Microvascular integrity and the time course of myocardial sodium accumulation after acute infarction

Loss of membrane permeability caused by ischemia leads to cellular sodium a ccumulation and myocardial edema. This phenomenon has important implication s to left ventricular structure and function in the first hours after myoca rdial infarction. We hypothesized that during this period of time, after pr olonged coronary occlusion and complete reflow, the rate of myocardial sodi um accumulation is governed by microvascular integrity. We used 3-dimension al Na-23 MRI to monitor myocardial sodium content changes over time in an i n vivo closed-chest canine model (n=13) of myocardial infarction and reperf usion. Infarcts with microvascular obstruction (MO) defined by both radioac tive microspheres and contrast-enhanced H-1 MRI showed a slower rate of sod ium accumulation as well as lower blood flow at 20 minutes and 6 hours afte r reperfusion, Conversely, the absence of MO was associated with faster rat es of sodium accumulation and greater blood flow restoration. In addition, infarct size by Na-23 MRI correlated best with infarct size by triphenyltet razolium chloride and contrast-enhanced H-1 MRI at 9 hours after reperfusio n. We conclude that in reperfused myocardial infarction, sodium accumulatio n is dependent on microvascular integrity and is slower in regions of MO co mpared with those with patent microvasculature, Finally, Na-23 MRI can be a useful tool for monitoring in vivo myocardial sodium content in acute myoc ardial infarction.