Cardiac amyloidosis masquerading as acute coronary syndrome
Yong Yong Tew1,2, Anne Scott3,4
1Edinburgh Heart Centre, Royal Infirmary of Edinburgh, Edinburgh, UK yongyongtew@gmail.com.
Insights
A patient with chest pain and left ventricular hypertrophy was diagnosed with primary AL amyloidosis. Early diagnosis and chemotherapy led to a stable condition at 1-year follow-up.
Area of Science:
- Cardiology
- Oncology
- Nephrology
Background:
- Distinguishing cardiac AL amyloidosis from coronary artery disease can be challenging.
- Left ventricular hypertrophy (LVH) in the absence of hypertension requires thorough investigation.
Observation:
- A 53-year-old man presented with chest pain, ECG changes, and elevated cardiac troponin I.
- Initial investigations revealed moderate coronary calcific disease but no flow limitation, and LVH on echocardiography.
- Cardiac MRI showed atypical late gadolinium enhancement patterns, not typical for amyloidosis.
Findings:
- A raised serum free kappa light chain and amyloid deposition in bone marrow confirmed primary AL amyloidosis with cardiac involvement.
- The patient's condition was initially misattributed to a 'plaque rupture' event.
Implications:
- This case highlights the importance of considering AL amyloidosis in patients with unexplained LVH and cardiac symptoms.
- Timely diagnosis through specific biomarkers and bone marrow examination is crucial for appropriate management.
- Chemotherapy offers a viable treatment option, leading to clinical stability in cardiac AL amyloidosis.
Abstract:
A 53-year-old man presented to a district general hospital with chest pain, ECG changes and a small high-sensitivity cardiac troponin I rise. There were no symptoms of heart failure. CT coronary angiography revealed moderate calcific disease and conventional angiography confirmed no flow limitation. Echocardiography showed left ventricular hypertrophy (LVH). His blood pressure remained normal throughout his admission. The tertiary centre labelled this as a 'plaque rupture' event but the LVH remained unexplained. Cardiac MRI displayed an unusual pattern of late gadolinium enhancement, which was not classical of amyloid. However, a raised serum free kappa light chain along with the deposition of amyloid on his bone marrow aspirate confirmed the diagnosis of primary AL amyloidosis with cardiac involvement. The patient went on to have chemotherapy and remained stable at 1-year follow-up.
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