# Transthyretin Cardiac Amyloidosis in a Very Elderly Patient With a History of Inferior Myocardial Infarction: A Case Report

## TL;DR

This case report describes a very elderly patient with transthyretin cardiac amyloidosis and a history of myocardial infarction, highlighting the importance of distinguishing true MI from pseudo-MI patterns in ECG findings.

## Contribution

The novelty lies in demonstrating that pathological Q waves in ATTR-CA can reflect a true prior MI rather than a pseudo-MI pattern.

## Key findings

- ECG findings showed abnormal Q waves and ST-T changes consistent with a prior inferior MI.
- Echocardiography revealed infero-septal wall motion abnormalities and wall thinning, supporting the MI diagnosis.
- ATTR-CA was confirmed with technetium-99m-pyrophosphate scintigraphy and monoclonal protein detection.

## Abstract

Transthyretin cardiac amyloidosis (ATTR-CA) involves the buildup of transthyretin protein in the heart muscle in the form of amyloid fibrils, which can affect heart structure and function. Common ECG findings of ATTR-CA include low QRS voltage and a pseudo-myocardial infarction (MI) pattern, defined as pathological Q waves or QS complexes in two consecutive leads without a history of MI or echocardiographic evidence of akinetic areas. Here, we present a case of ATTR-CA in a very elderly patient, in whom pathological Q waves on ECG were true indicators of a prior inferior MI. A 96-year-old woman with a history of inferior MI presented to her primary care clinic with a one-week history of nocturnal dyspnea. She had undergone coronary stent placement in the distal right coronary artery five years earlier for inferior MI. An ECG revealed abnormal Q waves, ST elevation of 0.5 mm, and T wave inversion in limb leads III and aVF, with no significant findings suggestive of left ventricular (LV) hypertrophy. Over a two-year period, QRS voltage progressively decreased in all leads, while the ST-T changes remained unchanged. Transthoracic echocardiogram (TTE) showed LV concentric hypertrophy with an increased wall thickness of 14 mm, except in the infero-septal region. In basal and mid-short-axis views, infero-septal wall motion was severely reduced, with notable wall thinning in contrast to the global LV hypertrophy observed elsewhere - findings consistent with prior inferior MI. The patient was ultimately diagnosed with ATTR-CA based on technetium-99m-pyrophosphate scintigraphy and monoclonal protein detection tests. Clinicians should recognize that pathological Q waves in ATTR-CA do not always indicate a pseudo-MI pattern. When both ECG and TTE suggest an MI pattern, further evaluation for coronary artery disease is warranted as part of the ATTR-CA diagnostic workup. In patients with both ATTR-CA and prior MI, a comprehensive clinical approach addressing both conditions is essential for optimizing prognosis.