Author + information
- Received October 4, 2018
- Revision received October 25, 2018
- Accepted October 25, 2018
- Published online January 28, 2019.
- Giuseppe D. Sanna, MD, PhDa,∗ (, )
- Giuseppe Nusdeo, MDa,
- Maria Rita Piras, MDb,
- Antonietta Forteleoni, MDa,
- Maria Rita Murru, BSc,
- Pier Sergio Saba, MD, PhDa,
- Simone Dore, PhDd,
- Giovanni Sotgiu, MD, PhDd,
- Guido Parodi, MD, PhDe and
- Antonello Ganau, MDe
- aClinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy
- bUnità di valutazione Alzheimer, Azienda Ospedaliero Universitaria Sassari, Ospedale San Camillo, Sassari, Italy
- cLaboratorio Centro Sclerosi Multipla, Università di Cagliari, Cagliari, Italy
- dClinical Epidemiology and Medical Statistics Unit, Department of Biomedical Sciences, University of Sassari, Sassari, Italy
- eUniversity of Sassari, Sassari, Italy
- ↵∗Address for correspondence:
Dr. Giuseppe Damiano Sanna, Clinical and Interventional Cardiology, Sassari University Hospital, Sassari (Italy), Via Enrico De Nicola, 07100 Sassari, Italy.
Objectives This case control study sought to assess the presence and characteristics of cardiac abnormalities in patients with Alzheimer disease (AD).
Background Protein 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.
Methods The 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).
Results Compared 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.
Conclusions This 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.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received October 4, 2018.
- Revision received October 25, 2018.
- Accepted October 25, 2018.
- 2019 American College of Cardiology Foundation
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