Differential anti-ischaemic effects of muscarinic receptor blockade in patients with obstructive coronary artery disease - impaired vs normal left ventricular function

Aims In patients with coronary artery disease acetylcholine (a muscarinic a gonist) causes vasoconstriction. The effect of atropine (a muscarinic antag onist) on coronary vasotone in patients with normal or impaired left ventri cular function is unknown. Methods and Results Twenty-four patients who required atropine infusion (to supplement heart rate response) during atrial pacing (pacing was conducted to assess ischaemia as part of an experimental protocol) were studied; 17 patients had normal and seven impaired left ventricular function (ejection fraction less than or equal to 0.40). Two control groups were selected from a large database (from patients in whom atrial pacing was carried out but to whom atropine was not administered) to match the normal (n = 20) and dys function (n = 10) groups. In the normal left ventricular function group atr opine increased rate pressure product by 12 +/- 4%, as compared to those wi thout atropine (P<0.05). Left ventricular end diastolic pressure increased less in the atropine group (+40 +/- 8% vs +78 +/- 6%; P<0.05). Arterial nor epinephrine increased similarly in both groups, but coronary flow (as asses sed by using a thermodiluting method in the coronary sinus) increased 23 +/ - 4% more in the atropine group (P<0.05). Further, there were lower levels of myocardial lactate production and ST-segment depression in the atropine group [lactate extraction +13 +/- 6% (atropine) vs -19 +/- 4% (controls), S T-segment depression 1.3 +/- 0.6 (atropine) vs 1.8 +/- 0.2 mm (control), bo th P<0.05 between groups]. In contrast, in the dysfunction group the overal l effect of atropine was less pronounced. Conclusion In patients with normal left ventricular function atropine impro ves coronary flow and reduces myocardial lactate production and ST-segment depression during atrial pacing, suggesting a reduction in myocardial ischa emia. (C) 1999 European Society of Cardiology.