Pulse Wave Analysis of the Aortic Pressure Waveform in Severe Left Ventricular Systolic Dysfunction

<jats:p> <jats:bold> <jats:italic>Background—</jats:italic> </jats:bold> The effect of moderate left ventricular systolic dysfunction (LVSD) on ventricular/vascular coupling and the aortic pressure waveform (AoPW) has been well described, but the effect of severe LVSD has not. </jats:p> <jats:p> <jats:bold> <jats:italic>Methods and Results—</jats:italic> </jats:bold> We used noninvasive, high-fidelity tonometry of the radial artery and a mathematical transfer function to generate the AoPW in 25 treated patients with LVSD (mean LV ejection fraction, 24±8.8%; range, 11% to 40%; 21 patients <30%). Pulse wave analysis of the AoPW was used to characterize ventricular/vascular coupling and compared with pulse wave analysis performed in 25 normal subjects matched for age, gender, height, body mass index, and heart rate. Measurements obtained using pulse wave analysis in LVSD patients indicated features of poor LV stroke performance and also reduced indices of arterial stiffness: increased travel time of the pressure wave (147±10 ms versus 132±21 ms; <jats:italic>P</jats:italic> <0.001); decreased systolic duration of reflected wave (134±24 ms versus 167±26 ms; <jats:italic>P</jats:italic> <0.001); ejection duration (277±22 ms versus 299±25 ms; <jats:italic>P</jats:italic> <0.008); percent systolic duration (32±5.3% versus 35±4.0%; <jats:italic>P</jats:italic> <0.02); aortic systolic pressure (100±16 mm Hg versus 121±16 mm Hg; <jats:italic>P</jats:italic> <0.001); unaugmented pressure (24±6.3 mm Hg versus 32±6.4 mm Hg; <jats:italic>P</jats:italic> <0.001); augmented pressure (4.8±3.1 mm Hg versus 9.6±4.5 mm Hg; <jats:italic>P</jats:italic> <0.001); pulse pressure (28±7.4 mm Hg versus 42±9.5 mm Hg; <jats:italic>P</jats:italic> <0.001); augmentation index (12±6.6% versus 23±7.6%; <jats:italic>P</jats:italic> <0.006); wasted LV effort (5.3±2.8×10 <jats:sup>2</jats:sup> dyne sec/cm <jats:sup>2</jats:sup> versus 17±10×10 <jats:sup>2</jats:sup> dyne sec/cm <jats:sup>2</jats:sup> ; <jats:italic>P</jats:italic> <0.001); systolic pressure time index (17±4.1×10 <jats:sup>2</jats:sup> mm Hg-sec/min versus 23±4.2×10 <jats:sup>2</jats:sup> mm Hg sec/min; <jats:italic>P</jats:italic> <0.001); and pressure systolic area (383±121 mm Hg sec/min versus 666±150 mm Hg sec/min; <jats:italic>P</jats:italic> <0.001). </jats:p> <jats:p> <jats:bold> <jats:italic>Conclusions—</jats:italic> </jats:bold> Severe LVSD causes measurable changes in the AoPW. Standardization of AoPW findings in LVSD patients may allow for the clinical use of radial artery pulse wave analysis to noninvasively determine the severity of dysfunction and aid in logical therapy. </jats:p>