this catalysis, and citrate, in the presence of acetyl-CoA, is cleaved to acetate and oxaloacetate.3. The acetyl group of acetyl-CoA however is liberated as acetate and the pro-S acetyl group of citrate is transformed to acetyl-CoA during the acetyl-CoA-dependent cleavage of citrate. This exchange reaction was demonstrated by isotopic experiments.4. Kinetic analysis of the reaction indicated the formation of an intermediate. This conclusion was substantiated by performing the acetyl-CoA-dependent cleavage of citrate in the presence of EDTA. The complexing agent inhibits the lyase activity of the enzyme and therefore leads to the accumulation of the intermediate, 38-citryl-CoA.5. The formation of 3s-citryl-CoA from acetyl-CoA and citrate in the presence of EDTA demonstrates the acyl exchange activity, the cleavage of this intermediate demonstrates the lyase activity of inactivated citrate lyase.6. Comparison of these results with the mechanism of action of native citrate Iyase led to the conclusion that the acetylated acyl carrier groups (enzyme-8-acetyl in citrate lyase ; CoA-8-acetyl on inactivated citrate lyase) are alike in both systems. This was supported by the demonstration of the presence of phosphopantetheine in the lyase.7. From these and other results, citrate lyase was characterized as a multienzyme complex. It was concluded that phosphopantetheine most likely represents the acyl-carrying group in this complex.The enzyme citrate lyase of molecular weight about 550 000 has been thoroughly investigated by use of physicochemical techniques [1, 21. Dissociation of the native enzyme was observed on incubation with EDTA or urea into catalytically inactive subunits from which the native enzyme complex could be partially reconstituted by rcaggregation under a variety of conditions, Virtually nothing was known however about the mechanism of action of this enzyme until =+ enzyme -X-acetyl + oxa1oaceta.b (3)The native complex exists in two states, the catalytically active enzyme which is acetylated (enzyme-X-COCH,) and the catalytically inactive enzyme which is not (enzyme-XH) [3]. Both forms are easily interconvertible. The active enzyme on

Ventricular tachycardias in coronary artery disease arise mostly from endocardial sites. However, little is known about the site of origin in other diseases. We present the case of an incessant, adenosine-sensitive ventricular tachycardia arising from the lateral wall of the left ventricle in a patient with mildly reduced left ventricular function. Intracardiac mapping suggested an epicardial origin, and the tachycardia was successfully ablated from a coronary sinus branch. After ablation, left ventricular function returned to normal. Transcoronary venous radiofrequency catheter ablation is a new approach for the treatment of ventricular tachycardia. Its value in the management of other types of ventricular tachycardia has yet to be determined.

Background-The defibrillation threshold (DFT) may be affected by biphasic shock duration (BSD), electrode configuration, and capacitance. The upper limit of vulnerability (ULV) may be used to estimate the DFT. For different lead configurations and phase 2 capacitances, we investigated in 18 pigs whether the use of ULV may predict waveforms with lowest DFT. Methods and Results-DFT and ULV were determined by up-down protocols for 10 BSDs. ULVs were measured by T-wave scanning during ventricular pacing (cycle length 500 ms). In protocol 1 (nϭ6), a pectoral "active can" was combined with an electrode in the superior vena cava as common cathode and a right ventricle electrode as anode (ACϩSVC). In protocol 2 and protocol 3 (nϭ6 each), only the "active can" was used as proximal electrode (AC). Capacitance was 150 F during both phases in protocol 1 and protocol 3 but 150 F (phase 1) and 300 F (phase 2) in protocol 2. ULV and DFT demonstrated a linear correlation in each protocol (rϭ0.78 to 0.84). Lowest DFTs were found at 10 ms for ACϩSVC and at 14 ms for AC (PϽ0.001). At optimal BSDs, voltage DFTs did not differ significantly between AC (527Ϯ57 V) and ACϩSVC (520Ϯ70 V). Switching capacitors for phase 2 in a way that reduced leading-edge voltage by 50% while doubling capacity did not change BSD for optimal voltage DFT but increased minimum DFT from 527Ϯ57 V to 653Ϯ133 V (Pϭ0.04). Conclusions-The BSD with lowest DFT is shorter for ACϩSVC than for AC. There is no significant difference in voltage DFT between both at optimal BSD. A lower phase 2 capacitance reduces DFTs irrespective of BSD. Because strength-duration curves for DFT and ULV correlate for different BSDs, lead systems, and phase 2 capacitances, ULV determination may allow the prediction of waveforms with lowest DFT. (Circulation. 1999;99:1516-1522.)

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(1) DFTs for biphasic shocks delivered by nonthoracotomy defibrillators are higher in the upright compared to the supine body position. (2) Differences remain significant 3 months after implantation. For both body positions, DFT decreases significantly from 1 week to 3 months after implantation. These findings have important implications for programming first shock energy to lower than maximal values or for development of devices with lower maximal stored energy.