IMPROVED LEFT-VENTRICULAR SYSTOLIC AND DIASTOLIC FUNCTION AFTER REGRESSION OF CARDIAC-HYPERTROPHY, TREATMENT WITHDRAWAL, AND REDEVELOPMENT OF HYPERTENSION

The aim of this study was to differentiate the effects of changes of arterial pressure from those of regression of left ventricular hypertrophy (LVH) on systolic and diastolic function at rest and during a rapid increase in afterload, induced by handgrip and cold pressor tests. An additional purpose was to assess the hemodynamic mechanisms responsible for the increase in arterial pressure after treatment withdrawal. Therefore, we evaluated the cardiac anatomy and function (TM echo) at rest and during handgrip and cold pressor tests in 23 hypertensive patients, before therapy and 20-30 days after withdrawal of treatment, which had lasted 6-12 months, when left ventricular mass index (LVMI) was significantly reduced (from 140 +/- 44 to 113 +/- 13 g/m2, p < 0.001) but the arterial pressure had increased again to pretreatment values (166 +/- 19/105 +/- 7 mm Hg before treatment vs. 162 +/- 15/100 +/- 12 mm Hg). The LVMI reduction was due to a decrease in LV wall thickness, whereas the LV internal dimensions did not change. Systolic function was evaluated by the relationship between LV end-systolic stress (ESS) and fractional shortening (FS): at rest as well as at the peak of handgrip and cold pressor tests, highly significant negative correlations between ESS and FS (range of -0.71 to -0.96) were found. Considering each point of relation between ESS and FS in hypertensive patients, in comparison with 95% prediction limits of the correlation obtained in normal subjects, a "supernormal" systolic function at rest was observed in 10 of 23 patients and a reduced systolic function was not present after treatment withdrawal and redevelopment of hypertension. The arterial pressure increase after treatment withdrawal was related to an increase in cardiac index (at rest, cardiac index from 2.5 +/- 0.6 before treatment to 3.1 +/- 0.7 L/min/m2, p < 0.001) and in particular in stroke index (from 38 +/- 8.8 to 47.7 +/- 11.5 ml/m2, p < 0.001), where as total peripheral resistance was reduced (from 53.04 +/- 14 to 41.1 +/- 12 U, p < 0.001). In conclusion, these results suggest that after regression of LVH and treatment withdrawal, systolic function is usually well maintained, both at rest and during acutely induced increase in afterload, and that the redevelopment of hypertension is mainly related to higher cardiac output.