Minimum left ventricular pressure during β -adrenergic stimulation in human subjects: Evidence for elastic recoil and diastolic "suction" in the normal heart

The influence of elastic recoil and restoring forces on diastolic left ventricular pressure decay and minimum left ventricular pressures has been demonstrated in animal models but has not been studied in the human heart. To investigate this issue in the normal human left ventricle, we studied eight patients with chest pain and normal coronary arteries with simultaneous measurement of left ventricular volume (by radionuclide angiography) and pressure (by micromanometer catheter) and coronary sinus blood flow. Electrocardiographic-gated data were obtained in the basal state, during rapid atrial pacing, and during isoproterenol infusion to a similar heart rate. Compared with pacing, isoproterenol increased ejection fraction and reduced end-systolic volume (p<0.005), end-systolic pressure (p<0.005), and the half-time of pressure decline after peak negative dP/dt (T1/2) (p<0.001). Negative diastolic pressure developed in seven of eight patients during isoproterenol (range, -0.5 to -2.4 mm Hg) but in only one of eight during pacing (-0.2 mm Hg). These reduced diastolic pressures during isoproterenol were accompanied by increased stroke volume (reflecting increased transmitral flow) and diminished pulmonary wedge pressure (reflecting left atrial pressure). The magnitude of reduction in minimum diastolic pressure during pacing and isoproterenol was related to the change in end-systolic volume (r0.79,p<0.001), ejection fraction (r-0.74, p<0.001), T1/2 (r0.57, p<0.02), and coronary sinus flow (r0.73, plt;0.005). Stronger correlations were observed in analyzing changes during isoproterenol alone. From similar end-systolic volumes, T1/2 and the time constant tau were lower (both p0.005), as was minimum diastolic pressure (p<0.05) during isoproterenol compared with pacing. Hence, isoproterenol infusion (simulating the catecholamine stimulation during exercise) significantly reduces minimum diastolic pressure in the normal human heart, resulting in the development of negative left ventricular pressures. The reduction in minimum left ventricular pressure is related to changes in left ventricular systolic volume, contractility, and coronary flow, and to the dynamics of isovolumic relaxation. This reduction in early diastolic pressure augments the left atrial - left ventricular pressure gradient during early diastole, enhancing the rate and magnitude of left ventricular filling required to maintain a high cardiac output at elevated heart rates.