Evidence map›Paper›PMID 30704603›Full record

ArticleJACC. Heart failure2019

Cardiac Abnormalities in Alzheimer Disease: Clinical Relevance Beyond Pathophysiological Rationale and Instrumental Findings?

Giuseppe D Sanna, Giuseppe Nusdeo, Maria Rita Piras, Antonietta Forteleoni, Maria Rita Murru, Pier Sergio Saba, Simone Dore, Giovanni Sotgiu, Guido Parodi, Antonello Ganau

Abstract read
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In one paragraph

Article in JACC. Heart failure, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% of its field
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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Neurovascular interactions in the ageing heart.Nature reviews. Cardiology · 2026
    Review
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  8. Alterations in the inflammatory homeostasis of aging-related cardiac dysfunction and Alzheimer's diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Giuseppe D SannaClinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy. Electronic address: giuseppedasanna@tiscali.it.
Giuseppe NusdeoClinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy.
Maria Rita PirasUnità di valutazione Alzheimer, Azienda Ospedaliero Universitaria Sassari, Ospedale San Camillo, Sassari, Italy.
Antonietta ForteleoniClinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy.
Maria Rita MurruLaboratorio Centro Sclerosi Multipla, Università di Cagliari, Cagliari, Italy.
Pier Sergio SabaClinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy.
Simone DoreClinical Epidemiology and Medical Statistics Unit, Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
Giovanni SotgiuClinical Epidemiology and Medical Statistics Unit, Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
Guido ParodiUniversity of Sassari, Sassari, Italy.
Antonello GanauUniversity of Sassari, Sassari, Italy.
University of Sassari · ITAzienda Ospedaliero Universitaria di Sassari · ITUniversity of Cagliari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis case control study sought to assess the presence and characteristics of cardiac abnormalities in patients with Alzheimer disease (AD).

backgroundProtein misfolding is involved in the pathophysiology of neurodegenerative disorders such as AD. Recently, amyloid-beta (Aβ) aggregates were identified within the cardiomyocytes and interstitium of patients with AD, suggesting that Aβ oligomers may reach and damage the heart.

methodsThe authors studied 32 patients with AD and 34 controls matched by age and sex, all of whom were free from cardiac or systemic diseases. A clinical evaluation, an electrocardiogram, and an echocardiogram were performed in all subjects. Furthermore, patients with AD underwent genetic analyses (of the PSEN1, PSEN2, APP, and APOE genes).

resultsCompared to the control group, patients with AD had a higher prevalence of low-voltage electrocardiographic QRS complexes (28% vs. 3%, respectively; p = 0.004), a lower voltage/mass ratio (p = 0.05), a greater echocardiographic interventricular septum (10.1 ± 1.3 mm vs. 9.3 ± 1.1 mm, respectively; p = 0.01), a greater maximum wall thickness (10.8 ± 1.7 mm vs. 9.3 ± 1.1 mm, respectively; p = 0.0001), and a 2-fold higher prevalence of diastolic dysfunction (70% vs. 35%, respectively; p = 0.007). Symptoms and signs of heart failure were absent in all patients with AD.

conclusionsThis study shows that electrocardiographic and echocardiographic abnormalities, including diastolic dysfunction, are present in patients with AD and that these studies reproduce the pattern of cardiac amyloidosis. These findings suggest that, in AD, there may be subclinical cardiac involvement likely associated with Aβ amyloid deposition. The clinical relevance of these cardiac abnormalities should be evaluated in larger prospective studies.

Indexed as

ElectrocardiographyAgedAlzheimer DiseaseCardiomyopathiesCase-Control StudiesDiastoleEchocardiography, Three-DimensionalFemaleFollow-Up StudiesHeart VentriclesHumansMaleProspective StudiesTomography, Emission-Computed, Single-PhotonVentricular Function, LeftAlzheimer diseaseamyloidosiscardiomyopathydiastolic dysfunctionprotein misfolding

Identifiers

PMID30704603
OpenAlexW2914620820

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.