Update on Incorporating Biomarkers with Imaging Findings for the Detection and Management of Cardiotoxicity.

PURPOSE OF REVIEW: Modern cancer therapy comes at a cost of increased risk of cardiotoxicity. The purpose of our paper is to provide an updated review highlighting research incorporating biomarkers and imaging findings for the detection of subclinical cardiac dysfunction and management of cancer treatment-related cardiotoxicity. RECENT FINDINGS: Biomarkers, particularly troponin, NTproBNP, and myeloperoxidase, have been shown to have a predictive role in the development of cancer treatment-related cardiotoxicity. Early reductions in global longitudinal strain and the more recently reported, circumferential strain, have been shown to be predictive of subsequent cardiotoxicity. Integrating troponin levels with longitudinal strain may have incremental value in predicting future cardiotoxicity. Initiating troponin-guided heart failure therapy following cancer treatment may impact the development of cardiotoxicity. Strain-guided heart failure therapy is currently under investigation. Early detection of subclinical cardiac dysfunction in high-risk cancer patients and subsequent medical intervention using biomarkers and imaging may help to alter the course of cancer treatment-induced cardiotoxicity. Current guidelines and expert consensus offer a general framework for monitoring high risk patients for cardiotoxicity. However, additional research is needed to provide a more sophisticated and structured approach in detecting and managing subclinical cardiac dysfunction with hopes of minimizing subsequent cardiotoxicity.

Novel anti-platelet agents in acute coronary syndrome: mechanisms of action and opportunities to tailor therapy.

Dual anti-platelet therapy, most commonly aspirin and clopidogrel, has been the standard of care for over a decade in patients who have experienced acute coronary syndrome, particularly when treated with coronary stenting. However, residual risk in patients receiving dual anti-platelet therapy post-acute coronary syndrome raises an unmet need for alternative therapy to clopidogrel. Consequently, novel anti-platelets agents including the P2Y12 receptor antagonists, such as prasugrel and ticagrelor, have emerged. Furthermore, using new methods to assess genetic polymorphisms and functional phenotypic assessments of platelet reactivity may become important in the development of personalized medicine and in developing tailored approaches to individual treatment. While robust large-scale evidence for genotypic- and phenotypic-guided therapy in improving outcomes is currently lacking, tremendous interest from various stakeholders including researchers, funding agencies, and industry continues to spur research endeavors in this arena. Further investigation is required in this emerging field to potentially offer improved platelet inhibition that may optimize cardioprotection and minimize bleeding risk in patients with acute coronary syndrome.

Ross procedure after prosthetic valve thrombosis in a patient with antiphospholipid syndrome and recurrent bleeding.

The Ross procedure allows replacement of a diseased aortic valve with pulmonary root autograft, possibly avoiding the highly thrombotic mechanical valves and immunologic deterioration of tissue valves in antiphospholipid syndrome (APS). Here, we present the use of the Ross procedure in a 42-year-old woman with mild intellectual disability, APS, and a complex anticoagulation history after she presented with thrombosis of her mechanical On-X aortic valve previously implanted for non-bacterial thrombotic endocarditis.

Ventricular Septal Defect from Takotsubo Syndrome.

Takotsubo Syndrome is a transient condition characterized by left ventricular systolic dysfunction with apical akinesis/dyskinesis and ballooning. Although the prognosis with medical management is excellent in most cases, rare cases of serious complications can occur. We present here a case of a 71-year-old woman presenting with acute decompensated heart failure with initial findings consistent with a myocardial infarction, who was found instead to have an acute ventricular septal defect as a complication of Takotsubo Syndrome.