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This report describes a patient in whom a MRI of the brain was performed without realizing that an ICD had been implanted 8 days previously. Electromagnetic noise induced during the MRI was detected as ventricular fibrillation and nearly caused inappropriate shocks. Charge time during MRI was prolonged. The battery indicator switched to "end of life," but this was reversed by capacitor reformation. These problems could have been avoided by inactivating the ICD prior to MRI. Three months later, the pacing threshold increased from 0.4 V per 0.5 ms at implantation to 2.8 V per 0.5. It is still uncertain whether radiofrequency current heating at the electrode tip caused the increased pacing threshold or if this would have occurred independently of the MRI. MRI of patients with an active ICD may cause life-threatening complications, and it is unknown if MRI may be safely performed if the ICD is inactivated. Therefore, MRI of patients with an ICD remains contraindicated.

RF catheter ablation is complicated by thromboembolism in about 1% of patients. Limited knowledge exists concerning when and how to use anticoagulation or antithrombotic treatment. We studied the activation of coagulation (prothrombin fragment 1 + 2 [PF1 + 2] and D-dimer), platelets (beta-thromboglobulin [beta-TG]) and fibrinolysis (plasmin-antiplasmin complexes [PAP]) during RF ablation of accessory pathways in 30 patients. They were randomized to receive heparin (100 IU/kg, intravenously) (1) immediately after introduction of the femoral venous sheaths (group I) or (2) after the initial electrophysiological study, prior to the delivery of RF current (groups II and III). Group II additionally received saline irrigation of all femoral sheaths. After the initial bolus, 1,000 IU of heparin was supplied hourly in all groups. Within groups II and III, median plasma values of PF1 + 2 and beta-TG more than tripled (P < or = 0.007) during the diagnostic study and gradually declined during heparin administration despite RF current delivery. Median D-dimer tripled (P = 0.005) and PAP doubled (NS) before heparin administration; then both remained around the upper reference values. In the early heparin group, however, PF1 + 2, D-dimer, and PAP did not rise at all, and beta-TG showed only a slight increase towards the end of the procedure. The differences between group I versus groups II and III were statistically significant prior to the first RF current delivery (PF1 + 2, D-dimer, and beta-TG) and by the end of the procedure (PF1 + 2, D-dimer, and PAP). In conclusion, "late" heparin administration allows hemostatic activation during the initial catheterization and diagnostic study. By administering intravenous heparin immediately after introduction of the venous sheaths, hemostatic activation is significantly decreased. Saline irrigation of the venous sheaths added nothing to late heparin administration.

Interruption of atrial flutter and fibrillation by RF catheter ablation may be favored by large, elongated lesions. We administered RF current in unipolar and bipolar mode in porcine right atrium. Bipolar ablation was performed between the tip electrodes of two serially coupled catheters. With 4-mm tip electrodes in vitro, lesion length increased from a mean (SD) of 7.9 (1.2) mm at 3 mm-interelectrode distance (i.e.d.) to 13.3 (3.3) mm at 9-mm IED, but decreased at 12-mm IED due to nonconfluent lesions (P < 0.0001). With 4 mm distal electrodes and 8 mm IED, bipolar lesions were 65% longer than corresponding unipolar ablations. Switching to bipolar mode increased the lesion length more than increasing electrode tip length to 6 mm in unipolar mode. Power and temperature controlled ablation created equally sized lesions. Twelve anesthetized pigs were randomized to unipolar or two catheter bipolar temperature controlled ablation of the right atrial free wall. Bipolar ablation created confluent lesions with endocardial length x width of 13.5 (5.8) x 7.3 (3.7) mm, unipolar ablation 6.4 (2.8) x 4.6 (1.4) mm (P < 0.001 when comparing length and P = 0.013 for lesion width). The atrial lesions in both groups were transmural and extended into hilar lung lesions with maximal depth of 3.0 (1.1) and 2.6 (1.0) mm, respectively (P = 0.44). Five bipolarly and four unipolarly ablated pigs developed right diaphragmal paresis. We conclude that bipolar ablation may be preferable in situations where large, elongated lesions are favorable. The two catheter technique is feasible in porcine right atrium. Both bipolar and unipolar ablation of the porcine right atrial free wall may frequently be complicated by injury to the phrenic nerve and adjacent lung tissue.

