Abstract
In ischemic heart disease, cardiac MRI, besides being the gold standard for evaluation of quantitative ventricular function, enables evaluation of myocardial wall thickness, T2-weighted imaging for myocardial edema and infarct quantification and transmurality. Delayed hyperenhancement sequences are highly predictive of scar formation, being associated with myocyte necrosis. The extent and transmurality of delayed hyperenhancement has prognostic implications and is inversely proportional to the degree of functional recovery after acute myocardial infarction. A greater transmural extent of infarction (eg, hyperenhancement involving >50% of the wall thickness) can predict regions that are less likely to improve in function after therapy. The ultimate focus of MRI in ischemic heart disease is in diagnosis, quantification of myocardium at risk, salvageable myocardium, perfusion defects and differentiation of viable myocardium from non viable myocardium to enable prognostication.
Keywords: Cardiac MRI, Ischemic heart disease, Viability
1. Clinical details
A 74-year-old male, normotensive, non-diabetic, smoker, no family history of ischemic heart disease with known coronary artery disease sustained myocardial infarction 20 years earlier. Coronary angiography revealed triple vessel disease for which he underwent CABG 18 years previously. The patient presented with dyspnea on exertion, relieved on rest. On admission pulse 60/min, BP 120/80 mm Hg. 2D echo Doppler Color revealed akinetic anterior septum, IVS, apex, anterior wall, LVEF 30%, normal LV dimensions with dilated LA. Trace MR. Cardiac MRI was requested for viability assessment.
2. Cardiac MRI depicted
LV Functional analysis: LVEDV: 146 ml, LVESV: 104 ml, LVEF: 29%, Stroke volume: 42 ml and Cardiac output: 2.2 l/min.
There was myocardial involvement in the basal anterior, anteroseptal and inferoseptal; mid cavity anterolateral, anterior, antero septal, inferoseptal, and inferior; apical septal, anterior, inferior and lateral wall and apex of the LV with segments of wall thinning (wall thickness <5 mm), severe hypokinesia to akinesia in part and apical dyskinesia with perfusion defect (Fig. 1) and post contrast hyperenhancement extending from the subendocardial to the epicardial surface, varying in transmurality from <25% to >75% wall thickness and near transmural infarction consistent with non viable myocardium (Fig. 2, Fig. 3). The extent of myocardial infarction was 19% of the LV myocardial volume. Ballooning of the LV apex was seen. Trace MR was evident. There was no MRI evidence of contained thrombus or mass. The interventricular septum was intact.
Fig. 1.
Defect on first pass perfusion at the site of myocardial thinning.
Fig. 2.
Delayed post contrast enhanced imaging on short axis views demonstrating subendocardial to near transmural scar formation in the anterior, antero septal and inferoseptal segments at mid cavity level.
Fig. 3.
Delayed post contrast enhanced imaging in the 4 chamber view demonstrating basal, mid cavity and apical septal subendocardial scar formation with near transmural involvement in part.
3. Conclusion
Myocardial viability is critical in the evaluation and management of patients with ischemic heart disease. Cardiac MRI with its improved spatial and temporal resolution now permits accurate and non invasive evaluation of cardiac morphology, function, regional and global myocardial wall motion abnormalities, myocardial edema, perfusion, ischemia and scar assessment.
Conflicts of interest
The author has none to declare.