Compensatory Mechanism in Regional Wall Dynamics of Left Ventricle in Patients with Hypertension

To assess the compensatory mechanism on regional systolic wall dynamics in hypertrophied left ventricle (LV), I analyzed the regional wall motion of LV in 13 patients with hypertension (HT) and 12 normal subjects with acute pressure overloading (N : by angiotensin II infusion). M-mode LV echocardiograms were recorded at four levels in LV (mitral valve, chordal, papillary muscle and apical levels), confirming the location with 2-D LV echocardiography. Fractional shortening of LV short axis (%△D), mean velocity of circumferential fiber shortening (mVcf), systolic meridional wall stress (WSt) in each level and fractional shortening of LV long axis (%△L) were measured. Force-velocity relation at each level were obtained by relating mVcf to WSt at various stress levels in N and HT, and the relations were fitting as exponential function. The %△D and mVcf in HT were significantly greater and WSt in HT was smaller than those in N with acute pressure overloading (p<0.05). The force-velocity relations at apical level was shifted to the left and down-ward, compared with that at basal level, in both N and HT, and the force-velocity relations at each level in N and HT were similar. The %△L in HT was significantly smaller than that in N with acute pressure overloading (12±3% vs 16±1%, p<0.01). These findings indicate that in chronic hypertensive heart compensatory mechanism is operative in short axis (especially in apical level) by decreasing systolic WSt, but no compensation may be present along the LV long axis, and that myocardial contractility of regional left ventricular wall in hypertensive heart is not different from that in normal subjects.