Abstract Background Left ventricular (LV) wall thickening and diastolic dysfunction on a transthoracic echocardiogram (TTE) without high voltage R wave in V5 leads on ECG leads to a diagnosis of cardiac amyloidosis. A final diagnosis is made by endomyocardial biopsy. However, amyloid sometimes invade the right ventricle (RV), and left (LA) and right (RA) atria to cause ECG changes such as sick sinus syndrome (SSS), arrhythmia, and QRS wave axis deviation. Purpose To predict sites of wall thickening and abnormal late enhancement (LE) on cardiac computed tomography (CT) and magnetic resonance imaging (MRI), suggesting amyloid invasion, using cardiac rhythm and other ECG findings in patients with cardiac amyloidosis confirmed by biopsy. Methods A total of 26 patients (11 females) with suspected cardiac amyloidosis, showing LV wall thickening by TTE without a high voltage R wave in V5 leads on ECG, underwent cardiac enhanced CT. LV wall thickening on CT in the early phase led to late phase acquisition to detect LE. 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 Two patients (cases 1 and 2) had SSS (junctional rhythm), one had atrial tachycardia, and the remaining two (cases 4 and 5) had a normal sinus rhythm. In case 1, ECG showed a left axis QRS wave deviation, no low voltage R wave in limb leads and a mild LA load. Wall thickening in the basal interventricular septum (IVS), LV inferior-posterior wall, LA on CT, 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 were observed. In case 2, ECG showed a normal QRS wave axis, no low voltage R wave in limb leads, no LA load, wall thickening in whole LV, RV, LA, and IVS on CT, and unclear (CT) or no (MRI) LE. In case 3, ECG showed a normal QRS wave axis, with low voltage R wave in limb leads, no LA load, wall thickening in LA and basal IVS on CT, LE in LA and basal IVS on CT, and LE in LA only on MRI. In case 4, ECG showed left axis QRS wave deviation, a low voltage R wave in limb leads, and no LA load, wall thickening in the LA and RV moderator band on CT, unclear LE on CT, and LE in whole LV, endocardium in the RV, and whole IVS on MRI. In case 5, ECG showed a right axis QRS wave deviation, low voltage R wave in limb leads, and a mild LA load, wall thickening in the IVS, LV lateral wall, LV anterior wall, RA, RV outflow tract, and RA appendage, and no LE on CT (MRI not performed). Conclusions This pilot study of a few patients with cardiac amyloidosis revealed few links between cardiac rhythm and other ECG findings with sites of wall thickening and abnormal LE. However, a longer-term study of more patients may lead to detecting an association between these variables with this methodology. Funding Acknowledgement Type of funding sources: None.