Cardiovascular Magnetic Resonance Imaging and Heart Failure

Abstract

Purpose of review: The purpose of this review is to summarize the application of cardiac magnetic resonance (CMR) in the diagnostic and prognostic evaluation of patients with heart failure (HF).

Recent findings: CMR is an important non-invasive imaging modality in the assessment of ventricular volumes and function and in the analysis of myocardial tissue characteristics. The information derived from CMR provides a comprehensive evaluation of HF. Its unique ability of tissue characterization not only helps to reveal the underlying etiologies of HF but also offers incremental prognostic information. CMR is a useful non-invasive tool for the diagnosis and assessment of prognosis in patients suffering from heart failure.

Keywords: Cardiomyopathy; Cardiovascular magnetic resonance; Heart failure; Late gadolinium enhancement.

Fig. 1

Ischemic cardiomyopathy images in cine, late gadolinium enhancement (LGE), stress perfusion, microvascular obstruction, and hemorrhage. a, b Still frames from 4-chamber cine in end-diastole and end-systole showing hypokinesis of the mid-ventricle to the apex with an apical aneurysm (between arrows) in a 65-year-old woman. c, d LGE images showing subendocardial delayed enhancement in the apical walls (between arrows) of the 65-year-old woman and subendocardial LGE in a 78-year-old man with an old myocardial infarction (MI). e, f Stress perfusion image showing perfusion defects of the anterior wall and the septum compared to the rest perfusion image, suggesting reversible ischemia (between arrows) in the 65-year-old woman. g LGE image showing microvascular obstruction in the basal inferoseptum (between arrows) in a 40-year-old man with acute MI. h T1 mapping showing the dark core of intramyocardial hemorrhage (between arrows) in the 78-year-old man with the corresponding LGE slice in image (d)

Fig. 2

Non-ischemic cardiomyopathy. Dilated cardiomyopathy images in cine, late gadolinium enhancement (LGE), and T1 mapping. a CMR end-diastolic frames from 4-chamber cine showing biventricular dilation in a 23-year-old man with chronic heart failure. b LGE imaging showing mid-myocardial delayed enhancement in the septum and the inferior wall (arrows). c T1 mapping shows diffusely elevated signals consistent with diffuse fibrosis. Hypertrophic cardiomyopathy (HCM) presentations in cine and late gadolinium enhancement. d, f 4-chamber or 2-chamber long-axis cine images showing different phenotypes of HCM. e, g LGE images showing patchy delayed enhancement (arrows) in corresponding patient cine views. d, f Asymmetric septal hypertrophy. e, g Apical HCM. Arrhythmogenic right ventricular cardiomyopathy. h Still frame from 4-chamber cine in end-diastole showing dilated, trabeculated right ventricle with regional thinning and microaneurysm (white arrows) in a 76-year-old man. i Late gadolinium enhancement image showing enhancement in the right ventricular wall (black arrows). The left ventricular LGE was due to a left circumflex occlusion in this patient, not left ventricular involvement in ARVC (white arrow). Amyloidosis. j, k Still frames from 2-chamber and 4-chamber cines showing bi-atrial enlargement, increased wall thickness of left ventricle, and trace pericardial effusion in a 65-year-old man. l Serial short-axis late gadolinium enhancement images showing diffuse transmural enhancement in the basal to mid-left ventricular myocardium, gradually decreasing to a global subendocardial pattern in the mid-ventricle. Note that the blood pool is dark which is related to abnormal blood pool gadolinium dynamics in the presence of diffuse amyloid deposition in the body

Fig. 3

Inflammatory cardiomyopathy. Acute myocarditis with late gadolinium enhancement (LGE) imaging, T1 and T2 mapping (top row), and follow-up in 3 months (second row) in a 27-year-old male. LGE images showing mid-myocardial to subepicardial LGE in the basal anterolateral wall on the short axis (a) and 2-chamber view (b) and in the apex on the 2-chamber view (B) (arrows). T1 mapping (c) and T2 mapping (d) at the base both showing elevated signal (yellow areas as compared to green areas which is normal). Three months later, there was diminished LGE signal in the corresponding short axis (e) and 2-chamber slices (f). At follow-up, T1 signal remained elevated (g), but T2 signal had returned to normal (h). Cancer immunotherapy–induced myocarditis and acute transplant rejection. Cine imaging of a 62-year-old female with immunotherapy-induced myocarditis (i) and LGE showing no convincing enhancement (j), but T1 mapping (k) and T2 mapping (l) both demonstrated signal elevation. LGE images (m, n) of a 34-year-old female with acute cellular rejection of the transplanted heart showing multifocal mid-myocardial delayed enhancement in the basal septum and basal inferior wall (m, arrows), and the entire subepicardium to mid-myocardium in the mid to apical myocardium (n, arrows). Sarcoidosis. LGE images of a 50-year-old man showing multifocal left ventricular subepicardial, mid-myocardial, and subendocardial delayed enhancement, and LGE of the right ventricle (o, p, arrows)

Fig. 4

Valvular disease example: aortic regurgitation. a Left ventricular outflow tract view in diastole showing aortic regurgitation jet (arrow) in a 56-year-old woman presented with heart failure. b Aortic through-plane phase contrast with magnitude and phase images of the same patient. c Aortic flow curve demonstrating quantitative analysis of forward aortic flow and regurgitant flow as negative flow persisted through the entire diastole (shaded area). This was post-processed from the phase contrast images (b)