Diastolic relaxation abnormalities during ischaemia and their association with high energy phosphate depletion, intracellular pH and myocardial blood flow.

Diastolic relaxation of cardiac muscle is an energy requiring process dependent upon restoration of a very low cytosolic calcium concentration. During demand ischaemia, induced by an increase in myocardial oxygen demand in the setting of restricted coronary blood flow, myocardial relaxation is impaired with a resultant decrease in left ventricular chamber distensibility. Metabolic studies suggest that high energy phosphate depletion alone cannot account for these relaxation abnormalities. Changes in myocardial pH and coronary blood flow modulate the impaired relaxation. The most likely hypothesis to explain impaired relaxation during demand ischaemia is that slow calcium uptake and incomplete calcium sequestration are characteristic of the physiology of angina pectoris and demand ischaemia, underlying the increased diastolic stiffness seen in these conditions.