Cardiac amyloidosis (CA) is a restrictive cardiomyopathy resulting from the deposition of amyloid fibrils in the myocardial interstitium. Most cases of CA result from fibrils composed of either monoclonal immunoglobulin light chains, or transthyretin protein transthyretin (wild-type or hereditary variants). Although the diagnosis of CA is based on invasive pathology demonstration of amyloid deposits, or non-invasive criteria using advanced cardiovascular imaging techniques, the 12-lead ECG plays a crucial importance in the suspicion of the diagnosis of CA when showing (a) low QRS voltages in limb leads contrasting with marked left ventricular hypertrophy on echocardiogram, (b) marked interatrial, atrioventricular and intraventricular conduction disturbances, (c) pseudo-infarct patterns contrasting with preserved left ventricular function, and finally (d) various types of atrial and ventricular arrhythmias. The treatment of CA has dramatically improved in the last few years with the increased usage of novel therapies. An early suspicion of the diagnosis has dramatically improved the result of treatment. The ECG is playing a crucial role in establishing this early diagnosis.