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Role of Cardiac Magnetic Resonance Imaging in the Detection of Cardiac Amyloidosis

Imran S. Syed, MD^_*,_*, James F. Glockner, MD, PhD, DaLi Feng, MD^_*, Philip A. Araoz, MD, Matthew W. Martinez, MD^_*,, William D. Edwards, MD, Morie A. Gertz, MD, Angela Dispenzieri, MD, Jae K. Oh, MD^_*, Diego Bellavia, MD, PhD^_*, A. Jamil Tajik, MD^||, Martha Grogan, MD^_*

^_* Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota
Division of Radiology, Mayo Clinic, Rochester, Minnesota
Division of Anatomic Pathology, Mayo Clinic, Rochester, Minnesota
Division of Hematology, Mayo Clinic, Rochester, Minnesota
^|| Division of Cardiovascular Diseases, Mayo Clinic, Scottsdale, Arizona

^_* Reprint requests and correspondence: Dr. Imran S. Syed, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905 (Email: syed.imran{at}mayo.edu).

Objectives: Our aim was to evaluate the role and mechanism of late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) in identifying cardiac amyloidosis (CA) and to investigate associations between LGE and clinical, morphologic, functional, and biochemical features.

Background: CA can be challenging to diagnose by echocardiography. Recent studies have demonstrated an emerging role for LGE-CMR.

Methods: LGE-CMR was performed in 120 patients with amyloidosis. Cardiac histology was available in 35 patients. The remaining 85 patients were divided into those with and without echocardiographic evidence of CA.

Results: Of the 35 patients with histologically verified CA, abnormal LGE was present in 34 (97%) patients and increased echocardiographic left ventricular wall thickness in 32 (91%) patients. Global transmural or subendocardial LGE (83%) was most common and was associated with greater interstitial amyloid deposition (p = 0.03). Suboptimal myocardial nulling (8%) and patchy focal LGE (6%) were also observed. LGE distribution matched the deposition pattern of interstitial amyloid. Among patients without cardiac histology, LGE was present in 86% of those with evidence of CA by echocardiography and in 47% of those without evidence of CA by echocardiography. In patients without echocardiographic evidence of CA, the presence of LGE was associated with worse clinical, electrocardiographic (ECG), and cardiac biomarker profiles. In all patients, LGE presence and pattern was associated with New York Heart Association functional class, ECG voltage, left ventricular mass index, right ventricular wall thickness, troponin-T, and B-type natriuretic peptide levels.

Conclusions: LGE is common in CA and detects interstitial expansion from amyloid deposition. Global transmural or subendocardial LGE is most common, but suboptimal myocardial nulling and focal patchy LGE are also observed. LGE-CMR may detect early cardiac abnormalities in patients with amyloidosis with normal left ventricular thickness. The presence and pattern of LGE is strongly associated with clinical, morphologic, functional, and biochemical markers of prognosis.

Key Words: amyloidosis • cardiac magnetic resonance • cardiomyopathy

Abbreviations and Acronyms   BNP = B-type natriuretic peptide   CA = cardiac amyloidosis   CMR = cardiac magnetic resonance   EF = ejection fraction   FOV = field of view   Gd = gadolinium   LGE = late gadolinium enhancement   LV = left ventricle/ventricular   LVMI = left ventricular mass index   NYHA = New York Heart Association   PF = patchy focal   RV = right ventricle/ventricular   SCA = senile cardiac amyloidosis   SN = suboptimal nulling   TE = echo time   TI = inversion time   TR = repetition time

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