Acute effect of clonidine on left ventricular pressure-volume relation in hypertensive patients with diastolic heart dysfunction

We sought to assess the haemodynamic effects of clonidine on left ventricul ar (LV) pressure-volume relation in patients with diastolic heart dysfuncti on due to essential hypertension. Towards this end, simultaneous recordings of LV volume (acoustic quantification) and LV pressure (micromanometer) we re obtained in 10 such patients before and after drug administration and co mpared to baseline findings on 10 matched normal controls. The following me asurements and calculations were obtained: maximal positive and negative fi rst derivative of LV pressure (peak +dP/dt and peak -dP/dt, respectively), LV minimal and end-diastolic pressure, peak systolic blood pressure, time c onstant of relaxation (TAU), LV stroke work and LV stiffness constant. The two invasive indexes, LV stiffness constant and TAU classified 10/10 patien ts as having abnormal LV diastolic function compared with 7/10 patients so classified by Doppler studies. Central sympathetic suppression by a single oral dose of clonidine 0.125 mg in heart rate and mean arterial pressure as well as a significant improvement of LV diastolic function indexes. Specif ically, the LV stiffness constant (ml(-1)), in normal subjects was 0.0028 v s 0.0152 (P<0.001) in hypertensive subjects at baseline, vs 0.0053 in hyper tensive after clonidine (P<0.001 vs baseline). Likewise, the E/A ratio, was 1.08 in normal subjects vs 0.88 (P<0.0001) in hypertensives at baseline, v s 1.28 in hypertensives after clonidine (P<0.0001 vs baseline). With clonid ine the diastolic portion of the pressure-volume curve was displaced downwa rd. In conclusion, clonidine can improve diastolic dysfunction without depr essing systolic LV performance. The improvement may be attributable in part to withdrawal of direct sympathetic influence on the myocardium and in par t to the indirect effect of systemic, pulmonary and coronary artery relaxat ion.