The aim of this study was to assess the feasibility of a cephalic vein cutdown and venography technique for implantation of a pacemaker or ICD and to determine the causes of failure of cephalic vein cutdown. In consecutive patients who underwent pacemaker or ICD implants, a modified cephalic vein guidewire technique was performed. This technique was attempted in 289 pacemaker implants and 26 ICD implants (155 men, 160 women; mean age 74 +/- 10 years). The success rate for implantation of a single chamber and a dual chamber device by using this technique alone was 84% (54/64) and 74% (185/251), respectively (P = 0.10). In an additional 7% of patients with dual chamber implant, the cephalic vein can be used for passage of the ventricular lead. A cephalic venogram was required in 82 patients and facilitated the passage of the guidewire in 62 (79%) of them. No complication related to vascular access was observed with this technique. This technique failed in 54 (17%) of 315 patients due to (1) failure of cephalic vein isolation (48%), (2) venous stenosis (24%), or (3) venous torturosity or anomalies (28%). There were no significant differences in the patient's age, sex, type of device, and the fluoroscopic time for lead placement between patients with or without successful lead placement using this technique (all P > 0.05). In conclusion, a simple modification of the cephalic vein guidewire technique together with venography has facilitated the placement of leads during pacemaker and ICD implant. This technique is safe and applicable in the majority of patients and avoids the risk of subclavian puncture.
Ventricular tachyarrhythmias may occur during intravenous arsenic trioxide (As 2 O 3 ). This has not happened during oral As 2 O 3 . Sixteen patients were studied by electrocardiography and 24-hour Holter monitoring at baseline, during and after oral As 2 O 3 (As 2 O 3 -ON, As 2 O 3 -OFF). QT and corrected QT (QTc) were significantly longer during As 2 O 3 -ON than in As 2 O 3 -OFF, but QT and QTc dispersions were comparable. The patients' 24-hour heart rates were higher during As 2 O 3 -ON than in As 2 O 3 -OFF. QTc intervals at each hour were longer during As 2 O 3 -ON than in As 2 O 3 -OFF. However, QTc prolongation of more than 30 milliseconds only occurred at one time point (2 hours) after oral As 2 O 3 , resulting in QTc of more than 500 milliseconds in 3 of 16 patients, all within 4 hours of oral As 2 O 3 . Although the standard deviation of normal RR interval was lower during As 2 O 3 -ON, ratios of low frequency to high frequency power for As 2 O 3 -ON and As 2 O 3 -OFF were comparable. No ventricular proarrhythmias were observed. These observations, due to the lower peak plasma arsenic reached during oral IntroductionArsenic trioxide (As 2 O 3 ) is efficacious in acute promyelocytic leukemia (APL). 1-4 It blocks potassium currents I Kr and I Ks , 5 causing QT prolongation. Ventricular tachyarrhythmias were reported in about 30% of patients treated with intravenous As 2 O 3 . [6][7][8][9] As 2 O 3 may be effective in other neoplasms, 10 making clinical trials of As 2 O 3 in these diseases pressing. However, reliance on intravenous As 2 O 3 hampers these efforts. Long-term intravenous As 2 O 3 is resource-demanding. Moreover, a potentially fatal cardiac toxicity is worrisome, especially in clinical trials.We have developed an oral formulation of As 2 O 3 . 4,11 Details of the preparation and pharmacokinetics of oral As 2 O 3 have been previously reported. 11 Oral As 2 O 3 gives a similar bioavailability, but lower peak plasma arsenic concentrations, as compared with intravenous As 2 O 3 . 11 Oral As 2 O 3 represents an advance in arsenic therapy. Patients take oral As 2 O 3 at home, rendering long-term therapy feasible, thus facilitating clinical trials. Most importantly, in more than 600 patient weeks of oral As 2 O 3 administered during 5 years, no ventricular tachyarrhythmias were observed. 4,11 Prolongation of QT or corrected QT (QTc) increases the risks of ventricular tachyarrhythmias. 12,13 QT-interval dispersion measures regional nonhomogeneities of ventricular repolarization. 14 Greater dispersions increase ventricular arrhythmias. 15 Heart rate variability (HRV) measures the beat-to-beat heart rate variations, correlating with changes in autonomic tone. HRV changes increase cardiac arrhythmias. 16 To explain the favorable cardiac side-effect profile of oral As 2 O 3 , we studied a cohort of patients on long-term oral As 2 O 3 , to determine the cardiac safety and changes of QT intervals and HVR. Study design PatientsWe studied 17 consecutive patients with relapsed APL (Table 1). All had normal ...
The aim of this study was to evaluate the cardiovascular autonomic function and vasovagal reaction in patients with paroxysmal atrial fibrillation without significant structural heart disease. Twenty-eight patients with paroxysmal atrial fibrillation (9 patients were categorized to have autonomic-mediated atrial fibrillation while atrial fibrillation in other patients was nonautonomic mediated) and 19 normal control subjects were recruited. Cardiovascular autonomic function tests included measuring heart rate response to standing, deep breathing, Valsalva maneuver, baroreflex sensitivity, 24-hour heart rate variability, and also head-up tilt test. Compared with normal subjects, no significant autonomic dysfunction was found in patients with autonomic-mediated and nonautonomic-mediated atrial fibrillation. All subjects had negative baseline tilt test. With isoproterenol provocation, six patients developed atrial fibrillation. Four of 9 patients and 3 of 19 patients with autonomic mediated and nonautonomic mediated atrial fibrillation had a positive tilt test respectively, while none occurred in the controls. A significant percentage (32%) of patients with paroxysmal atrial fibrillation had episodes of atrial fibrillation provoked by changes in autonomic tone, although there was no underlying abnormal cardiac autonomic function nor sympathetic-parasympathetic imbalance. A heightened susceptibility to vasovagal cardiovascular response may have important implications on the occurrence and symptomatology of patients with paroxysmal atrial fibrillation.
A 13-year-old girl presented with incessant ventricular tachycardia complicating acute Coxsackie B3 myocarditis. Electro-physiologic assessment revealed that the tachycardia could not be terminated, overdrive suppressed or accelerated by programmed electrical stimulation, but was transiently slowed by intravenous adenosine triphosphate and had marked spontaneous and sympathoautonomic-mediated fluctuation in the tachycardia cycle length. These features were atypical of reentry and triggered automaticity and suggested that abnormal automaticity was the likely tachycardia mechanism. Intravenous amiodarone slowed the ventricular tachycardia, but the patient eventually succumbed from rapidly progressive left ventricular failure. Postmortem pathohistologic examination confirmed the diagnosis of acute myocarditis.
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