Giuseppe D Sanna1, Giuseppe Nusdeo2, Maria Rita Piras3, Antonietta Forteleoni2, Maria Rita Murru4, Pier Sergio Saba2, Simone Dore5, Giovanni Sotgiu5, Guido Parodi6, Antonello Ganau6. 1. Clinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy. Electronic address: giuseppedasanna@tiscali.it. 2. Clinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy. 3. Unità di valutazione Alzheimer, Azienda Ospedaliero Universitaria Sassari, Ospedale San Camillo, Sassari, Italy. 4. Laboratorio Centro Sclerosi Multipla, Università di Cagliari, Cagliari, Italy. 5. Clinical Epidemiology and Medical Statistics Unit, Department of Biomedical Sciences, University of Sassari, Sassari, Italy. 6. University of Sassari, Sassari, Italy.
Abstract
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.
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.
Authors: Yulia N Grigorova; Ondrej Juhasz; Jeffrey M Long; Valentina I Zernetkina; Mikayla L Hall; Wen Wei; Christopher H Morrell; Natalia Petrashevskaya; Audrey Morrow; Katherine H LaNasa; Alexei Y Bagrov; Peter R Rapp; Edward G Lakatta; Olga V Fedorova Journal: Int J Mol Sci Date: 2022-04-20 Impact factor: 6.208
Authors: Zahra Raisi-Estabragh; Amine M'Charrak; Celeste McCracken; Luca Biasiolli; Maddalena Ardissino; Elizabeth M Curtis; Nay Aung; Claudia K Suemoto; Clare Mackay; Sana Suri; Thomas E Nichols; Nicholas C Harvey; Steffen E Petersen; Stefan Neubauer Journal: Eur Heart J Cardiovasc Imaging Date: 2022-04-18 Impact factor: 9.130