Abstract
The electrophysiologic effects of hydralazine were evaluated in nine hypertensive patients with Sinoatrial dysfunction. Intravenous hydralazine, 0.15 mg/kg, caused no significant reduction in arterial blood pressure. Yet this dose of hydralazine increased heart rate from 61.9 ± 4.1 beats/ min (mean ± standard error of the mean) to 68.6 ± 4.9 ( P < 0.001). Sinus nodal recovery time upon termination of atrial pacing shortened from 3,207 ± 1,098 to 2,064 ± 573 msec ( P < 0.05) and second escape cycles shortened as well ( P < 0.025). Acceleration of heart rate and abbreviation of recovery time did not closely correlate with change in blood pressure ( r = 0.41 and 0.18, respectively). Junctional escape beats became more frequent and junctional escape time shortened from 2,525 ± 692 to 1,705 ± 382 msec ( P < 0.05). Sinoatrial conduction time tended to shorten, but a significant change was not observed. Atrial tachyarrhythmias did not occur and atrial refractoriness was unchanged. Thus, a minimal blood pressure response to hydralazine was associated with enhanced automaticity. Hydralazine merits clinical trial for treatment of sick sinus syndrome with concomitant hypertension.
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