CardioNerds co-founder Amit Goyal, Dr. Dinu Balanescu, Dr. Teodora Donisan, and Dr. Anjali Agarwalla get the cardiologist perspective of Cancer Therapy-Related Cardiac Dysfunction (CTRCD) from Dr. Joerg Hermann. We previously learned from the oncologist perspective with Dr. Susan Dent in Episode #261! In this episode, we discuss the history of cancer therapies and our developing understanding of how these life-saving medications can cause cardiac toxicities. As we manage patients in the CardioNerds CardioOncology clinic, we ask Dr. Hermann how the general cardiologist should approach patients with a cancer diagnosis, when should a patient be referred to a cardiooncology specialist, and what are the common cardiotoxicities to look out for. We’ll also place a quick consult to our guest expert’s goldendoodle! Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan. Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann Patients with malignancy will incur several “hits” in addition to their malignancy and its subsequent treatment — these include their genetics, environment, and comorbidities. The role of the cardiologist is to identify how the combination of these “hits” can bring cardiovascular disease to the forefront and where we can intervene upon it. The sooner we recognize cardiotoxicity, the better the outcome for our patients. Patients should receive baseline risk assessment with TTE and biomarkers with routine surveillance. You cannot assign a percentage to cardiac risk in cancer. Patients require a multidisciplinary approach with constant monitoring and surveillance. Consider exercise testing when conducting pre-treatment risk assessment and during monitoring. Peak VO2 abnormalities is often the first marker of cardiotoxicity — though note that it correlates well with global longitudinal strain (GLS). If someone develops a cardiovascular complication of chemotherapy, this should prompt referral to cardiooncology. Show notes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Cardiologist Perspective with Dr. Joerg Hermann What types of cardiovascular pathology occur in the setting of cancer and its treatment? We conventionally thought of cardiotoxicities as being of two types: Type 1: irreversible cardiac injury that does not improve despite withdrawal of offending chemotherapeutic (protype = classic anthracycline cardiotoxicity) Type 2: reversible cardiac dysfunction that improves with discontinuation of chemotherapeutic (prototype = classic traztuzumab cardiotoxicity) However, we have begun moving away from this thought process as it has become more evident that injuries historically thought of as “type 1” may not be as relentless as previously understood, and that patients with type 2 dysfunction may not actually be returning to completely normal after the offending agent is withdrawn. As such, this episode proposes two other ways to frame our understanding of cardiotoxicities: a clinical/practical approach, based on symptoms (symptomatic vs asymptomatic — this is the approach used by the ESC guidelines), and a mechanistic approach: direct effect on cardiac myocytes, indirect effects (e.g., effect on coronaries), and inflammatory effects. The 2021 International Cardiooncology Society (ICOS) consensus statement defines five major forms of cancer therapy related cardiac dysfunction (CTRCD): Cardiac dysfunction/heart failure:Asymptomatic: defined by changes in ejection fraction. This may be mild (LVEF 50% AND either new decline in GLS by 15% from baseline or new rise in troponin or NTproBNP), moderate (new LVEF reduction by ≥10 percentage points to 40 - 49% AND either new decline in GLS by 15% from baseline or new rise in troponin or NTproBNP), or severe (new LVEF reduction to

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