Hepatic Resection Slows Progression of Carcinoid Heart Disease

Resection of hepatic carcinoid metastases is associated with a decreased risk of progression of carcinoid heart lesions and with improved survival and prognosis, claims a new study.

Researchers at The Mayo Clinic (Rochester, MN, USA) analyzed the effect of hepatic resection on progression of cardiac lesions and prognosis in 77 patients with carcinoid heart disease who had serial echocardiograms done at least one year apart. Ten of these patients had resections performed during the observation period.

The study results showed that progression of cardiac lesions was seen in one of the ten patients (10%) who underwent hepatic resection during follow-up, compared with 42 of 67 patients (63%) who did not undergo hepatic resection during that period. Patients who had no resection also had a significantly greater increase in echocardiographic (ECG) score and significantly higher 5-hydroxyindoleacetic acid (5-HIAA)--a breakdown product of the chemical messenger serotonin--levels than did patients who underwent hepatic resection. Five-year survival after carcinoid heart disease diagnosis was significantly greater in patients who had hepatic resection (86.5%, versus 29.0% in patients without hepatic resection). The study was published in the February 2008 issue of Mayo Clinic Proceedings.

"Our findings suggest that, in patients with carcinoid heart disease who are eligible for hepatic resection, surgical debulking of the tumor burden in the liver can improve survival,” concluded lead author Alain M. Bernheim, M.D., and colleagues. "Eligible patients with metastatic carcinoid tumors and carcinoid heart disease should be considered for hepatic surgery before their tumors have reached an inoperable state.”

Carcinoid heart disease--a slow-growing but malignant type of tumor originating in the cells of the neuroendocrine system-- is associated with liver metastases that permit large quantities of vasoactive substances to reach the right side of the heart without being inactivated by the damaged first-pass liver metabolism.


Related Links:
The Mayo Clinic