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Microvascular integrity and the time course of myocardial sodium accumulation after acute infarction
C E Rochitte1, R J Kim, H B Hillenbrand
1Cardiology Division, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Insights
Myocardial sodium accumulation after reperfused myocardial infarction is slower in areas with microvascular obstruction. Three-dimensional sodium-23 MRI effectively monitors sodium content and infarct size in acute myocardial infarction.
Area of Science:
- Cardiovascular Research
- Medical Imaging
- Biomedical Engineering
Background:
- Ischemia-induced loss of membrane permeability causes sodium accumulation and myocardial edema.
- These changes significantly impact left ventricular structure and function post-myocardial infarction.
- Microvascular integrity is a key factor in managing sodium levels during reperfusion.
Purpose of the Study:
- To investigate the relationship between microvascular integrity and myocardial sodium accumulation rates.
- To assess the utility of 3-dimensional (23)Na MRI in monitoring sodium content changes in acute myocardial infarction.
- To correlate (23)Na MRI findings with established methods for infarct size and microvascular obstruction assessment.
Main Methods:
- Utilized a canine model of myocardial infarction and reperfusion.
- Employed 3-dimensional (23)Na MRI to track changes in myocardial sodium content over time.
- Quantified microvascular obstruction (MO) using radioactive microspheres and contrast-enhanced (1)H MRI.
- Compared sodium accumulation rates and blood flow in regions with and without MO.
Main Results:
- Infarcts with microvascular obstruction exhibited slower sodium accumulation and reduced blood flow compared to areas without MO.
- Absence of MO correlated with faster sodium accumulation and improved blood flow restoration.
- (23)Na MRI-determined infarct size showed strong correlation with triphenyltetrazolium chloride and contrast-enhanced (1)H MRI at 9 hours post-reperfusion.
Conclusions:
- Myocardial sodium accumulation in reperfused myocardial infarction is dependent on microvascular integrity.
- Regions with microvascular obstruction demonstrate slower sodium accumulation.
- (23)Na MRI is a valuable tool for in vivo monitoring of myocardial sodium content in acute myocardial infarction.
Abstract:
Loss of membrane permeability caused by ischemia leads to cellular sodium accumulation and myocardial edema. This phenomenon has important implications to left ventricular structure and function in the first hours after myocardial infarction. We hypothesized that during this period of time, after prolonged coronary occlusion and complete reflow, the rate of myocardial sodium accumulation is governed by microvascular integrity. We used 3-dimensional (23)Na MRI to monitor myocardial sodium content changes over time in an in vivo closed-chest canine model (n=13) of myocardial infarction and reperfusion. Infarcts with microvascular obstruction (MO) defined by both radioactive microspheres and contrast-enhanced (1)H MRI showed a slower rate of sodium accumulation as well as lower blood flow at 20 minutes and 6 hours after reperfusion. Conversely, the absence of MO was associated with faster rates of sodium accumulation and greater blood flow restoration. In addition, infarct size by (23)Na MRI correlated best with infarct size by triphenyltetrazolium chloride and contrast-enhanced (1)H MRI at 9 hours after reperfusion. We conclude that in reperfused myocardial infarction, sodium accumulation is dependent on microvascular integrity and is slower in regions of MO compared with those with patent microvasculature. Finally, (23)Na MRI can be a useful tool for monitoring in vivo myocardial sodium content in acute myocardial infarction.