Role of cardiovascular magnetic resonance in acute and chronic ischemic heart disease

Abstract

Cardiovascular magnetic resonance (CMR) is a multi-parametric, multi-planar, non-invasive imaging technique, which allows accurate determination of biventricular function and precise myocardial tissue characterization in a one-stop-shop technique, free from the use of ionizing radiations. Though CMR has been increasingly applied over the last two decades in every-day clinical practice, its widest application has been in the assessment of ischemic cardiomyopathy.

Keywords: Acute myocardial infarction; Cardiovascular magnetic resonance; Chronic ischemic heart disease.

Fig. 1

Myocardial infarction: overview. T2-weighted two chamber long axis view showing myocardial oedema in the basal to mid-cavity inferior wall (a) with concomitant subendocardial late gadolinium enhancement (LGE) in the post-contrast sequence (b) in a patient with acute subendocardial infarction in the proximal to mid right coronary artery territory. T2-weighted three chamber long axis view showing myocardial oedema in the mid-apical anteroseptum with evidence of a hypo-intense core (c, white arrow), consistent with intramyocardial haemorrhage, in a patient with transmural infarction in the distal left anterior descending territory (d) with persistence of microvascular obstruction (d, white arrow). Four chamber long axis post-contrast view showing subendocardial LGE of the mid-cavity anterolateral wall (e). Two chamber long axis post-contrast view showing transmural LGE of the mid-apical inferior wall (f)

Fig. 2

Complications of acute myocardial infarction. Two chamber long axis post-contrast sequence showing contained chronic rupture of the anterior wall (a, white arrow) in a patient with transmural myocardial infarction in the left anterior descending territory. Three chamber long axis cine sequence showing large pseudo-aneurysm of the mid-cavity inferolateral wall (b) with evidence of flow (b, white arrow-head) between a “tunnel-like” connection with the left ventricle in a patient with trasmural infarction in the left circumflex territory. Mid-cavity short-axis post-contrast sequence showing myocardial infarction of the papillary muscles (c). Mid-cavity short-axis post-contrast sequence showing myocardial infarction of the right ventricular inferior wall (d, black arrow) in a patient with transmural infarction in the basal inferior wall. Early (e) and late (f) four chamber long axis gadolinium enhancement sequences showing a large apical thrombus in a patient with transmural myocardial infarction in the distal left anterior descending territory (f)

Fig. 3

Acute coronary syndromes with normal angiogram. Early gadolinium enhancement sequences showing extensive epicardial enhancement (a, black arrow) and corresponding late gadolinium (LGE) on the post-contrast sequences (b, black arrow) in a patient with acute myocarditis. T2-weighted images showing focal discrete oedema in the mid-cavity inferolateral wall (c, white arrow) with corresponding LGE on post-contrast sequences (d, white arrow) in a patient with embolic myocardial infarction in the mid left circumflex territory. T2-weighted sequences showing acute myocardial oedema in the apical segments (e) with no evidence of late gadolinium enhancement (LGE) on the post-contrast sequences (f) in a patient with Tako-Tsubo cardiomyopathy

Fig. 4

Myocardial viability and left ventricular (LV) recovery after revascularization. Long-axis two (a) and four chamber (b) cine sequences showing marked thinning of the LV anterior and anteroseptal walls in a patient with severe disease of the mid-distal left anterior descending (LAD); post-contrast sequences showing viable myocardium in the mid-distal LAD territory as late gadolinium enhancement (LGE) is limited to the subendocardium (c, d, white arrow). Long-axis two (e) and four chamber (f) cine sequences showing recovery of LV wall thickness 3 months after revascularization of the LAD

Fig. 5

Stress perfusion CMR. Three slice (base, mid and apex—a, b and c, respectively) short axis stress perfusion sequences acquired at peak adenosine infusion showing two separate areas of hypoperfusion, in the proximal to distal inferior (a–c, white arrow) and mid-cavity anterior walls (b, white arrow), with a normal rest perfusion (d–f) and only a discrete area of subendocardial late gadolinium enhancement in the mid-cavity anterior wall (h) on post-contrast images (g–i). Overall, these findings are consistent with inducible myocardial ischemia in all right coronary artery territory with ischemia superimposed to the infarcted area in the mid left anterior descending territory