Intrathoracic Pressure Deviations Attenuate Left Ventricular Filling and Stroke Volume Without Pronounced Myocardial Mechanical Alterations in Healthy Adults

Intrathoracic pressure modulates cardiac loading conditions, which then influence left ventricular (LV) chamber function, and may occur with underlying myocardial mechanical alterations. We investigated the independent effects of inspiratory negative and expiratory positive intrathoracic pressure on septal geometry, LV chamber function, and rotation, twist, and strain indices. After baseline, twenty healthy adults (11M/9F, 23±4 years) performed resistive breathing to manipulate inspiratory (−30, −20, −10 cmH₂O) or expiratory (+10, +20 cmH₂O) intrathoracic pressure. Echocardiography was used to acquire LV-focused 2D images, and mitral Doppler inflow and annular tissue velocity spectra. Images were analyzed for LV chamber volumes, tissue velocities, trans-mitral filling velocities, and speckle-tracking derived LV longitudinal, radial, and circumferential strain and strain-rate, basal and apical rotation, and twist. Across negative pressure trials, most profoundly at −30 cmH₂O, we observed progressive end-diastolic septal flattening (3.9±0.4 vs. 3.2±0.4 cm, P<0.05) and decreases in LV end-diastolic volume (103±23 vs. 115±25 mL, P<0.05) and stroke volume, while end-systolic volume was unchanged. However, LV apical and basal rotation, twist (13.3±3.6 vs. 13.9±3.7 degrees, P=0.890), and circumferential, radial, and longitudinal strain indices were largely unchanged. During positive pressure trials, we observed main effects for septal flattening (P=0.014) confined to inspiration, and modestly reduced LV end-diastolic volume (P<0.001), end-systolic volume (P=0.033), and stroke volume. Again, myocardial mechanics parameters changed little. Collectively, our data suggest that both positive and negative intrathoracic pressures can exacerbate direct ventricular interaction through opposing mechanisms that attenuate LV end-diastolic volume and stroke volume, but without specific changes in myocardial mechanics or mitral inflow.