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

Overview
Journal Cureus
Date 2025 Mar 12
PMID 40070618
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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 aV, 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.

References
1.
Kitaoka H, Izumi C, Izumiya Y, Inomata T, Ueda M, Kubo T . JCS 2020 Guideline on Diagnosis and Treatment of Cardiac Amyloidosis. Circ J. 2020; 84(9):1610-1671. DOI: 10.1253/circj.CJ-20-0110. View

2.
Gillmore J, Maurer M, Falk R, Merlini G, Damy T, Dispenzieri A . Nonbiopsy Diagnosis of Cardiac Transthyretin Amyloidosis. Circulation. 2016; 133(24):2404-12. DOI: 10.1161/CIRCULATIONAHA.116.021612. View

3.
Murtagh B, Hammill S, Gertz M, Kyle R, Tajik A, Grogan M . Electrocardiographic findings in primary systemic amyloidosis and biopsy-proven cardiac involvement. Am J Cardiol. 2005; 95(4):535-7. DOI: 10.1016/j.amjcard.2004.10.028. View

4.
Nagueh S, Smiseth O, Appleton C, Byrd 3rd B, Dokainish H, Edvardsen T . Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2016; 29(4):277-314. DOI: 10.1016/j.echo.2016.01.011. View

5.
Perfetto F, Zampieri M, Bandini G, Fedi R, Tarquini R, Santi R . Transthyretin Cardiac Amyloidosis: A Cardio-Orthopedic Disease. Biomedicines. 2022; 10(12). PMC: 9775219. DOI: 10.3390/biomedicines10123226. View