Contractile performance following regression of left ventricular hypertrophy in hypertensive patients.

The left ventricular end systolic stress-end systolic dimension (ESS-ESD) relation was used to assess the effect of regression in left ventricular hypertrophy on myocardial contractility in 14 hypertensive patients (mean age 47 years) treated with guanfacine (a sympatholytic central alpha-adrenergic agonist) for 10 weeks. Echocardiography (M-mode under two-dimensional guidance) was used to determine left ventricular dimensions, posterior wall thickness (PWT) and septal thickness (ST) before and during the last week of therapy. Left ventricular mass (LVM) expressed as cross-sectional area (CSA) and meridianal wall stress at end systole were derived. Echocardiography was carried out at rest and during i.v. infusion of sodium nitroprusside to alter left ventricular afterload. A minimum of four systolic arterial pressure-ESD points were available for analysis and the value for the slope ESS-ESD was calculated for each patient. Guanfacine produced a significant decrease (P < 0.005) in arterial pressure, wall thickness and CSA. The linear ESS-ESD slope was similar in patients with and without left ventricular hypertrophy and did not change in the whole group or in four patients who had a decrease in CSA of > 10%. It is concluded that guanfacine can induce regression of left ventricular hypertrophy in hypertensive patients and that a decrease in LVM does not influence the intrinsic contractile performance of the left ventricular.