Modification of the baroreceptor control of atrio-ventricular conduction induced by digitalis in man.

Several studies in animals and in man have suggested that the inhibitory influence of baroreceptors on heart rate and peripheral circulation is enhanced by digitalis. Because the atrio-ventricular node represents a key site for the clinical action of digitalis we studied how baroreceptor control of atrio-ventricular conduction is modified by digitalis at therapeutical doses. In eight subjects heart rate was kept constant by atrial pacing to assess neural influences on atrio-ventricular conduction rate without the modifications caused by simultaneous changes in cardiac cycle length. Arterial baroreceptors were stimulated by increasing or reducing blood pressure (intra-arterial recording), via an iv bolus of phenylephrine or nitroglycerine. The baroreflex sensitivity was assessed in ms . mmHg-1 as the slope of the linear regressions relating the rise or fall in systolic blood pressure to the lengthening or shortening in St- (atrial stimulus artifact) Q interval (ECG recording). The study was performed before and 45 min after iv administration of digitalis (0.8 mg of Lanatoside C). Baroreflex sensitivity during baroreceptor stimulation was 2.9 +/- 1.1 ms . mmHg-1 (mean +/- SE) before digitalis, whereas after digitalis a significantly and markedly greater value of 5.6 +/- 1.5 ms . mmHg-1 was found. Baroreflex sensitivity during baroreceptor deactivation was 0.9 +/- 0.1 ms . mmHg-1 before digitalis, and was not significantly affected by the drug. Thus in man the baroreceptor control of atrio-ventricular conduction is strikingly potentiated by digitalis although this potentiation is only evident in the upper portion of the stimulus-response curve of the reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreceptor control of atrioventricular conduction in man.

Although human baroreflexes are known to exert a powerful physiological control on heart rate, little information exists on the physiological control they exert on the atrioventricular conduction system. In 11 normotensive subjects with normal atrioventricular conduction, we altered baroreceptor activity by injection of pressor and depressor drugs (phenylephrine and trinitroglycerin) and recorded mean arterial pressure (MAP, catheter measurements), R-R interval, and pre-His and post-His intervals (A-H and H-V, His bundle recording). With the subjects in sinus rhythm, increasing MAP by 21+/- 1 mm Hg caused a marked lengthening (250 +/- 28 msec), and decreasing MAP by 17 +/- 2 mm Hg a marked shortening (142 +/- 16 msec) of the R-R interval. There was little change in the A-H interval and no change at all in the H-V interval. However, when the R-R interval was kept constant in these subjects by atrial pacing, a similar increase and decrease in MAP caused, respectively, a marked lengthening (49 +/- 6 msec) and shortening (19 +/- 3 msec) of the A-H interval, although the H-V interval remained unaffected. Thus physiological ranges of baroreceptor activation have a marked influence on the atrioventricular node but apparently not on the ventricular portion of the atrioventricular conduction system. This influence is unmasked when pacing prevents the baroreceptor influence on the sinoatrial node.

[A study of atrio-ventricular conduction in subjects with the Lown-Ganong-Levine syndrome (author's transl)]. / Studio della conduzione atrio-ventricolare in soggetti con sindrome di Lown-Ganong-Levine

Eight subjects with the Lown-Ganong-Levine syndrome were studied by means of His bundle recordings during sinus rhythm and during atrial pacing. During sinus rhythm in all cases, the A-H interval was lesser than the mean value observed in 10 control subjects. Atrial pacing at rates up to 190/min produced three types of responses. Four patients showed an initial increment in A-H interval, followed by a plateau response at higher rates. One patient showed an initial increment and a plateau response in A-H interval at low and intermediate rates, followed by a sudden and conspicuous increment at higher rates, indicating conduction of impulse through the A-V node, due to refractoriness of the by-pass tract. Three patients showed a progressive increase in A-H interval similar to that of normal subjects but to a lesser degree. The possible mechanisms for the different types of response are discussed.