The present study investigated the effects of propofol (P) as sole anaesthetic agent of left ventricular (LV) function using gated radionuclide ventriculography (RNV) in unpremedicated patients with chronic coronary arterial disease (CAD). After informed consent, seven ASA 111 patients (51–74 yr) undergoing major urologic surgery took part in this study. All patients suffered from documented angina pectoris secondary to CAD. None gave a history of congestive heart failure or valvular heart disease. No patients were premedicated, but all received their chronic medications (nifedipine and isosorbide) up to and including the morning of surgery. The study was performed in the Nuclear Medicine Laboratory just before surgery. Heart rate (HR) was obtained from standard limb lead II of the ECG. A 7.5 F thermodilution Swan-Ganz catheter and a radial artery cannula were inserted under local anaesthesia. All patients were studied by RNV using red blood cells (RBC) labelled in vivo with 99m-technetium (Tc). A first RBC-Tc preparation containing 2–3 mCi f Tc was counted 10 cm from a gamma-camera. A first-pass study was carried out in the left anterior oblique position following the bolus i.v. injection of the source, allowing the evaluation of the isotopic dilution cardiac output (CO iso) and the attenuation factor (F). Then, a second RBC-Tc preparation containing 20–25 mCi of Tc was injected intravenously. At equilibrium, 16 ECG-synchronized frames were acquired by computer for processing. Mean end-diastolic (ED) and end-systolic (ES) counts, left ventricular-end diastolic and systolic areas and ejection fraction (EF) were calculated every 1.5 min. Using the F, end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), and densitometric CO (CO dens) were obtained. The first CO dens and CO iso were compared for validation of the method in each patient. Series of measurements including HR, mean arterial pressure (P̄a), right atrial pressure (Pra), pulmonary capillary wegde pressure (Ppw), thermodilution cardiac output (CO th), EF, EDV, ESV and distribution in percent of the regional ejection fractions were collected, and derived values were calculated. A baseline study was performed before anaesthetic induction (awake). Anaesthesia was induced with P (2 mg · kg −1), followed by an infusion of P (100 μg · kg −1 · min −1). Vecuronium (0.05 mg · kg −1) was administered and controlled ventilation (F io 2 1) was instituted (F eco 2 : 4–4.5 %). Data acquisitions were serially obtained over the 15 min following the end of the bolus i.v. injection of P : between 1 and 2.5 min, 3 and 4.5 min, 6 and 7.5 min, 9 and 10.5 min, 12 and 13.5 min and 15 and 16.5 min. In addition, arterial and mixed venous blood samples were drawn before P, and 3, 6 and 15 min after the start of P infusion. After the last data acquisition, the patient was transported to the operating room. All data were given as mean ± sd. ANOVA and paired t test were used for statistical analysis. The correlation between specific variables was tested with a linear regression method; p <0.05 was considered as significant. Propofol decreased P̄a and cardiac index, while HR and systemic vascular resistances remained unchanged. The systolic index decreased as a result of the decrease in Pra and Ppw. Propofol had no myocardial depressant effect in as much as EDV, ESV and EF were unchanged during constant afterload. Absence of variation in the distribution of regional ejection fractions was one argument in favour of a lack of imbalance between myocardial oxygen demand and supply.