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Published on: February 17, 2018
Cardiac encephalopathy and congestive heart failure: a hypothesis about the relationship
1Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. lcaplan@bidmc.harvard.edu
Insights
Congestive heart failure patients may develop a unique neurologic syndrome resembling normal pressure hydrocephalus due to cranial fluid retention. This previously unreported condition causes apathy and abulia, impacting cognitive function in heart failure patients.
Area of Science:
- Neurology
- Cardiology
- Nephrology
- Hepatology
Background:
- Congestive heart failure (CHF) frequently leads to neurological dysfunction, presenting as cardiac encephalopathy with metabolic features.
- Existing literature lacks comprehensive understanding of specific neurological syndromes associated with CHF.
Observation:
- A distinct, previously undocumented syndrome is observed in some CHF patients, mimicking normal pressure hydrocephalus (NPH).
- This syndrome is characterized by apathy and abulia, with preserved alertness, suggesting a specific neurological impact.
Findings:
- The syndrome is hypothesized to result from fluid retention within the cranial cavity.
- Similar presentations can occur in conditions causing anasarca, such as severe liver/kidney disease or hypoalbuminemia.
Implications:
- This condition may be underrecognized by cardiologists and neurologists, impacting patient diagnosis and care.
- Further research is needed to confirm the pathophysiology and establish definitive diagnostic criteria for this CHF-related neurological syndrome.
Abstract:
Many patients with congestive heart failure develop neurologic dysfunction. This may take the form of a cardiac encephalopathy that shares clinical features with other metabolic encephalopathies. The causes are multiple. There is a particular, previously unreported, syndrome that occasionally develops in some patients with congestive heart failure that resembles the findings in patients with normal pressure hydrocephalus. This syndrome is characterized by apathy and abulia with preserved alertness; it is caused by fluid retention within the cranial cavity. The syndrome may also develop in patients with other conditions that cause anasarca, e.g., severe liver or kidney disease or hypoalbuminemia. Because patients with these conditions are often quite ill, it has been difficult to verify the pathophysiologic aspects of the syndrome so that its mechanism must remain a hypothesis that awaits more definitive study in a series of patients. I have not seen this syndrome discussed in any cardiology or neurology texts or reports, and it seems to be completely unknown to cardiologists and neurologists. I have recognized about one patient per year with this syndrome.
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