Rapidly progressive dyspnea in gastrointestinal stromal tumor (GIST) with imatinib cardiac toxicity

• Published in: Journal of community hospital internal medicine perspectives 2018-03, Vol.8 (2), p.87-91
• Main Authors: Ghias, Adnan Asif Parvez, Bhayani, Shahzeem, Gemmel, David J, Garg, Sudershan K
• Format: Article
• Language: English
• Subjects: Biopsy; Cancer; cardiac toxicity; Cardiology; Cardiotoxicity; Case Report; Case reports; Drug dosages; Dyspnea; Echocardiography; Enzyme inhibitors; fluid retention; Gastrointestinal cancer; Gastrointestinal stromal tumors; Geriatrics; GISTs; Health risks; Heart; Heart diseases; Heart failure; Hypertension; Imatinib; imatinib toxicity; Inhibitor drugs; Leukemia; LV dysfunction; Medical imaging; Metastases; Metastasis; Older people; Patients; Pretreatment; Protein-tyrosine kinase; rare; Respiration; Retention; Targeted cancer therapy; Toxicity; Tumors; Tyrosine; Ventricle
• ISSN: 2000-9666; 2000-9666
• DOI: 10.1080/20009666.2018.1454787

Gastrointestinal stromal tumors (GISTs) are rare and current estimates range from 4,000 to 6,000 number of GIST cases in the USA annually. Imatinib, a tyrosine kinase inhibitor, has shown a survival benefit in GISTs, and the presence of KIT mutation status is predictive of response. The current case discusses rapidly progressive dyspnea and heart failure in an elderly male with metastatic GIST who was started on imatinib. Although reported as a rare and sporadic side effect of imatinib, the current case illustrates rapidity and the clinical significance of cardiotoxicity, with onset at 2 weeks. Cases of imatinib-induced cardiotoxicity can range from being mild ventricular dysfunction to overt heart failure. Prior to starting imatinib, our patient had a history of hypertension. He subsequently ended up developing heart failure as acknowledged by the echocardiogram (ECHO). In general, elderly with preexisting cardiovascular comorbidity are at greater risk. The goal in such situations is immediate discontinuation or reduction of the imatinib dosage. The case prompts for awareness of imatinib cardiotoxicity. Moreover, a pretreatment cardiac assessment along with monitoring throughout therapy is therefore advisable. Also, imatinib-induced cardiotoxicity should be differentiated from imatinib-associated fluid retention, in which ECHO findings can be normal. This case report raises the concern for accelerated cardiotoxicity profile of imatinib. Further prospective studies with multidisciplinary input are needed to establish this association further.