1. This study was designed to determine how left ventricular relaxation function in patients with essential hypertension is impaired by arterial haemodynamic load that is increased in early ejection phase. These patients did not suffer from cardiac hypertrophy or disturbed coronary perfusion. We used a high-fidelity multisensor catheter to record pressure and flow signals in the ascending aorta. The timing and magnitude of wave reflection were obtained by decomposing the measured waves into their forward and backward components. Radionuclide angiography was employed to obtain the time-activity curve. The left ventricular relaxation function was assessed by analysing the time-activity curve, which was filtered using Fourier expansion with the number of harmonics for minimum error.
2. In comparison with age-matched normotensive subjects (seven subjects with mean blood pressure 97 mmHg), hypertensive subjects (seven subjects with mean blood pressure 138 mmHg) had a shorter backward wave arrival time (193 ± 26 versus 258 ± 35 ms) and a higher reflection factor (0.58 ± 0.12 versus 0.42 ± 0.07). Isovolumic relaxation period was prolonged in hypertensive subjects (118 ± 19 versus 90 ± 19 ms). There was an inverse correlation between isovolumic relaxation period and backward wave arrival time in all 14 subjects (r = −0.67, P < 0.05). In contrast, there were no significant differences in cardiac output and time to peak ejection rate between the two groups.
3. Our analyses revealed that early return of the enhanced wave reflection may profoundly impair left ventricular relaxation function in patients with hypertension. The prolonged isovolumic relaxation and unaltered cardiac output suggested that relaxation abnormalities may have a tendency to precede systolic dysfunction in our hypertensive subjects.