Asymptomatic Cardiac Abnormalities Present in Alzheimer Disease
By Will Boggs MD
NEW YORK—Patients with Alzheimer disease can have asymptomatic electrocardiographic and echocardiographic abnormalities suggestive of an infiltrative process, researchers report.
"Cerebral and heart diseases may share some pathophysiologic mechanisms, and they should represent potential common therapeutic targets in the future," Dr. Giuseppe D. Sanna from Sassari University Hospital, in Sassari, Italy, told Reuters Health by email.
Some research suggests that protein misfolding might affect both the brain and the heart in patients with Alzheimer disease (AD), but clinical evidence of cardiac involvement in AD remains scarce.
Dr. Sanna and colleagues assessed the presence and characteristics of cardiac abnormalities in 32 individuals with AD who were free of cardiovascular or systemic disease and 34 matched controls who were awaiting minor noncardiac surgery.
The AD group had a significantly higher prevalence of low-voltage QRS complexes and lower total QRS scores on their ECGs, compared with the control group, but otherwise showed no significant differences, the researchers report in the February issue of JACC: Heart Failure.
On echocardiography, patients with AD showed significantly greater maximum wall thickness and intraventricular septum thickness, as well as a significantly higher prevalence of diastolic dysfunction (70% vs. 35% among controls).
Compared with controls, AD patients also had significantly lower total QRS scores/LV mass index ratios.
"This amyloid-like cardiac pattern reflects a peculiar involvement of the heart and suggests a shared disease mechanism (i.e., deposition of the same material resulting from protein misfolding) that affects both brain and heart in AD," the researchers suggest.
Polymorphisms of the PSEN1 and PSEN2 genes were present in five AD patients, but none of them was associated with dilated cardiomyopathy or peculiar cardiac patterns.
"The clinical implications of our results should be confirmed in larger prospective studies," Dr. Sanna said. "The 'cardiomyopathic' process in AD patients is probably slow; therefore, we rarely observe an overt clinical phenotype."
Dr. Mathew Maurer from Columbia University Irving Medical Center, New York Presbyterian Hospital, in New York City, who co-authored an accompanying editorial, told Reuters Health by email, "The observation by the investigators that the voltage-to-mass ratio was low in subjects with Alzheimer's disease compared to age and gender matched controls (suggests) that an infiltrative phenotype consistent with cardiac amyloidosis could be present."
"Further study utilizing emerging imaging techniques, such as cardiac PET scan and technetium pyrophosphate scintigraphy, could elucidate if amyloidosis is present in the hearts of patients with Alzheimer's disease," he said.
"Protein misfolding is the mechanism underlying the development of all forms of amyloidosis (involving both the brain and heart)," Dr. Maurer said. He added that his group has shown this to be treatable in patients with transthyretin cardiac amyloidosis, inspiring hope "for patients with other neurodegenerative diseases caused by abnormal proteostasis."
Dr. Federica del Monte from the Medical University of South Carolina, in Charleston, who earlier reported the presence of compromised myocardial function and intramyocardial deposits of amyloid-beta in patients with AD, told Reuters Health by email, "We are delighted that the findings of our previously published study were replicated and that this study supports the robust clinical findings of our report."
"The main message of both reports is that, with the therapeutic advances prolonging life in AD patients, there will be more and more patients with cognitive dysfunction and AD and heart failure," she said, underscoring "the need for specialized cross discipline training and careful assessment of the therapeutic regimens."
JACC Heart Fail 2019.
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