Rejection of atrial sensing artifacts by a pacing lead with short tip-to-ring spacing.

AIMS: The ability of a new pacing lead design, with a 10 mm tip-to-ring spacing, to facilitate rejection of sensed far field R-waves and myopotentials was evaluated. METHODS AND RESULTS: Measurements were performed in 66 patients. The occurrence of far field R-wave sensing and myopotential sensing was determined by means of the surface ECG and the ECG markers provided by the pacemaker. At an atrial sensitivity of 0.25 mV and an atrial blanking of 50 ms far field R-wave sensing was observed in 12 patients (18.2%) and at an atrial sensitivity of 1.0 mV no far-field R-wave sensing was observed. Myopotentials were sensed in 3 patients. In all patients the measured P-wave amplitude was at least twice the estimated amplitude of the far field R-wave at an atrial blanking of 50 ms. CONCLUSION: The results from this study show that a small tip-to-ring spacing allows for programming of a high atrial sensitivity and short atrial blanking with an acceptably low risk for atrial artifact sensing.

Value of the addition of amlodipine to atenolol in patients with angina pectoris despite adequate beta blockade.

Anginal patients who remain symptomatic despite optimally dosed beta blockade may also be given dihydropyridine calcium antagonists. This treatment regimen was examined in a double-blind parallel, randomized, controlled study in 147 patients with angina and positive bicycle exercise tests despite optimal beta blockade with atenolol (heart rate at rest <60 beats/min). Patients were randomized to atenolol and/or placebo (control), and atenolol and/or amlodipine. The main outcome measurement was exercise tolerance after 8 weeks compared with baseline. After 8 weeks, no significant differences in time to 0.1-mV ST-segment depression, time to chest pain, and time to end of exercise were observed. The number of patients with chest pain during exercise decreased significantly in the amlodipine group (p = 0.04 vs controls). The subgroup of patients with an early (<6 minutes) onset of chest pain at baseline showed a significant increase in time to chest pain after amlodipine (p = 0.0001 vs controls). In the amlodipine group, ST depression and rate-pressure product at submaximum comparable workload decreased to 0.4 mm (0.56) (p = 0.03 vs controls) and 1.223 (2.652) beats/ min x mm Hg (p = 0.01 vs controls). The number of patients in each group with adverse events was not different. The addition of amlodipine to the treatment of patients with myocardial ischemia, despite optimal beta blockade, is well tolerated and may lead to improvement in symptomatic anginal patients, who have a rapid onset of exercise-induced ischemia.