Myocardial ischaemia during tachycardia--not due to an increase in myocardial oxygen demand.
It is generally believed that an increase in heart rate will be accompanied by an increase in myocardial oxygen demand (MVO2), but in a recent publication this concept has been challenged; we present data supporting the view that an increase in heart rate is not necessarily accompanied by an increase in MVO2. Our data are based on studies on dogs in five phases: (a) normal coronary arteries; (i) with normal heart rate; (ii) with tachycardia induced by a pacemaker; and (iii) with normal heart rate; and (b) with a constricted left anterior descending coronary artery: (i) with normal heart rate; and (ii) with induced tachycardia. MVO2 remained unchanged both per beat and per unit of time. Neither global nor regional myocardial function in the area supplied by the constricted artery changed during tachycardia. The reason for myocardial ischaemia should therefore not be attributed to an increase in MVO2 if the diameter of the heart is not increased, and attention should rather be focused on inadequate diastolic perfusion time and possible redistribution of blood from the potentially ischaemic zone.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D003327:Coronary Disease / Q000209:etiology*; D004285:Dogs; D006321:Heart / Q000503:physiopathology; D006339:Heart Rate; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D013610:Tachycardia / Q000150:complications* / Q000378:metabolism; D013997:Time Factors
D002245:Carbon Dioxide