Does nitrite reduce ischaemia-reperfusion injury in patients with acute ST segment elevation myocardial infarction?

Heart attacks are common and are due to a blockage of one of the arteries that supply the heart with blood. The associated lack of oxygen supply causes death of the heart muscle supplied by this artery. Prompt opening of the blocked artery (eg by inflation of a balloon in the artery) limits the extent of this damage. However, the restoration of blood flow itself causes a degree of damage to the heart muscle. In this study we plan to investigate whether a drug called sodium nitrite given to patients suffering from heart attacks immediately before opening the blocked artery will reduce the damage to the heart muscle. This is important because when a large amount of heart muscle is damaged the patient is at risk of developing heart failure a condition associated with breathlessness and a poor survival.

The anion nitrite is reduced to nitric oxide under hypoxic and/or acidotic conditions, resulting in targeted delivery of nitric oxide to hypoxic tissues. Recent work in animal models has shown that nitrite administration at doses well below those which have any effect on blood pressure potently protects against ischaemia- reperfusion injury when administered either before ischaemia or immediately before reperfusion. This proposal will evaluate whether nitrite administration protects against ischaemia-reperfusion injury and reduces infarct size in patients presenting with acute ST segment elevation myocardial infarction.