Effect of adjunctive intracoronary adenosine on myocardial ischemia, hemodynamic function and left ventricular performance during percutaneous transluminal coronary angioplasty: clinical access to ischemic preconditioning?

Abstract

Background: Ischemic preconditioning has been defined as a mechanism that renders the heart more resistant to subsequent ischemia. Adenosine plays an important role in the pathogenesis of ischemic preconditioning.

Objective: To assess whether intracoronary administration of adenosine prevents the deterioration of left ventricular performance and hemodynamic function by allowing adaptation to myocardial ischemia in the setting of percutaneous transluminal coronary angioplasty (PTCA).

Design: This was a prospectively randomized doubly blinded trial.

Methods: We investigated 20 patients undergoing PTCA of the left anterior descending coronary artery supplying myocardium with normal left ventricular function in the setting of stable angina pectoris. Patients were randomly allocated to be administered adenosine intracoronarily (20 mg/10 min) or an equal amount of saline, providing a control population. Results of standardized chest pain questionnaires, tolerated inflation times, ST-segment shifts, left ventricular and aortic pressures, isovolumetric phase indexes, and indexes of volume and ejection fraction during the course of PTCA between the two groups were compared.

Results: Patients administered adenosine tolerated significantly longer balloon-inflation times (188 +/- 41 versus 153 +/- 36 s; P = 0.03), which were associated with less pronounced signs of ischemia, and exhibited less deterioration of isovolumetric phase indexes during PTCA. Deterioration of left ventricular ejection fraction was slightly less severe with adenosine (72 +/- 5% before PTCA versus 64 +/- 6% during angioplasty) than it was for the control group (71 +/- 7% before PTCA versus 60 +/- 7% during angioplasty; P = 0.11).

Conclusions: Intracoronary application of adenosine prior to coronary angioplasty increases tolerance of ischemia and prevents deterioration of left ventricular hemodynamics during ischemia. One potential explanation of these results is that induction of ischemic preconditioning took place.