TY - JOUR
T1 - Modification of left ventricular diastolic behavior by isometric handgrip exercise
AU - Ludbrook, P. A.
AU - Byrne, J. D.
AU - Reed, F. R.
AU - McKnight, R. C.
PY - 1980
Y1 - 1980
N2 - To clarify the basis of increased left ventricular (LV) end-diastolic pressure associated with isometric exercise, LV diastolic and systolic function were examined in 25 patients during sustained handgrip. During handgrip, average systemic arterial mean pressure increased by 20 mm Hg, and LV systolic pressure rose by 31 mm Hg, though in five patients, no increase in mean arterial or LV systolic pressure occurred. LV end-diastolic pressure rose by 10 mm Hg, right ventricular systolic and end-diastolic pressures increased by 10 and 5 mm Hg, respectively (p<0.01 for all pressures). LV end-systolic volume rose by 23%, but end-diastolic volume was unchanged. Reduction of ejection fraction by 13% and mean circumferential fiber shortening rate by 7% indicated further impairment of LV function, though ejection fraction was unchanged or augmented in 14 patients. In all patients, diastolic pressure-volume curves were displaced upward and to the right, without change in the rate constant of the exponentially fit pressure-volume or normalized pressure-volume elasticity relations, operational end-diastolic stiffness or the rate of isovolumic relaxation. Thus, upward transposition of diastolic pressure-volume relations during handgrip does not depend on changes in LV chamber elastic properties or relaxation, LV systolic function or coronary perfusion pressure, but appears, by inference, to be caused by the concomitantly increased right ventricular pressures, perhaps mediated in part by pericardial constraint in association with right ventricular distension.
AB - To clarify the basis of increased left ventricular (LV) end-diastolic pressure associated with isometric exercise, LV diastolic and systolic function were examined in 25 patients during sustained handgrip. During handgrip, average systemic arterial mean pressure increased by 20 mm Hg, and LV systolic pressure rose by 31 mm Hg, though in five patients, no increase in mean arterial or LV systolic pressure occurred. LV end-diastolic pressure rose by 10 mm Hg, right ventricular systolic and end-diastolic pressures increased by 10 and 5 mm Hg, respectively (p<0.01 for all pressures). LV end-systolic volume rose by 23%, but end-diastolic volume was unchanged. Reduction of ejection fraction by 13% and mean circumferential fiber shortening rate by 7% indicated further impairment of LV function, though ejection fraction was unchanged or augmented in 14 patients. In all patients, diastolic pressure-volume curves were displaced upward and to the right, without change in the rate constant of the exponentially fit pressure-volume or normalized pressure-volume elasticity relations, operational end-diastolic stiffness or the rate of isovolumic relaxation. Thus, upward transposition of diastolic pressure-volume relations during handgrip does not depend on changes in LV chamber elastic properties or relaxation, LV systolic function or coronary perfusion pressure, but appears, by inference, to be caused by the concomitantly increased right ventricular pressures, perhaps mediated in part by pericardial constraint in association with right ventricular distension.
UR - http://www.scopus.com/inward/record.url?scp=0018954061&partnerID=8YFLogxK
U2 - 10.1161/01.CIR.62.2.357
DO - 10.1161/01.CIR.62.2.357
M3 - Article
C2 - 7397977
AN - SCOPUS:0018954061
SN - 0009-7322
VL - 62
SP - 357
EP - 370
JO - Circulation
JF - Circulation
IS - 2
ER -