Electrophysiology study was performed in 93 patients with bifascicular block and unexplained syncope. Clinical evidence of organic heart disease was present in 33 (35%). Electrophysiological abnormalities were detected in 45 patients (48%). Of these, 36 had distal conduction disease, including 28 with an HV interval greater than 55 ms (mean 76.4 ms), and eight who developed infraHisian block following either intravenous procainamide (four) or atrial pacing (four). Sick sinus syndrome was evident in six patients and a further two had carotid sinus hypersensitivity. Sustained monomorphic ventricular tachycardia (VT) was induced in only three patients, two of whom also had prolonged HV interval. Among the 93 patients, 45 had therapy which was guided by positive findings at electrophysiology study (Group 1). Of these, 42 received permanent pacemakers, two were treated with combined permanent pacing and antiarrhythmic drug therapy, and one was treated with antiarrhythmic drug alone. In addition, eight patients without electrophysiologic abnormalities were treated empirically by pacing (Group 2). Finally, 40 patients without electrophysiologic abnormalities received no specific therapy (group 3). At a mean follow-up of 39 months (range two-125 months), recurrence of syncope had occurred in 4% of Group 1 patients, and 25% of Group 3 patients (p less than 0.05). No patient in Group 2 had had recurrence. Total mortality was 40%, including 47% of patients in Group 1, 25% of Group 2, and 35% of Group 3. Death was sudden in seven patients. We concluded that among patients with bifascicular block and syncope, therapy directed by findings at electrophysiology study was associated with symptomatic improvement, but mortality was not significantly influenced.(ABSTRACT TRUNCATED AT 250 WORDS)
17 subjects with essential hypertension (14 male, 3 female - ages: 40-69 years), 13 of whom continued their previous anti-hypertensive therapy, completed a double-blind cross-over trial of ketanserin 40 mg twice daily versus placebo tablets twice daily - each treatment phase was six weeks in duration. For the group as a whole, blood pressure (BP) was reduced in the ketanserin phase compared with the placebo phase; supine mean BP decrease: 4 +/- 1 mm Hg (p less than 0.05); standing mean BP decrease: 7 +/- 1 mm Hg (p less than 0.001). Heart rate (HR) was also significantly decreased in the ketanserin phase by 5 +/- 1 beats/minute (p less than 0.001). When individual subgroups were analysed the reductions in BP and HR were greater in subjects already receiving anti-hypertensives, diuretic and/or beta blockers. Changes were observed in 24 hour urine sodium and potassium excretion - sodium (mmol/day): placebo 137 +/- 17, ketanserin 174 +/- 19 (p less than 0.05); potassium (mmol/day): placebo 74 +/- 8, ketanserin 57 +/- 5. For the group as a whole there were no significant adverse effects during the ketanserin phase, although two subjects had a dose reduction of ketanserin because of drowsiness and dizziness. Two additional subjects withdrew from the study due to adverse effects, one in the placebo phase. In conclusion ketanserin in the dose administered has a modest hypotensive effect which is best seen in subjects already receiving other anti-hypertensive agents.
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