Lampros Katsaros

Afterload-induced left ventricular diastolic dysfunction during myocardial ischaemia and reperfusion.

What is the central question of this study? While the load dependence of the diastolic function is established for the normal heart, little is known about the response of the acutely ischaemic and reperfused myocardium to alterations in afterload. What is the main finding and its importance? Using a model that simulates the clinical scenario of acute ischaemia–reperfusion, we show that increased afterload aggravates diastolic dysfunction during both acute ischaemia and reperfusion. In addition, increased afterload induces diastolic dyssynchrony, which might be the underlying mechanism of the diastolic dysfunction of the ischaemic myocardium. These findings provide us with new information regarding how better to manage patients who undergo revascularization therapy after acute myocardial infarction.

MITOCHONDRIAL NA+/CA2+ EXCHANGER INHIBITION DURING REPERFUSION EXHIBITS POTENTIAL CARDIOPROTECTIVE EFFECT, IN A PORCINE ISCHEMIA-REPERFUSION MODEL

Inhibition of mitochondrial Na+/Ca2+ exchanger has been recently recognized as a novel therapeutic target for the prevention of arrhythmias in heart failure. We examined the effects of CGP-37157, an inhibitor of the mitochondrial Na+/Ca2+ exchanger, administered at the onset of reperfusion, on