Utility and safety of axillo-subclavian venous imaging with carbon dioxide (CO) prior to chronic lead system revisions.

BACKGROUND: Prior to attempting placement of one or more electrodes to revise existing rhythm control devices, patency of the central veins should be documented, in view of a high incidence of significant chronic occlusions. Since iodinated contrast venography may be contraindicated in select situations, imaging of the axillo-subclavian venous system with gaseous carbon dioxide (CO(2)) was evaluated prospectively in 23 consecutive individuals who were considered for revision of previously implanted pacemaker or automatic cardioverter defibrillator lead systems. METHODS: Approximately 20 mL of CO(2) were manually infused via CO(2) primed injection tubing into a vein at or above the level of the antecubital fossa ipsilateral to the side of prior lead placements. Digital subtraction imaging over the axillo-subclavian region, lower neck, and mediastinum was performed. Formal interpretation was obtained from one of three interventional radiologists and at least one electrophysiologist. RESULTS: Significant venous occlusions were identified in five (22%) patients. Vascular access utilized for the subsequent 18 revisions performed included the imaged patent ipsilateral vein in 14 patients and the contralateral, right-sided subclavian venous system in three patients. One patient required epicardial left ventricular lead placement. There were no complications from venography. CONCLUSIONS: Axillo-subclavian venography with gaseous CO(2) in patients undergoing pacemaker or implantable cardioverter defibrillator lead revisions is feasible and safe when use of iodinated dye is contraindicated. This technique should be employed in patients with azotemia, dye contrast allergies, or significant inflammation in the vicinity of the intravenous line insertion.

Twelve-lead ECG features to identify ventricular tachycardia arising from the epicardial right ventricle.

BACKGROUND: Usefulness of 12-lead ECG for predicting an epicardial origin for ventricular tachycardia (VT) arising from the right ventricle (RV) has not been assessed. An epicardial approach is sometimes warranted to eliminate RV VT. OBJECTIVES: The purpose of this study was investigate the hypothesis that specific ECG features identify an epicardial origin for RV VT. METHODS: To mimic an endocardial or epicardial origin, we paced representative sites in 13 patients undergoing RV endocardial/epicardial mapping (134/180 pace map sites). RESULTS: QRS duration from epicardial vs endocardial sites was not different (183 +/- 27 ms vs 185 +/- 28 ms, P = .3). Reported cut-off values for identifying epicardial left ventricular origin, pseudo-delta wave (> or =34 ms), intrinsicoid deflection time (> or =85 ms), and RS complex (> or =121 ms) did not apply to the RV. A Q wave in lead II, III, or aVF was more likely noted from inferior epicardial vs endocardial sites (53/73 vs 16/43, P <.01). A Q wave in lead I was more frequently present from epicardial vs endocardial anterior RV sites (30/82 vs 5/52, P <.001). QS in lead V(2) was noted from anatomically matched epicardial anterior RV sites (22/33 vs 13/33, P <.05). In the RV outflow tract, no ECG feature distinguishing epicardial/endocardial origin reached statistical significance. CONCLUSION: A Q wave or QS in leads that best reflect local activation suggest an epicardial origin for RV depolarization and may help in identifying a probable epicardial site of origin for RV VT. QRS duration and reported criteria for epicardial origin of VT in the left ventricle do not identify a probable epicardial origin in the RV.

Increasing left ventricular pacing output decreases interventricular conduction time in patients with biventricular pacing systems.

OBJECTIVE: To evaluate the effect of increasing LV pacing output on interventricular timing in patients with biventricular pacing systems. BACKGROUND: Clinical improvement with biventricular pacing is likely related to reduction in ventricular dysynchrony in patients with cardiomyopathy. We hypothesized that increasing left ventricular pacing output would reduce interventricular conduction time and could affect ventricular synchrony. METHODS: Forty-two sequential patients with biventricular pacing systems that permitted independent LV pacing were selected at the time of routine device interrogation. The interval between LV pacing stimulus and onset of the RV electrogram was measured during LV pacing at capture threshold and at maximum pacing output for each patient. RESULTS: The average time from LV pacing stimulus to right ventricular electrogram onset was 142.5 +/- 32.5 ms (range 90-230 ms) at threshold and 132.3 +/- 30.4 ms (range 90-220 ms) at maximum pacing output, with a mean decrease in conduction time of 10.2 +/- 10.9 ms (range 0-45 ms). There was significantly greater interventricular conduction shortening with increased pacing output in patients with ischemic cardiomyopathy compared to others (14.9 +/- 11.9 ms vs 4.0 +/- 4.6 ms; P < 0.01). CONCLUSIONS: Conduction time from LV to RV shortens as LV pacing output is increased. This effect is seen to a greater degree in patients with ischemic cardiomyopathy, possibly related to the presence of myocardial scar near the pacing electrode. Further investigation is needed to assess the clinical outcomes related to this new method for optimizing resynchronization therapy.

Accidental intravenous colchicine poisoning.

Colchicine is a commonly used drug for the treatment of gout and other indications. Toxicity from intentional oral overdoses of colchicine has been reported. Two cases are reported here in which colchicine was given by intravenous injection, and patients presented with multiorgan toxicity. The authors tested plasma and urine colchicine levels in these patients and found them significantly elevated. Testing of the vial from which the colchicine injections were given showed that the vial was mislabeled and contained 10-fold greater concentration of drug than the labeling indicated. These patients thus received a bolus dose of 20 mg of intravenous colchicine rather than the intended 2-mg dose. An intravenous dose of this magnitude has not previously been reported.