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Acute effect of clonidine on left ventricular pressure-volume relation in hypertensive patients with diastolic heart
C Stefanadis1, A Manolis, J Dernellis
1Hippokration Hospital, Department of Cardiology, University of Athens, Greece.
Insights
Clonidine effectively improved diastolic dysfunction in hypertensive patients by reducing sympathetic activity. This treatment enhanced left ventricular (LV) diastolic function without negatively impacting systolic performance.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Essential hypertension frequently leads to left ventricular (LV) diastolic dysfunction.
- Diastolic dysfunction impairs the heart's ability to relax and fill, impacting overall cardiac function.
- Assessing LV pressure-volume relations provides detailed insights into diastolic mechanics.
Purpose of the Study:
- To evaluate the hemodynamic effects of clonidine on LV pressure-volume relations in patients with essential hypertension and diastolic dysfunction.
- To determine if clonidine can improve impaired diastolic function in this patient population.
- To compare the diagnostic accuracy of invasive LV stiffness and time constant of relaxation (TAU) with Doppler studies for diastolic dysfunction.
Main Methods:
- Simultaneous LV pressure and volume measurements were recorded in 10 hypertensive patients with diastolic dysfunction and 10 healthy controls.
- Measurements were taken at baseline and after administration of a single oral dose of clonidine (0.125 mg).
- Key hemodynamic parameters including LV stiffness constant and TAU were calculated and compared.
Main Results:
- Clonidine significantly improved LV diastolic function indexes, including LV stiffness constant and E/A ratio, in hypertensive patients.
- The diastolic portion of the LV pressure-volume curve shifted downward after clonidine administration.
- Clonidine reduced heart rate and mean arterial pressure but did not impair systolic LV performance.
Conclusions:
- Clonidine demonstrates efficacy in improving diastolic dysfunction associated with essential hypertension.
- The therapeutic benefits of clonidine may stem from reduced sympathetic tone and systemic vasodilation.
- Clonidine offers a potential treatment option for diastolic dysfunction without compromising systolic heart function.
Abstract:
We sought to assess the haemodynamic effects of clonidine on left ventricular (LV) pressure-volume relation in patients with diastolic heart dysfunction due to essential hypertension. Towards this end, simultaneous recordings of LV volume (acoustic quantification) and LV pressure (micromanometer) were obtained in 10 such patients before and after drug administration and compared to baseline findings on 10 matched normal controls. The following measurements and calculations were obtained: maximal positive and negative first derivative of LV pressure (peak +dP/dt and peak -dP/dt, respectively), LV minimal and end-diastolic pressure, peak systolic blood pressure, time constant of relaxation (TAU), LV stroke work and LV stiffness constant. The two invasive indexes, LV stiffness constant and TAU classified 10/10 patients 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 these patients resulted within 60 min in a decrease of heart rate and mean arterial pressure as well as a significant improvement of LV diastolic function indexes. Specifically, the LV stiffness constant (ml(-1)), in normal subjects was 0.0028 vs 0.0152 (P < 0.001) in hypertensive subjects at baseline, vs 0.0053 in hypertensive 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, vs 1.28 in hypertensives after clonidine (P < 0.0001 vs baseline). With clonidine the diastolic portion of the pressure-volume curve was displaced downward. In conclusion, clonidine can improve diastolic dysfunction without depressing systolic LV performance. The improvement may be attributable in part to withdrawal of direct sympathetic influence on the myocardium and in part to the indirect effect of systemic, pulmonary and coronary artery relaxation.