Temperature monitoring during RF ablation has been proposed as a means of controlling the creation of the lesion. However, in vivo studies have shown poor correlation between lesion size and catheter tip temperature. Thus, we hypothesized a difference between catheter tip and tissue temperatures during RF catheter ablation, and that this difference may depend on flow passing the ablation site, tip electrode length, and catheter-tissue orientation. In vitro studies were performed using four different ablation catheters (tip electrode length: 2, 4, or 6 mm) with a thermistor or a thermocouple as temperature sensor. Set temperature was 70 degrees C and pulse duration was 30 seconds. Pieces of porcine left ventricle were immersed in a bath of isotonic saline-dextrose solution at 37 degrees C. The ablation catheters were positioned perpendicularly, obliquely, or parallel to the endocardium. A temperature sensor was inserted from the epicardial side and positioned 1 mm beneath the catheter-tissue interface. Experiments were made with a flow of 200 mL/min passing the ablation site or with no flow. The catheter tip and tissue temperatures differed significantly (P < 0.0001) during ablation. This difference increased with time, with flow passing the ablation site, with the length of the tip electrode, and when the catheter was positioned perpendicularly or obliquely to the endocardium as compared to the parallel catheter-tissue orientation (P < 0.05). In conclusion, the tissue temperature may far exceed the catheter tip temperature, and intramyocardial superheating resulting in steam formation and popping may occur despite a relatively low catheter tip temperature.

The aim of the present study was twofold: to assess the safety of ablating the atrial free wall using RF current; and to assess the effect of a single dose of intravenous heparin followed by aspirin once daily to prevent thrombus formation after RF ablation. Temperature and power guided catheter ablation were evaluated. Twenty pigs were randomized to power or temperature guided unipolar RF catheter ablation. Ten animals received a bolus of heparin (150 U/kg) followed by 150-mg aspirin daily, and ten served as controls. A mid-sternal thoracotomy was performed 5-7 days later. The ability of a lesion to resist an increased transmural atrial pressure was examined by inflating a cuff around the pulmonal artery. Transmural lesions were found in all animals. Right atrial pressure was increased from 5 to 30 mmHg with no sign of perforation. In 11 of 20 (55%) animals, 1-3 lesions were found in the lungs (diameter 4-18 mm). The localization of these lesions corresponded to the lesions in the atria. There were no differences in the energy delivery modes with regard to the number of animals with lung lesions. Lesions with thrombus formation were found in four animals in the heparin/aspirin group and in nine animals in the control group. The incidence of thrombi was significantly smaller in the treatment group. There were no differences between temperature and power guided catheter ablation with regard to the size of the atrial lesions or to the incidence of thrombus formation. Transmural lesions induced in the right atrium by RF energy are resistant to increases in transmural pressure. However, lung tissue overlying the ablated target may be injured by the RF energy delivered. The combination of a single dose intravenous heparin followed by aspirin daily may reduce the incidence of thrombus formation.

Monophasic action potentials (MAP) were obtained from the outflow tract of the right ventricle during apical pacing in 20 patients with coronary artery disease. The electrical restitution was studied by interpolation of extrasystoles with various coupling intervals to the preceding steady-state beat at basic paced cycle lengths (CL) of 700, 600, and 500 msec. At higher frequencies the ventricular effective refractory periods (V-ERP) and duration of MAPs became shorter and the electrical restitution curves were displaced downwards (P less than 0.001). With increasing diastolic intervals preceding the extrasystole up to a maximum of 100 msec, the duration of premature MAPs increased at all frequencies. An obvious hump of the electrical restitution curve was observed at coupling intervals of 100 msec due to a later transient decrease (P less than 0.01) in duration of MAPs at the basic CL of 500 msec. No significant hump was observed at lower heart rates. Thus, a different time course of the electrical restitution was observed at various CLs. The intraventricular conduction intervals were shorter at the shorter basic CLs when compared to the 700 msec cycles (P less than 0.05). The conduction intervals were also modified by the coupling interval between the interpolated stimulus and the preceding steady-state action potential (AP). The premature beats elicited 30 msec or earlier after refractoriness were conducted more slowly at all basic cycle lengths (P less than 0.005), and those between 60 and 150 msec after the V-ERP more rapidly (P less than 0.01) than the steady-state beats. These observations have implications for the protocols used for introducing two or more frequencies during programmed stimulation in man. Furthermore, the conduction pattern in vivo cannot be interpreted from single cell studies.