What the Cardiologist Needs to Consider in the Management of Oncologic Patients with STEMI-Like Syndrome: A Case Report and Literature Review

Abstract

In pre-hospital care, an accurate and quick diagnosis of ST-segment elevation myocardial infarction (STEMI) is imperative to promptly kick-off the STEMI network with a direct transfer to the cardiac catheterization laboratory (cath lab) in order to reduce myocardial infarction size and mortality. Aa atherosclerotic plaque rupture is the main mechanism responsible for STEMI. However, in a small percentage of patients, emergency coronarography does not reveal any significant coronary stenosis. The fluoropyrimidine agents such as 5-Fluorouracil (5-FU) and capecitabine, widely used to treat gastrointestinal, breast, head and neck cancers, either as a single agent or in combination with other chemotherapies, can cause potentially lethal cardiac side effects. Here, we present the case of a patient with 5-FU cardiotoxicity resulting in an acute coronary syndrome (ACS) with recurrent episodes of chest pain and ST-segment elevation.. Our case report highlights the importance of widening the knowledge among cardiologists of the side effects of chemotherapeutic drugs, especially considering the rising number of cancer patients around the world and that fluoropyrimidines are the main treatment for many types of cancer, both in adjuvant and advanced settings.

Evaluation of 5-Fluorouracil-Induced Cardiotoxicity: Role of Cardiac Biomarkers

“…It has been shown that several risk factors might increase the risk of cardiotoxicity, including age (elderly and very young), previous chest radiotherapy, BMI and particularly a history of cardiovascular disease [17,25,26]. However, in general, there is no strong evidence to prove these factors to be associated with an increased risk of 5-FU-induced cardiotoxicity in healthy patients, genetically prone patients, underlying heart diseases and renal insufficiency should be considered as paramount risk factors [27,28].…”

“…Taking into account the fact that cardiac biomarkers such as N-terminal pro-brain natriuretic peptide, creatine phosphokinase, and cardiac troponins have been shown to have a low negative predictive value, indicating an inability to rule out cardiotoxicity even in presence of normal levels of such biomarkers. On the other hand, with silent ischemia as a relatively common manifestation of cardiotoxicity, which has been demonstrated to be well recognized during Holter monitoring, patients close monitoring throughout the chemotherapy should be considered an integral part of diagnosing cardiotoxicity [28].…”

A contemporary update on cancer and takotsubo syndrome

“…In other cases, either the presence of not hemodynamically significant coronary artery disease was reported, or a history of previous coronary artery disease resulted as a predictor of cardiotoxicity development. In such scenarios plaque instability or vasospasm causing a narrowing of the coronary lumen on top of a pre-existing plaque might not be excluded ( 19 , 64 , 65 ). Finally, recent findings suggest that the main mechanisms of pyrimidine-associated cardiotoxicity are direct vascular (endothelial) and myocardial damage ( 59 , 61 ).…”