Catheter ablation of ventricular tachycardia in coronary artery disease is feasible in patients with one configuration of monomorphic sustained ventricular tachycardia. There is no significant difference with respect to the type of energy applied. The follow-up data show that in a selected group of patients with coronary artery disease, catheter ablation offers a therapy alternative.

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Strategic electroanatomic mapping with fast identification of the area of tachycardia origin and high density mapping only of this target area allowed fast and successful localization and ablation of right and left free wall and septal ectopic atrial foci.

Objective-To amplify the description of myocardial stunning. Design-Control versus 30 min after a 20 min no flow ischaemia. Experimental animals-i 5 isolated rabbit hearts perfused with erythrocyte suspension. Main outcome measures-Left ventricular systolic function in terms of aortic flow, peak systolic pressure (LVPmax), dP/dtmax, and the end systolic pressurevolume relation (ESPVR); early relaxation from dP/dtmin and rate of left ventricular pressure decay (T). Passive properties: ventricular and myocardial stiffness. Coronary resistance from coronary blood flow and perfusion pressure. Total myocardial oxygen consumption (MVo,tot). Total mechanical energy via pressure-volume area (PVA). Contractile efficiency (Econ) and MVo, of the unloaded contracting heart (MVo2unl).External mechanical efficiency (Eext) from stroke work and MVo2tot.Results-Systolic variables in stunned myocardium were significantly decreased (mean (SD)): aortic flow: 38 (13) v 9 (11) mllmin; LVPmax: 112 (19) 138 (73) v 125 (58) mm Hg/ml, but the volume axis intercept was shifted rightward: 0 30 (0.37) v 0*65 (0.25) ml. Likewise, early relaxation was impaired: dP/dtmin (-1275 (250) v -975 (250) mm Hg/s) and T (37 (7) v 46 (10) ms). LVPed was significantly decreased at 19 (12) v 12 (7) mm Hg, and both the ventricular (end diastolic pressure-volume relation) and the myocardial stiffness (constant k) were increased by 75% and 31%, respectively. Coronary resistance increased non-significantly from 0-83 (0.31) to 1.04 (0.41) mm HgI(mlnmin/100 g). Decreases in PVA (570 (280) v 270 (200) mm Hgnml/100 g), MVo2tot (40 (9) v 34 (8) ulIbeat/100 g), and MVo,unl (26 (9) v 22 (6),uIIbeat/100 g) did not reach significance, in contrast to significant decreases in Econ (31 (18) Conclusions-Ventricular systolic function is decreased after brief episodes of ischaemia. The decrease in diastolic function probably amplifies the systolic deterioration during myocardial stunning. Passive diastolic properties are also changed, shown by increases in both ventricular and myocardial stiffness. The increase in coronary resistance indicates stunning at the vascular level which could limit oxygen supply. With maintained MVo,tot during stunning, external efficiency is decreased. Possible candidates for this metabolic stunning are inadequate excitation-contraction coupling and disturbed 02 utilisation by the contractile apparatus. (Heart 1996;75:55-61) Keywords: stunning; coronary resistance; efficiency; isolated heart After brief periods of ischaemia, myocardial function remains depressed for hours or even days. This is known as myocardial stunning.1 2 Although there are many published reports on myocardial stunning,3-5 the phenomenon is far from completely understood. Many of the studies focus only on systolic properties6-8 as one aspect of that particular myocardial state.Depending on the duration and severity of the ischaemic insult, postischaemic myocardium can become entirely2 or almost entirely akinetic.910 In the present study, we reve...

1 This study was performed to investigate whether cardiac positive inotropic as well as peripheral vasodilator properties of adibendan contribute to its overall haemodynamic profile in conscious dogs. 2 Haemodynamic measurements were carried out in conscious chronically instrumented dogs after administration of adibendan, sodium nitroprusside or dobutamine. 3 The cardiovascular changes induced by adibendan (0.01 and 0.03mg kg-1) resembled those of dobutamine (1.0-4.0Ogkg1 min -): left ventricular dP/dt60 (LV dP/dt60), stroke volume (SV) and cardiac output (CO) increased to a similar extent, but mean arterial pressure (MAP) and heart rate (HR) remained unchanged. 4 In contrast to dobutamine, higher doses of adibendan (0.1-1.Omgkg-) decreased MAP and LVEDP. These effects were of a similar magnitude to those observed following nitroprusside administration (0.5-12.5 ug kg1 min 1). In contrast to nitroprusside, adibendan still showed additional effects on LV dP/dt60 and CO. 5From these results, it is concluded that both the peripheral vasodilator and the cardiac positive inotropic action of adibendan contribute to its overall haemodynamic profile.