November 2026 Br J Cardiol 2026;33(4) doi:10.5837/bjc.2026.053 Online First
Morris Simwa, Peter J Cowburn
Pathophysiology The pathophysiology of CHD involves chronic exposure of the endocardium to vasoactive substances released by functioning NETs, leading to fibrotic plaque deposition.3 Valve leaflet thickening, retraction and fixation develop over time and result in predominantly right-sided valvular regurgitation, often accompanied by varying degrees of stenosis. The vasoactive substances produced in carcinoid syndrome, primarily serotonin, undergo metabolism in the liver, lung and brain.4,5 In patients with hepatic metastases, liver clearance is bypassed, and persistent systemic exposure leaves the right heart vulnerable to damage. The left h
November 2026 Br J Cardiol 2026;33(4) doi:10.5837/bjc.2026.054 Online First
James Hickson, Wen Hui Tei, Uditha Hewarathna, Mark Hayes
Introduction Carcinoid heart disease (CHD) represents a rare yet important aetiology of intrinsic tricuspid and pulmonary valve pathology, associated with significant morbidity and mortality due to right heart failure. With timely medical therapy and, when indicated, surgical intervention, substantial improvements in both quality of life and long-term survival can be achieved. Notably, clinical manifestations indicative of cardiac involvement often remain subtle until CHD reaches an advanced stage. The cardiac manifestations stem from the paraneoplastic effects elicited by vasoactive substances, notably 5-hydroxytryptamine (5-HT or serotonin)
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