Chemotherapy Induced Cardiotoxicity: A State of the Art Review on General Mechanisms, Prevention, Treatment and Recent Advances in Novel Therapeutics.

As medicine advances to employ sophisticated anticancer agents to treat a vast array of oncological conditions, it is worth considering side effects associated with several chemotherapeutics. One adverse effect observed with several classes of chemotherapy agents is cardiotoxicity which leads to reduced ejection fraction (EF), cardiac arrhythmias, hypertension and Ischemia/myocardial infarction that can significantly impact the quality of life and patient outcomes. Research into possible mechanisms has elucidated several mechanisms, such as ROS generation, calcium overload and apoptosis. However, there is a relative scarcity of literature detailing the relationship between the exact mechanism of cardiotoxicity for each anticancer agent and observed clinical effects. This review comprehensively describes cardiotoxicity associated with various classes of anticancer agents and possible mechanisms. Further research exploring possible mechanisms for cardiotoxicity observed with anticancer agents could provide valuable insight into susceptibility for developing symptoms and management guidelines. Chemotherapeutics are associated with several side effects. Several classes of chemotherapy agents cause cardiotoxicity leading to a reduced ejection fraction (EF), cardiac arrhythmias, hypertension, and Ischemia/myocardial infarction. Research into possible mechanisms has elucidated several mechanisms, such as ROS generation, calcium overload, and apoptosis. However, there is a relative scarcity of literature detailing the relationship between the exact mechanism of cardiotoxicity for each anticancer agent and observed clinical effects. This review describes cardiotoxicity associated with various classes of anticancer agents and possible mechanisms. Further research exploring mechanisms for cardiotoxicity observed with anticancer agents could provide insight that will guide management.

Utilization of sacubitril-valsartan for right ventricular failure in a patient with arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular (RV) cardiomyopathy is an autosomal dominant inherited cardiomyopathy that is characterized by an increased risk of ventricular arrhythmias, sudden cardiac death and, less commonly, heart failure. The authors present the case of a 36-year-old woman with familial lamin cardiomyopathy with positive LMNA mutation and genetic testing revealing LMNA and TMEM43 mutations consistent with arrhythmogenic RV cardiomyopathy. The patient presented with clinical signs of RV failure. Transthoracic echocardiogram showed newly reduced RV function in the absence of left ventricular involvement. Cardiac MRI demonstrated diffuse late gadolinium enhancement of the mid-level and apical RV anterior free wall. Diuretics were started, and sacubitril-valsartan was added when the patient's symptoms persisted. Diuretics were then discontinued, and sacubitril-valsartan was the primary therapy. This is the first reported case of symptomatic and imaging-proven RV recovery in a patient with symptomatic RV failure in the setting of arrhythmogenic RV cardiomyopathy treated with sacubitril-valsartan.

The authors present the case of a 36-year-old woman who was found to have arrhythmogenic right ventricular cardiomyopathy, a rare inherited cardiomyopathy. This condition is caused by various mutations that lead to cardiac muscle cells being replaced with fibrofatty tissue and manifests as heart arrhythmias, sudden cardiac death or heart failure. The patient presented with symptoms of right heart failure. Imaging found a new reduction in right ventricular function, confirming the diagnosis of right heart failure. The patient was treated initially with diuretics. However, her symptoms persisted despite treatment and sacubitril­valsartan was started, after which she symptomatically improved. Repeat imaging showed improvement in right ventricular function with sacubitril­valsartan therapy.

Proton beam therapy causing pericarditis - a rare case of radiation induced cardiotoxicity.

Acute pericarditis is caused by the inflammation of the pericardium which can result in an effusion around the heart. Proton beam therapy causing radiation-induced pericarditis is not a well-known cause of pericarditis. We present a case of a patient with Li-Fraumeni Syndrome who developed acute onset pericarditis, presumed to be secondary to proton beam therapy.

A case report: rapid progression of coronary atherosclerosis in a patient taking Targretin (Bexarotene).

Anti-neoplastic drugs have made major advancements in oncology, however they are not without cardiovascular consequences. We present a patient with cutaneous T-cell lymphoma receiving Targretin therapy who presented with accelerated atherosclerosis. His triglyceride level (TG) was greater than 1000 mg/dL, which rapidly improved with discontinuation of Targretin.