TY - JOUR
T1 - Coronary reperfusion enhances recovery of atrial natriuretic peptide secretion
T2 - Salvaging endocrine function in patients with acute right ventricular infarction
AU - Yasuda, Satoshi
AU - Nonogi, Hiroshi
AU - Miyazaki, Shunichi
AU - Goto, Yoichi
AU - Haze, Kazuo
PY - 1994/2
Y1 - 1994/2
N2 - Background: The heart has been demonstrated not only to be a pumping organ but also an endocrine organ secreting atrial natriuretic peptide (ANP). We hypothesized that myocardial ischemia may affect ANP secretion and that reperfusion therapy for acute myocardial infarction can preserve endocrine function of the heart. Methods and Results: Twenty patients with acute right ventricular infarction were examined who underwent reperfusion therapy on admission. These patients had proximal occlusion of the dominant right coronary artery involving the right atrial branches: 9 patients with successful reperfusion (SRP group) and the remaining 11 patients with unsuccessful reperfusion (URP group). Within 24 hours after the onset of infarction, a volume loading test was performed after reperfusion therapy with measurements for plasma ANP levels and hemodynamics. Before the volume loading test, the plasma ANP level and mean right atrial pressure were similar between these two groups. However, in the URP group, percent increase in ANP in response to volume loading was strikingly smaller (URP, 45±18% versus SRP, 133±25%; P<.01) despite similar percent increase in mean right atrial pressure (URP, 100±46% versus SRP, 86±23%). The peak ANP level occurred significantly later in the URP group (69±16 hours) than in the SRP group (28±9 hours, P<.001) after the onset of infarction. Conclusions: The response of ANP release to volume loading is attenuated in patients with right ventricular infarction without coronary reperfusion. However, successful reperfusion induces a rapid recovery of cardiac endocrine function as well as its mechanical function. A sufficiently elevated plasma ANP level may be a useful predictor of hemodynamic improvement in patients with right ventricular infarction.
AB - Background: The heart has been demonstrated not only to be a pumping organ but also an endocrine organ secreting atrial natriuretic peptide (ANP). We hypothesized that myocardial ischemia may affect ANP secretion and that reperfusion therapy for acute myocardial infarction can preserve endocrine function of the heart. Methods and Results: Twenty patients with acute right ventricular infarction were examined who underwent reperfusion therapy on admission. These patients had proximal occlusion of the dominant right coronary artery involving the right atrial branches: 9 patients with successful reperfusion (SRP group) and the remaining 11 patients with unsuccessful reperfusion (URP group). Within 24 hours after the onset of infarction, a volume loading test was performed after reperfusion therapy with measurements for plasma ANP levels and hemodynamics. Before the volume loading test, the plasma ANP level and mean right atrial pressure were similar between these two groups. However, in the URP group, percent increase in ANP in response to volume loading was strikingly smaller (URP, 45±18% versus SRP, 133±25%; P<.01) despite similar percent increase in mean right atrial pressure (URP, 100±46% versus SRP, 86±23%). The peak ANP level occurred significantly later in the URP group (69±16 hours) than in the SRP group (28±9 hours, P<.001) after the onset of infarction. Conclusions: The response of ANP release to volume loading is attenuated in patients with right ventricular infarction without coronary reperfusion. However, successful reperfusion induces a rapid recovery of cardiac endocrine function as well as its mechanical function. A sufficiently elevated plasma ANP level may be a useful predictor of hemodynamic improvement in patients with right ventricular infarction.
KW - infarction
KW - peptides
KW - reperfusion
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UR - http://www.scopus.com/inward/citedby.url?scp=0027958349&partnerID=8YFLogxK
U2 - 10.1161/01.CIR.89.2.558
DO - 10.1161/01.CIR.89.2.558
M3 - Article
C2 - 8313544
AN - SCOPUS:0027958349
VL - 89
SP - 558
EP - 566
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 2
ER -