Key result
I-123 MIBG imaging reveals marked cardiac sympathetic denervation in AL amyloidosis without heart failure.
Why the study?
Myocardial adrenergic denervation had not been described in patients with primary (AL) amyloidosis without congestive heart failure.
Case Report (n=3)
This is the first report demonstrating marked cardiac sympathetic denervation in patients with AL amyloidosis without congestive heart failure, which may be implicated in the pathogenesis of cardiac conduction disturbances.
Answers are grounded in this paper and cite their sources.
May signal early cardiac denervation in AL amyloidosis without HF; hypothesis-generating and requires validation in larger cohorts.
Three patients, 2 women and 1 man, with primary (AL) amyloidosis without congestive heart failure are described; all 3 patients presented reduced I-123 metaiodobenzylguanidine (MIBG) myocardial uptake suggesting marked cardiac sympathetic denervation. This is the first time myocardial adrenergic denervation is described in patients with AL amyloidosis without evidence of congestive heart failure; the observed denervation could be implicated in the pathogenesis of cardiac conduction disturbances which are common in this disease.
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Lekakis et al. (2003) conducted a case report in Primary (AL) amyloidosis without congestive heart failure (n=3). I-123 metaiodobenzylguanidine (MIBG) imaging was evaluated on Reduced I-123 MIBG myocardial uptake. Reduced I-123 MIBG myocardial uptake, suggesting marked cardiac sympathetic denervation, was observed in 3 patients with primary (AL) amyloidosis without congestive heart failure.
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