Background Increased systolic wall stress has been regarded as the key mechanism by which left ventricular hypertrophy (LVH) develops in pressure or volume overload due to heart valve diseases. However, the variations of LVH have also been well recognised when systolic wall stress does not differ. We have therefore investigated the possible role of myocardial power, the time course of systolic wall stress along with pressure and volume loading status in determining LVH.

Methods TOE and LV high fidelity pressures were recorded immediately before heart valve surgery in 109 patients (age 64 ± 12 yr, 73 males). Of whom, 63 were AS, 21 were AR, 25 were MR. Transverse LV cavity dimension and wall thickness were derived from mid-cavity M-mode echocardiograms along with LV pressure by digitising. Thus mean systolic wall stress, peak myocardial power, time from ECG q wave to peak wall stress, LV mass index, LV wall thickness to radius, aortic peak pressure gradient, and MR volume were all determined.

Results There is no difference in LV systolic wall stress in 3 valve groups. Aortic valve pressure gradient and MR volume are the key regulator of LV geometry; while LV peak power and duration of stress development positively correlated with LVMI. LV systolic stress is negatively correlated with T/R and LVMI. These were demonstrated by stepwise regression analysis: T/R= 0.84 + 0.0027 AVPG- 0.0040 MR Volume – 0.0016 LV stress, r2=0.72, p < 0.001; LVMI = −51 – 0.38 AVPG – 0.28 LVMS + 11.4 LV Power + 0.96 Time to peak stress, r2=0.46, p < 0.001.

Conclusion As expected, pressure or volume overload determines LV geometry. The significant variations of LV mass among heart valve diseases cannot be explained on the basis of systolic wall stress. However, the rate of myocardial energy output (peak power) and the duration of force development (q-peak stress) have played more important role in LVH. LV wall stress appears to be the consequence rather than the cause of LVH. These findings have important implications for our understanding in the mechanism of LV hypertrophy in heart valve diseases.