Myocardial oxygen consumption (MVO2) is defined by the equation: MVO2 = coronary blood flow x arteriovenous difference in O2 content. The average value for a heart of 300 g is 30 to 35 ml/min. In the absence of physiological variations in the arteriovenous difference in O2 content, MVO2 is related to coronary blood flow and the typical anti-anginal agent is one which prevents or reduces increases in MVO2. MVO2 depends on several factors: 1. intraparietal tension, which depends on intraventricular pressure and volume and in which the oxygen demands of pressure overload are much higher than those of volume overload; 2. contractility or myocardial inotropism: 50 per cent increase in the velocity of left ventricular contraction increases MVO2 by 40 per cent; 3. heart rate; 4. external cardiac work--the work accomplished during the ejection phase; this represents about 15 per cent of the MVO2; 5. the energy of electrical activation; this represents about 0,5 per cent of the MVO2; 6. the oxygen requirements of basal myocardial metabolism which represent about 20 per cent of the MVO2; 7. ventricular relaxation: is a factor to be added to those described above; this consumes about 15 per cent of the total energy of a cardiac beat; it may be increased with Isoproterenol or decreased by increasing the calcium concentration. This mechanism may explain the physiopathological impact of calcium inhibitors in effort angina or angina due to increased MVO2.