Evidence map›Paper›PMID 28739313›Full record

ReviewTrends in cardiovascular medicine2018

Cardiac amyloidosis: An update on pathophysiology, diagnosis, and treatment.

Omar K Siddiqi, Frederick L Ruberg

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Trends in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 8 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

160 citing papers in PubMed, 8 syntheses or guidelines pooled it.

  1. Pooled it
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  3. Guideline
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  9. Efficacy and Safety of Anselamimab in Immunoglobulin Light Chain Amyloidosis: Results From the Randomized CARES Trials.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026
    Trial
  10. The pathophysiology of wild-type transthyretin amyloidosis: implications for exercise intolerance.American journal of physiology. Heart and circulatory physiology · 2026
    Review
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100 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Omar K SiddiqiSection of Cardiovascular Medicine, Department of Medicine, Boston University School of Medicine, Boston Medical Center, 88 East Newton Street, Boston, MA; Amyloidosis Center, Boston University School of Medicine, Boston Medical Center, Boston, MA.
Frederick L RubergSection of Cardiovascular Medicine, Department of Medicine, Boston University School of Medicine, Boston Medical Center, 88 East Newton Street, Boston, MA; Amyloidosis Center, Boston University School of Medicine, Boston Medical Center, Boston, MA; Department of Radiology, Boston University School of Medicine, Boston Medical Center, Boston, MA. Electronic address: frruberg@bu.edu.

Funding

Serum biomarker identification of cardiac amyloidosis in elderly African Americans.R21AG050206 · NIA · BOSTON MEDICAL CENTER · PI RUBERG, FREDERICK LIEF · 2015 to 2016
$479k
NIA NIH HHS R21 AG050206
6 · The paper itself

Abstract

The amyloidoses are a group of systemic diseases characterized by organ deposition of misfolded protein fragments of diverse origins. The natural history of the disease, involvement of other organs, and treatment options vary significantly based on the protein of origin. In AL amyloidosis, amyloid protein is derived from immunoglobulin light chains, and most often involves the kidneys and the heart. ATTR amyloidosis is categorized as mutant or wild-type depending on the genetic sequence of the transthyretin (TTR) protein produced by the liver. Wild-type ATTR amyloidosis mainly involves the heart, although the reported occurrence of bilateral carpal tunnel syndrome, spinal stenosis and biceps tendon rupture in these patients speaks to more generalized protein deposition. Mutant TTR is marked by cardiac and/or peripheral nervous system involvement. Cardiac involvement is associated with symptoms of heart failure, and dictates the clinical course of the disease. Cardiac amyloidosis can be diagnosed noninvasively by echocardiography, cardiac MRI, or nuclear scintigraphy. Endomyocardial biopsy may be needed in the case of equivocal imaging findings or discordant data. Treatment is aimed at relieving congestive symptoms and targeting the underlying amyloidogenic process. This includes anti-plasma cell therapy in AL amyloidosis, and stabilization of the TTR tetramer or inhibition of TTR protein production in ATTR amyloidosis. Cardiac transplantation can be considered in highly selected patients in tandem with therapy aimed at suppressing the amyloidogenic process, and appears associated with durable long-term survival.

Indexed as

Amyloid Neuropathies, FamilialCardiomyopathy, RestrictiveGenetic MarkersGenetic Predisposition to DiseaseHumansMutationPhenotypePredictive Value of TestsRisk FactorsTreatment OutcomeGenetic MarkersAL amyloidosisRestrictive cardiomyopathyTransthyretin amyloidosis

Identifiers

PMID28739313
PMCPMC5741539

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.