Nifedipine infusion increased subepicardial myocardial blood flow and reduced epicardial ST-segment elevation, but did not reduce ischaemia-induced conduction delay or arrhythmias.
Does nifedipine infusion improve myocardial blood flow and reduce arrhythmias in a dog model of severe myocardial ischaemia?
In a canine model of severe myocardial ischemia, nifedipine improved subepicardial blood flow but failed to prevent ischemia-induced conduction delays or reperfusion arrhythmias.
The effects of nifedipine were studied in a model of local myocardial ischaemia, comprising anaesthetized thoracotomized dogs in which a critical constriction of the left circumflex coronary artery (LCX) was combined with sudden occlusion of the left anterior descending coronary artery (LAD). Since more than one coronary artery is involved in ischaemic heart disease, the model seems to reflect the clinical situation very closely. In this model, infusion of 1 microgram kg-1 min-1 nifedipine increased myocardial blood flow within the stenosed area served by the LCX as well as in the myocardial region supplied by the LAD, mainly in the subepicardium. Accordingly, the drug reduced ischaemic ST-segment elevation only in the epicardium. It is suggested that nifedipine directed flow to the sub-epicardium of the ischaemic area by improving the collateral circulation. This redistribution of flow resulted in a decrease in the endo/epicardial flow ratio. Nifedipine did not change the inhomogeneity of electrical activation indicating that it has no effect on the ischaemia-induced conduction delay. At the same time nifedipine was not able to reduce either the number of extrasystoles appearing in the early postocclusion and reperfusion phase or the incidence of ventricular fibrillation occurring mainly during reperfusion.
Szekeres et al. (Fri,) conducted a other in Severe myocardial ischaemia. Nifedipine was evaluated on Myocardial blood flow, ST-segment elevation, electrical activation, and arrhythmias. Nifedipine infusion increased subepicardial myocardial blood flow and reduced epicardial ST-segment elevation, but did not reduce ischaemia-induced conduction delay or arrhythmias.