ACTA FAC. MED. NAISS. 2004; 21 (3): 107-118

     Original article

Veselin Mitrović¹, Markus Hamel¹, Milutin Mirić², Michael Weber¹, Matthias Rau¹, Jochen Thormann¹, Christian Hamm¹

¹Kerckhoff-Klinik GmbH, Dept. of Cardiology, Bad Nauheim, Germany;
²Dedinje, Cardiovascular Institute, Belgrade, Serbia and Montenegro

    Moxonidine, a new centrally active imidazoline receptoragonist, might represent a new clinically beneficial antihypertensive principle. This is the first in vestigation regard ing the effects of moxonidine on coronary and sys temic hemodynamics, metabolic markers of ischemia and neurohumoral parameters. We stud ied moxonidine (single dose of 0.4 mg p.o.) in 22 pa tients with hypertension (WHO I-II) and left ventricular (LV) hypertrophy, ST segment depressions during exercise, pectanginal complaints and negative coronarograms. Assessments included arterial blood pressure, cardiac out - put, pulmonary artery pressure mean (PAPm), pulmonary capillary wedge pressure (PCWP) and coronary sinus flow (CSF) by intravascular Dopp ler tech nique. The average moxonidine-induced parameter changes (p<0.05, at least), at about 2 hours later, were as fol lows: a de crease in systolic/diastolic pressure by 28/10 mmHg, and in heart rate by 5 bpm, associated with a decline of PAPm by 17% and of PCWP by 26%. LV-work was re duced by 26%, MVO₂ by 18% and CSF by 16%. Average peak velocity in CS fell by 18% and coronary flow reserve (with adenosine) in creased by 12%. CS-02 sat u ration rose by 4%, accompanied by an in crease in lactate extraction by 17%, a decrease in norepinephrine spillover by 30% and in arte rial endothelin by 20%.
    Conclusion: moxonidine produces clinically relevant sympathicolysis with beneficial effects on hemodynamics, coronary circulation and neurohumoral parameters.

    Key words: essential hypertension, coronary reserve, moxonidine, adenosine, hemodynamics, neurohormones