Why the study?
Does induced tachycardia acutely increase atrial natriuretic peptide levels in coronary sinus and arterial plasma?
Does induced tachycardia acutely increase atrial natriuretic peptide levels in coronary sinus and arterial plasma?
Induced tachycardia acutely increases atrial natriuretic peptide levels in both coronary sinus and arterial plasma, with arterial changes correlating with right atrial pressure and noradrenaline levels.
Tachycardia-induced ANP release may affect acute hemodynamics; leaves open its clinical relevance in arrhythmias pending confirmatory studies.
Atrial natriuretic peptide (ANP) was measured in coronary sinus (CS) plasma in seven patients with induced tachycardia. Right atrial pressure (RAP) and femoral artery (FA) levels of ANP, noradrenaline (NA) and adrenaline (A) were measured before and after 5 min with tachycardia. During tachycardia, ANP in CS plasma increased from 381 +/- 273 (mean +/- SD) to 1376 +/- 1191 pmol l-1 (p < 0.0001), and ANP levels in FA plasma from 89 +/- 48 to 231 +/- 151 pmol l-1 (p < 0.005). A significant increase was observed for peak RAP, whereas mean RAP remained unaltered. While no correlation existed between the increase in CS plasma ANP level and RAP, significant correlations were found between the changes in FA plasma ANP and RAP, and between FA plasma levels of ANP and NA. Following tachycardia, significant correlations were found both between ANP in CS and FA plasma and between the changes in these plasma levels. Whereas the changes in FA plasma levels of ANP during tachycardia seems dependent of RAP and arterial plasma levels of NA, the CS plasma ANP level appears to be independent of the two factors, probably because CS plasma ANP are drained mainly from the left side of the heart.
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ØIE et al. (1994) studied this question.
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