84 year-old male with history of myocardial infarction, now presenting with new onset of chest pain.

Figure 1: Image demonstrates a region of delayed enhancement (bright vs. normal myocardium which is dark) in the anterior wall of the left ventricle. This region of delayed enhancement represents an area of prior infarct with scar tissue.

Figure 2: Image through the mid left ventricle shows a larger area of delayed enhancement (bright) in the anterior and anterolateral left ventricular wall in the distribution of the left anterior descending artery.

Figure 3: Static image from oblique coronal true FISP cine through the aortic root demonstrates the aortic valve leaflets, which have limited motion during systole (Movie 2). There is a flow jet in between the margins on the leaflets consistent with stenosis of the aortic valve.

Figure 4: Static image from an oblique axial true FISP cine image through the aortic root at the level of the aortic valves demonstrates the reduced aortic valve orifice area during systole (area < 2 cm2) consistent with mild aortic stenosis.

Movie 1: Short axis cine true FISP at the level of the mid left ventricle demonstrates wall thinning with akinesis of the anterolateral LV wall, consistent with previous myocardial infarction.

Movie 2: Oblique coronal cine true FISP at the level of the aortic root demonstrates a flow jet distal to the aortic valve orifice indicative of aortic stenosis. The aortic valve leaflets are also visible and demonstrate limited motion during systole.

Movie 3: Oblique axial cine true FISP at the level of the aortic valve demonstrates markedly limited motion of the aortic valve leaflets during systole and a reduced aortic valve orifice area (area < 2 cm2). These findings are consistent with mild aortic stenosis.

[Measurement of aortic valve area: area > 1.5 cm2 indicates mild stenosis;
area between 1.0 – 1.5 cm2 indicates moderate stenosis; area < 1.0 cm2 indicates severe stenosis].

Myocardial Infarction of the anterolateral wall of the left ventricle with mild aortic stenosis.
(Reference Application Tip: Viability imaging)

Ischemic heart disease (IHD) is the leading cause of morbidity and mortality in modern industrialized countries worldwide. It is caused by an insufficient supply of oxygen to the myocardium in relation to oxygen demands either at rest or during stress (e.g. exercise). IHD can be caused by a variety of pathophysiologic conditions of which atherosclerosis (coronary artery disease) is the most common. Acute myocardial infarction occurs when blood flow, and therefore oxygen supply, to the myocardium declines below a critical level causing acute death of myocardial cells. Myocardial infarction, which can be transmural or subendocardial, most frequently occurs in the left ventricle, although patients with inferior wall infarction can have right ventricle involvement. The major complications of myocardial infarction include: heart failure, cardiac rupture, true left ventricular aneurysm, false (pseudo) aneurysm, acute mitral regurgitation from papillary muscle rupture, ventricular septal rupture (defect) and mural thrombus with or without peripheral embolization, and acute pericarditis (Dressler’s syndrome).

The concept of myocardial viability is based on the fact that even severely dysfunctional myocardium in patients with ischemic heart disease may show functional improvement after revascularization. It is characterized by maintenance of myocardial structural integrity and metabolic activity, although myocardial contractile function may be decreased. The ability to distinguish viable myocardium from myocardium that has been irreversibly injured is important for therapeutic strategy, especially because revascularization of viable but dysfunctional myocardium can significantly improve long-term patient survival. The greater the extent of viability, the better the outcome post-reperfusion, with greater left ventricular functional improvements, greater reduction in heart failure symptoms, and better exercise tolerance. Therefore, clinical methods that allow for the distinction between viable and non-viable myocardium are important to help determine the patient population with ischemic heart disease who will benefit from interventional or surgical revascularization. Such clinical methods include low-dose dobutamine stress echocardiography, single photon emission computed tomography (SPECT), and 18F-flurodeoxyglucose positron emission tomography (FDG-PET).

In recent years, magnetic resonance imaging (MRI) techniques have emerged as a powerful tool for characterizing ischemic heart disease in the setting of myocardial ischemia and myocardial infarction and, thus, myocardial viability. MRI provides high-quality three-dimensional dynamic imaging of the heart allowing for assessment of global and regional left ventricular function, first-pass myocardial perfusion, and direct imaging of the non-viable myocardial scar. In addition, MRI provides the ability to image the entire myocardial wall, which allows for the measurement of the extent of infarction across the wall (degree of subendocardial vs. transmural involvement). On MR imaging, acutely infarcted myocardium demonstrates increased signal intensity on T2-wieghted spin-echo images. However, T2-weighted spin-echo images do not identify chronic infarcts and can overestimate infarct size by including myocardial areas at risk. In addition, T2-weighted images have a low signal to noise ratio.

Gadolinium-DTPA enhanced MRI provides better quality and high resolution images where areas of infarction appears as hyper-enhanced regions relative to non-infarcted tissue on images acquired late after contrast injection. Contrast enhanced MRI also allows for assessment of infarct microvascular perfusion. After myocardial infarction, the differences in myocardial wash-in and wash-out kinetics of gadolinium enable definition of 3 patterns of myocardial enhancement:

1. Normal (non-ischemic) myocardium: Characterized by rapid wash-in of contrast agent on first-pass images (<30 s) with progressive washout over the next minutes.
2. Infarcted myocardium: Characterized by a slower wash-in but more importantly by a delayed wash-out (>30 min). This delayed contrast enhancement (up to 10 minutes after contrast administration) is likely due to both increased concentration of the gadolinium molecule, impaired washout of the molecule relative to more rapid wash-out from normal myocardium, and due to an increase in the extracellular space and edema at the site of the infarction. Approximately 30 days following the event, the area of infarction will demonstrate thinning of the myocardium and decreased signal on T2 images or gradient echo images due to the presence of fibrosis.
3. Regions of microvascular obstruction: In these regions there is inadequate perfusion despite revascularization of the obstructed coronary artery. These areas are characterized by dramatically delayed contrast wash-in resulting in very low (black) signal intensity on first pass MRI images relative to normal, non-ischemic or necrotic but reperfused myocardium.

Cine MRI sequences of the heart can provide high spatial and temporal resolution in addition to great contrast between the blood pool and myocardium. Cine sequence images, which can be obtained from multiple views along the long or short axis of the left ventricle, can be used to depict the regional wall motion abnormalities and to quantify ventricular volumes. In addition, these images can also depict mechanical complications after myocardial infarction including a true or false aneurysm, septal rupture, mitral regurgitation and pericardial effusion.

References:

1. Higgins CB and A De Roos. Cardiovascular MRI & MRA. Philadelphia: Lippincott Williams & Wilkins, 2003.
2. Maythem Saeed. Minireview: New Concepts in Characterization of Ischemically Injured Myocardium by MRI. Experimental Biology and Medicine. 2001: 367-376.
3. Schneider G, Ahlhelm F, Seidel R, et al. Contrast-Enhanced Cardiovascular Magnetic Resonance Imaging. Topics in Magnetic Resonance Imaging. 2003; 14(5): 386-402.
4. Jorn JW Sandstede. Assessment of Myocardial Viability by MR Imaging. European Radiology. 2003; 13(1): 52-61.
5. Wagner A, Mahrholdt H, Sechtem U, Kim RJ, and RM Judd. MR Imaging of Myocardial Perfusion and Viability. Magnetic Resonance Imaging Clinics of North America. 2003; 11(1): 49-66.