Response by Herrmann et al to Letter Regarding Article, “Vascular Toxicities of Cancer Therapies: The Old and the New—An Evolving Avenue”

Oxaliplatin-Induced Acute ST Segment Elevation Mimicking Myocardial Infarction: A Case Report

“…Chemotherapeutic agents are well known to influence molecular signaling pathways, which may affect vascular smooth muscle cells and induce vasoconstriction/vasospasms [20,21]. For cisplatin, when combined with bleomycin and vinca alkaloids, chest pain may be provoked with an incidence of 40%, which is caused molecularly by endothelial dysfunction.…”

“…For cisplatin, when combined with bleomycin and vinca alkaloids, chest pain may be provoked with an incidence of 40%, which is caused molecularly by endothelial dysfunction. Whether nitrogen monoxide, vascular endothelial growth factor receptor interactions, or Rho kinase activation may be involved in the molecular steps induced by platinum-derived chemotherapeutics and especially by oxaliplatin, has not yet been established [20,21]. Additionally, platinum-based agents exert an activating effect on thrombocytes alleviating coagulation and release of thromboxan A2, which in turn may provoke vasoconstriction in the smooth muscle cells of the endothelium [15,22].…”

Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond

“…The inhibition of VEGF and its receptors represents a main (but not sole) mechanism by which antiangiogenic drugs can cause vascular toxicity [20]. Among them, bevacizumab is a monoclonal antibody that targets VEGF-A, thus preventing its interaction with VEGFR and leading to inhibition of tumor angiogenesis.…”

The ethics of radiation exposure in cancer-treated patients

“…In addition to the medical radiation exposure for monitoring of LV function by serial MUGA assessments, it must be pointed out that, besides the risk of heart failure and LV dysfunction secondary to bortezomib, 23 the patient in this case study was exposed to other significant cardiotoxic side effects of bortezomib, a proteasome inhibitor, including the risks of acute myocardial infarction and pulmonary hypertension, 24 which cannot be detected by serial MUGA. Coordination of multidisciplinary care with regularly scheduled echocardiograms (preferably 3D) to assess cardiac function may have helped to avoid unnecessary radiation exposure [113 mSv] from excessive serial MUGA tests, while also helping to monitor for the development of these other cardiotoxic side effects.…”