Jan G. Van Emous

Assessment of Myocardial Viability by Intracellular 23Na Magnetic Resonance Imaging

Background—Because of rapid changes in myocardial intracellular Na+ (Na+i) during ischemia and reperfusion (R), 23Na magnetic resonance imaging (MRI) appears to be an ideal diagnostic modality for early detection of myocardial ischemia and viability. So far, cardiac 23Na MRI data are limited and mostly concerned with imaging of total Na+. For proper interpretation, imaging of both Na+i and extracellular Na+ is essential. In this study, we tested whether Na+i imaging can be used to assess viability after low-flow (LF) ischemia. Methods and Results—Isolated rat hearts were subjected to LF (1%, 2%, or 3% of control coronary flow) and R. A shift reagent was used to separate Na+i and extracellular Na+ resonances. Acquisition-weighted 23Na chemical shift imaging (CSI) was alternated with 23Na MR spectroscopy. Already during control perfusion, Na+i could be clearly seen on the images. Na+i image intensity increased with increasing severity of ischemia. During R, Na+i image intensity remained highest in 1% LF hearts. Not only did we find very good correlations between Na+i image intensity at end-R and end-diastolic pressure (R=0.85, P<0.001) and recovery of the rate-pressure product (R=−0.88, P<0.001) at end-R, but most interestingly, also Na+i image intensity at end-LF was well correlated with end-diastolic pressure (R=0.78, P<0.01) and with recovery of the rate-pressure product (R=−0.81, P<0.01) at end-R. Furthermore, Na+i image intensity at end-LF was well correlated with creatine kinase release during R (R=0.79, P<0.05) as well as with infarct size (R=0.77, P<0.05). Conclusions—These data indicate that 23Na CSI is a promising tool for the assessment of myocardial viability.

Changes of intracellular sodium T2 relaxation times during ischemia and reperfusion in isolated rat hearts.

The effect of ischemia and reperfusion on transverse relax ation (T2) of intracellular Na+ (Na+i) was measured with 5‐min time resolution in isolated rat hearts. Nai T2 relaxation was biexponential with 28 ± 7% fast (T2f)and 72 ± 7% slow (T2s) decay. This ratio was constant throughout the protocol. Dur ing 20 min of ischemia, Nai T2s increased from 18.9 ± 2.7 ms to 26.4 ± 1.1 ms (P < 0.001), whereas T2f did not change significantly (3.1 ± 1.8 versus 2.3 ± 1.6 ms during control), and Na+i increased from 9.0 ± 1.0 to 19.5 ± 1.0 mmol/liter (P < 0.001). T2s and Na+i declined again during reperfusion. Changes in T2s relaxation correlated significantly (r = 0.73, P < 0.001) with the time course of Na+i.

Glycolytic ATP production is not essential for Na+-K+ ATPase function and contractile recovery during postischemic reperfusion in isolated rat hearts

Accumulation of intracellular sodium (Nai +) during ischemia is an important determinant of calcium overload upon reperfusion via Na + -Ca 2 + exchange. Postischemic reperfusion of ischemic myocardium results in an immediate decrease of Na + via (resumption) of Na + -K + ATPase activity [1]. Since energy from glycolysis may be preferentially used to fuel membrane functions [2], in the present study the requirement of glycolytic ATP for the postischemic decline of Nai + was evaluated.