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Incidentally detected cardiac amyloidosis on 99mTc-MDP bone scintigraphy
1Department of Radiology, King Faisal Specialist Hospital & Research Center, MBC#28 P.O. Box 3354, Riyadh, Saudi Arabia.
Insights
Methylene diphosphate (MDP) shows potential for diagnosing cardiac amyloidosis (CA), a cause of heart failure. This widely available tracer may serve as a noninvasive diagnostic tool, comparable to other bone-seeking agents.
Area of Science:
- Cardiology
- Nuclear Medicine
- Radiology
Background:
- Cardiac amyloidosis (CA) is a significant cause of restrictive cardiomyopathy and heart failure with preserved ejection fraction (HFpEF).
- Current diagnostic tracers for CA, including 99mTc-DPD, 99mTc-PYP, and 99mTc-HMDP, are not widely accessible.
- Methylene diphosphate (MDP) is a widely available bone-seeking tracer, but its utility in CA diagnosis is based on limited case reports.
Abstract:
Cardiac amyloidosis (CA) is an important cause of restrictive cardiomyopathy and heart failure with preserved ejection fraction (HFpEF). At present, 3 bone-seeking tracers, 99mTc-diphosphono-1,2-propanodicarboxylic acid (99mTc-DPD), 99mTc-pyrophosphate (99mTc-PYP), and 99mTc-hydroxymethylene diphosphonate (99mTc-HMDP), have been evaluated for detecting CA, but they are not widely available. In contrast, methylene diphosphate (MDP) is widely available. However, only sporadic case reports have shown that MDP can accumulate in patients with CA. We report an 86-year-old man with multiple medical problems, including hypertension, hyperlipidemia, HFpEF, and a history of treated prostate cancer, who was referred for a 99mTc-MDP bone scan to rule out bone metastasis. The bone scan was negative for bone metastasis, but there was mild tracer accumulation in the heart, suggestive of CA. Subsequently, CA was diagnosed on 99mTc-PYP imaging. MDP may play a role comparable to other bone-seeking tracers in the diagnosis of CA and may be used as a noninvasive adjunct in the diagnosis of CA. Future research should compare MDP with other bone-seeking tracers for the diagnosis of CA. In addition, mechanistic studies on tracer binding to amyloid fibrils may help understand the pathophysiology of CA and facilitate the development of better and more specific tracers for CA.
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