The effect of nitroglycerin on pacing-induced changes in myocardial oxygen consumption and metabolic coronary vasodilation in patients with coronary artery disease

In the present study, we assessed the potential effect of nitroglycerin IV (NTG), a donor of exogenous nitric oxide, on metabolic coronary flow control in patients with coronary artery disease. In 12 patients scheduled for coronary artery surgery, arterial blood pressure, pulmonary capillary wedge pressure, coronary sinus blood flow (continuous thermodilution), myocardial Oxygen supply (DVO2), and myocardial oxygen consumption (MVO2) were measured at sinus rhythm and in response to atrial pacing at 30 bpm greater than baseline sinus rate. These measurements were repeated during infusion of NTG 1 and 2 mu g.kg(-1).min(-1). At control, in the absence of NTG, MVO2 increased from 13.7 +/- 3.4 mL O-2/min during sinus rhythm to 19.3 +/- 5.5 mL O-2/min during pacing. NTG 1 and 2 mu g.kg(-1).min(-1) blunted the pacing-induced increase in MVO2 dose-dependently. During NTG 1 mu g.kg(-1).min(-1), MVO2 increased from 12.9 +/- 3.3 mL O-2/min at sinus rhythm to 17.3 +/- 4.7 mt O-2/min during pacing (P = 0.01 versus control pacing); during NTG 2 mu g.kg(-1).min(-1), MVO2 increased from 13.4 +/- 3.3 mL O-2/min to 15.9 +/- 3.7 mL O-2/min (P = 0.008 versus control pacing). However, the pacing-induced increase in DVO2 per mL O-2/min increase in MVO2 (Delta DVO2/Delta MVO2), was significantly greater during the infusion of NTG 2 mu g. kg(-1).min(-1) (1.85 +/- 0.56; P = 0.023) compared with control (1.51 +/- 0.22). This was associated with an increase in coronary sinus hemoglobin oxygen saturation (30% +/- 5% at control pacing and 34% +/- 6% during pacing with NTG 2 mu g.kg(-1).min(-1) P = 0.018), which indicates that during the infusion of NTG, there was more metabolic coronary vasodilation than achievable solely on the basis of the metabolic stimulus. Implications: Our findings suggest that nitroglycerin, a donor of exogenous nitric oxide, reduces pacing-induced increases in myocardial oxygen consumption and enhances metabolic coronary vasodilation in patients with coronary artery disease, in whom endogenous nitric oxide activity may be reduced.