Comparison of sites of wall thickening and abnormal late enhancement on cardiac CT and magnetic resonance imaging with electrocardiography findings in patients with confirmed cardiac amyloidosis
Authors: Funabashi N , Kobayashi Y 
Published: February 2022

Funding Acknowledgements

Type of funding sources: None.

Background

Left ventricular (LV) wall thickening and diastolic dysfunction on a transthoracic echocardiogram (TTE) without a high voltage R wave on V5 leads on an ECG leads to a diagnosis of cardiac amyloidosis. A final diagnosis is made by endomyocardial biopsy. However, amyloid sometimes invades the right ventricle (RV), and left (LA) and right (RA) atria, causing ECG changes such as sick sinus syndrome (SSS), arrhythmia, and QRS wave axis deviation.

Purpose

To elucidate the relationship between sites of wall thickening and abnormal late enhancement (LE) on cardiac computed tomography (CT) and magnetic resonance imaging (MRI), suggesting amyloid invasion, with ECG findings in patients with cardiac amyloidosis confirmed by biopsy.

Methods

A total of 26 patients (11 females) with suspected cardiac amyloidosis, who had LV wall thickening by TTE without a high voltage R wave in V5 leads on ECG, underwent cardiac CT. LV wall thickening observed on CT in the early phase led to a late phase acquisition. Five patients (3 females, mean age 73 years) were diagnosed with cardiac amyloidosis: complicated multiple myeloma, 2; senile ATTR (transthyretin) amyloidosis, 1; immunoglobulin light chain (AL) amyloidosis, 1; and transthyretin mutation, 1. Four patients underwent cardiac MRI.

Results

Case 1 had wall thickening in the basal interventricular septum (IVS), LV inferior-posterior wall, LA on CT, abnormal LE in the endocardium in whole LV, RV, and RA on CT, and LE in the endocardium in whole LV, RV, LA, and IVS on MRI. ECG showed SSS (junctional rhythm), left axis QRS wave deviation, no low voltage R wave in limb leads, and a mild LA load. Case 2 had wall thickening in whole LV, RV, LA, and IVS on CT, and unclear (CT) or no (MRI) abnormal LE. ECG revealed SSS (junctional rhythm), a normal QRS axis, no low voltage R wave in limb leads, and no LA load. Case 3 had wall thickening in the LA and basal IVS on CT, abnormal LE in the LA and basal IVS on CT, and LE in the LA only on MRI. ECG revealed atrial tachycardia, a normal QRS axis with low voltage R wave in limb leads, and no LA load. Case 4 had wall thickening in the LA, an RV moderator band on CT, an unclear LE on CT, and LE in whole LV, endocardium in the RV, and whole IVS on MRI. ECG showed a normal sinus rhythm, left axis QRS wave deviation, with low voltage R wave in limb leads, and no LA load. Case 5 had wall thickening in the IVS, LV lateral wall, LV anterior wall, RA, RV outflow tract, and RA appendage, and no abnormal LE on CT (MRI not performed). ECG revealed a normal sinus rhythm, right axis QRS wave deviation, with low voltage R wave in limb leads, and a mild LA load.

Conclusions

In this pilot study of a small number of patients with cardiac amyloidosis, few relationships between sites of wall thickening and abnormal LE on ECG were found. However, a long-term follow-up study with more patients may reveal relationships between such parameters using this methodology. Abstract Figure. Classification by wall thickening on CT