Regional myocardial perfusion and performance

The function of the heart is to pump blood from the veins into the arteries in response to the need of the tissues for oxygen and substrates. During its action the heart itself needs these nutrients. Factors that mainly determine the myocardial oxygen demand are (fig.0.1): heart rate, myocardial contractile performance (contractility) and ventricular wall tension. The oxygen supply is delivered by the coronary perfusion. Under normal conditions of coronary perfusion an equilibrium between the demand and the supply is present and adaptation is possible during a wide range of circumstances where myocardial oxygen demand is increased. A limitation of the coronary inflow, due to a coronary stenosis, quickly leads to an oxygen deficit. Even at slight flow reductions a redistribution of blood flow from the endocardium to the epicardium leads to endocardial malfunction. Therefore, the distribution of the blood flow within the myocardium is also a determinant of myocardial oxygen supply (fig.0.1). Acute myocardial ischaemia leads within seconds to an impaired segmental contractile function. When the ischaemic area constitutes a considerable fraction of the left ventricular muscle mass, a decrease in overall contractile function, cardiac output and arterial blood pressure occurs. Furthermore, the cardiac electro-physiological stability is disturbed, which frequently leads to arrhythmias of various severities including ventricular fibrillation. The pharmacological treatment of ischaemia is directed to restore the myocardial oxygen demand and supply relationship, either by decreasing the demand or by increasing the supply, whereas antiarrhythmic therapy is used to stabilize the haemodynamic condition and to reduce the risk of fatal arrhythmias. Enhancement of the oxygen supply can theoretically be realized by augmentation of perfusion pressure or perfusion time, while another approach is to lower the coronary vascular resistance or to augment the blood flow through interarterial collateral channels. The reduction of myocardial oxygen demand is carried out by reducing heart rate, myocardial contractility or intramyocardial wall tension. The present thesis, where an attempt is made to gain insight into the transmural distribution of the myocardial blood flow and its relationship with segmental function, has been broadly subdivided into four parts