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Recommendations for head-up tilt testing (HUT) often include the prolonged abstaining from food and water consumption (nothing by mouth [NPO]) and intravenous fluids administration before HUT. After the baseline test, supine equilibration periods are recommended before and between each dose of medication. The aim of this study was to determine if similar results are obtainable with a simpler protocol. After 2-3 hours NPO, 1,540 HUTs were performed at 70 degrees for 30 minutes unless predetermined endpoints were reached. Then, with the patient remaining in the tilted position, isoproterenol (ISO) (1 microgram/min), titrated every 3 minutes to a maximum of 5 micrograms/min (n = 803 patients), sublingual nitroglycerin (NTG) (300-400 micrograms) (n = 143 patients), or edrophonium (EDP) (5 mg) repeated once after 3 minutes (n = 46 patients) were administered. No aspiration or other adverse effects attributable to the abbreviated fasting period were observed. ISO was well tolerated as doses were increased. Vasovagal manifestations developed in 31% of ISO tests, in 11% with EDP, and in 50% with NTG (P < 0.001). Time consumed with rehydration before and postural changes during HUTs may be avoided when ISO is administered. With NTG the response may be excessive.

Catheter ablation using direct current (DC) shock has proved invaluable in the management of a variety of tachycardias. However, sporadic reports of fatal arrhythmias following ablation have raised the question of the proarrhythmic potential of DC shock ablation. The present study was undertaken in 45 patients to assess prospectively any proarrhythmia related to DC shock ablation, using matched pre- and postablation Holter monitors and programmed electrical stimulation (PES). Nineteen of these patients had Holter monitors for three successive postablation days to observe trends. There was unmatched data in 11 additional patients. All 56 patients provided prospective follow-up for clinical events. There was no immediate sustained VT/VF at the time of the ablation. Four patients had sustained VT in the first 72 hours after ablation; three episodes were similar to the preablation clinical arrhythmias; one patient had torsades de pointes interrupting bradycardia. Twelve patients met Holter, PES, or clinical criteria for proarrhythmia; none were treated on the basis of these findings. On Holter monitoring, there were significant increases in VPCs/hour and couplets/hour in patients undergoing atrial or atrioventricular junctional ablations; and an increase in couplets after accessory pathway ablations. Increases in these categories were not significant for VT patients; nor were increases in episodes of VT/hour or atrial arrhythmias significant in any group. Patients were followed for 44 +/- 33 months, with an actuarial survival of 95% at 1 year, 88% at 3 years, and 85% at 4 years. There were six deaths during follow-up. Two patients had sudden death: one at 2 months had early evidence of proarrhythmia; the other at 32 months may have represented later myocardia deterioration. One patient died of heart failure at 77 months; and there were three noncardiac deaths. DC shock ablation in humans is much less proarrhythmic than in dogs. The low incidence of clinical proarrhythmic events during prolonged follow-up after discharge resulted in low sensitivity, specificity, and positive predictive values for Holter and PES, although the negative predictive values of these tests were greater than 90%. Only one of 12 patients who met criteria for proarrhythmia in the days immediately following ablation had subsequent clinical events consistent with proarrhythmia. These results may be useful as standards for comparison with results of radiofrequency or other ablation modalities.

Over a 39 month period, 143 patients with coronary artery disease had programmed stimulation (PES) for recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF). Twenty-two patients underwent operations. Ages ranged from 40 to 71 years; 20 of the 22 were men. All patients had coronary artery disease and 11 had left ventricular aneurysms. The mean ejection fraction was 31% (16% to 50%). Eighteen of the 22 patients underwent operations for drug-resistant ventricular arrhythmias (more than six different drugs plus drug combinations tested per patient). Nineteen patients had intraoperative mapping, endocardial resection, and/or an encircling endocardial ventriculotomy. Three patients with ischemia-related VT had coronary artery bypass (CABG) alone. The 30 day operative mortality was 14%. Thirteen of 19 (68%) operative survivors were effectively controlled with operation alone or a combination of operation and previously ineffective drug therapy. Of the six patients whose VT was inducible postoperatively, three have experienced episodes of sustained VT and one patient died suddenly. Three of these patients have the automatic implantable defibrillator. Operation guided by endocardial mapping is effective alone or in combination with drugs in this select group of patients. If the patients' VT was uninducible postoperatively with or without the addition of antiarrhythmic therapy, late deaths (3/19) were due to poor myocardial reserve and coronary artery disease, not the reemergence of sustained ventricular arrhythmias during a mean follow-up of 15 months.

Catheter or intraoperative activation mapping studies, or both, were performed in 17 patients with coronary artery disease with two to four distinct configurations of ventricular tachycardia, resistant to a mean of 12.1 +/- 6.0 antiarrhythmic drug trials per patient. Mapping studies were performed to guide anticipated surgical ablation of arrhythmias. Activation map data were adequate to determine sites of origin of 30 (64%) of 47 observed tachycardia configurations. These 30 ventricular tachycardias (26 observed clinically) were mapped to 22 separate endocardial sites of origin. Sites of origin of distinct tachycardias were identical or closely adjacent (within 3 cm) in six patients and widely separate (greater than or equal to 4 cm) in eight patients (47% of the group). Activation maps were not adequate to determine sites of origin of 17 (36%) of the 47 tachycardias, including all configurations in three patients. Fifteen patients underwent surgery for control of ventricular tachycardia: aggressive, map-guided endocardial resection (mean 26.5 +/- 14.2 cm2) in 12 patients with identified sites of tachycardia origin and extensive resection of visible endocardial scar (2 patients) or encircling endocardial ventriculotomy (1 patient) in those in whom the sites of origin of all clinical tachycardias remained undetermined. Two inoperable patients were treated with amiodarone. During postoperative electrophysiologic tests (11 of 13 surgical survivors), ventricular tachyarrhythmias were initially uninducible in only 4 of 11 patients. However, in two patients only nonclinical arrhythmias (ventricular flutter) were induced. Six (21%) of 29 clinical tachycardias whose sites of origin were either not determined or not resected (right septum or papillary muscle) remained inducible in five patients. Using previously ineffective antiarrhythmic drugs, initially inducible arrhythmias became uninducible (two patients), or harder to induce than preoperatively (five patients). As a result of surgical resections alone or in combination with previously ineffective drugs (and amiodarone in two inoperable patients), there were no recurrences of ventricular tachycardia in 14 (93%) of 15 patients discharged during 19.0 +/- 14.3 months of follow-up study. Thus, activation mapping may commonly reveal separate apparent sites of origin for clinically observed, morphologically distinct, highly drug-refractory ventricular tachycardias in patients with coronary artery disease with multiple tachycardia configurations. Extensive surgical resection of identified sites of origin may be required to ablate arrhythmias in these patients.(ABSTRACT TRUNCATED AT 400 WORDS)