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I want to talk today about cardio
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oncology drugs and side effects it's a
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topic that I struggled myself with
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grasping there is a myriad of new cancer
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drugs especially the targeted therapies
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with so many names so many targets and
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so many toxicities that it is hard for a
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general cardiologist to keep up with but
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we have to keep up because even patients
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with metastatic cancers are surviving
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thanks to those Therapies and they are
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presenting to us with cardiac
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complications or a need for cardiac
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prevention and
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surveillance I searched and I use many
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references for this stock these are the
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most important references those are all
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the references I used but these are the
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most important ones the 2022 ESC
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guidelines are the most important ones
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they have very nice tables and
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descriptions of specific
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toxicities and you have two expert panel
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recommendations recently published in a
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jack cardio
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oncology first we need to understand the
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four types of systemic cancer therapies
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we have the traditional chemotherapy
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number two we have the hormonal therapy
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that is used in breast cancer but also
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in prostate cancer and the ones used in
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prostate cancer are more complex and
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they do lead to a lot of cardiovascular
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complications
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you have the Androgen deprivation
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therapy such as GnRH Agonist GNR
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antagonist and androgen receptor
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antagonist that I will describe later
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then you have most importantly among the
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new therapies the targeted therapy and I
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used to confuse this with immune therapy
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targeted therapy is very different from
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immune therapy this therapy consists of
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two sorts of therapy one you have the
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antibodies against growth factor
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receptors on the cancer cell membrane on
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the surface of the cancer cell those are
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specific growth factor receptors to
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specific cancers that promote cancer
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cell growth and pro proliferation and
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Metabolism so blocking those will lead
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to cancer cell death the second type of
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targeted therapy are not antibodies they
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are small molecules that go inside the
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cells not on the surface of the cell
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inside the cells and they attack signal
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transduction Pathways which regulate
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cancer cell cycle and growth and
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disrupting those signal Pathways will
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also lead to cancer cell destruction
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frequently those signal pathways are
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linked to growth factor receptors unlike
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chemotherapy this therapy tries to
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Target abnormal receptors or Pathways
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inside the cell
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that are specifically expressed by
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cancer cells or overexpressed by cancer
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cells compared to normal
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cells and this is an illustration of
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that so you have growth factor receptors
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on the surface of the cancer cells such
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as her two which is expressed on some
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subtypes of breast cancer cells the her
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two positive breast cancer cells you
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have the egfr epidermal growth factor
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receptor the platel derived growth
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factor receptor cd20
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cd38 then you have growth factor
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receptor on the surface of the vessels
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feeding the cancer cell such as most
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importantly the
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vegfr vascular endot growth factor
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receptor that's the most important
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receptor that is targeted in many types
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of cancers those surface receptors on
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the cancer cell or the vessels are
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targeted by antibod
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then you have the intracellular
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signaling molecules most of which are
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kinases you see their names here they
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end with k k for
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kise many of which are tyrosin kise such
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as here tyros and kyes a lot of those
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are linked to the growth factor
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receptors that's how the growth factor
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receptor promote cellular growth via
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those signaling kinases these targeted
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kinas es like the surface receptors are
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overexpressed in specific Cancers and
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promote cellular growth proliferation
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cellular metabolism they promote
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angiogenesis especially uh the
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transduction pathway for the
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vegfr they also inhibit apoptosis so
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targeting those receptors or pathway
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kinases will lead to cancer cell
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destruction
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unfortunately those receptors and
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kinases are overexpressed in cancer
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cells but they are also expressed in
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normal cells such as myocardial cells
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skin cells and gastrointestinal cells
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hence we get the side effects
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specifically the cardiovascular side
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effect and the vascular effect
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particularly those that Target the
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arterial Pathways and receptors hence
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you can get for example arterial throm
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including Mi you can get Venus trombi as
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well and since those receptors and
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pathways are present in myocardial cells
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you can get myocardial cell dysfunction
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dis
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metabolism and hence you can get
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cardiomyopathy because of those targeted
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therapies here is a slide talking again
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about those very important targeted
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therapies so the first type is
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monoclonal antibodies they target cancer
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cell surface receptors
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such as growth factor receptors or CD
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receptors on immune cells in lymphoma
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and Myoma or they can Target cancer cell
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arteries and vessels surface endogenesis
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regulator such as those here those
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targeted therapies that are antibodies
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targeting the surface their names end in
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mb for antibodies and they are given
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intravenously not orally and they can
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Target the her 2 the egfr or the V egfr
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or multiple of the CDs cd2 or cd38 this
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is an example aab targeting cd20 on Loma
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cells you have dumu targeting cd38 on
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Myoma cells you have trastuzumab
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famously in breast cancer targeting her
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2 which is a form of
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egfr you have BAS suab very important
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and widely used monoclonal antibody
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targeted therapy which binds to the egfr
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and inhibit the growth of tumor blood
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vessels in colon cancer and many other
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cancers you have the panitumumab which
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Targets egfr in colon
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cancer now the second type of targeted
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therapy are the small molecu drugs owing
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to their low weight they penetrate the
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cancer cell membrane and damage
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intracellular signaling molecules
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mainly those various kinases frequently
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link to various gross Factor receptors
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for example the tyosin kyes of v egfr
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and
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egfr they may Target Jack Mech and
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K their names end in nebb or
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occasionally Li unlike mab for
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monoclonal antibodies you need to know
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that because you'll hear those names
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over and over so when you hear a can
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drug that ends in m its monoclonal
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antibody typically a monoclonal antibody
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targeted therapy against the surface
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receptor if they end in Nee or
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occasionally Le those are small molecule
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targeted therapy typically anti- kinases
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frequently tyrosin kinas they may end in
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Meb for proteosome Inhibitors use in
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multiple Myoma and they are given orally
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those are small molecules that are given
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orally
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unlike intravenously for the MB
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monoclonal
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antibodies and these are some examples
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of small molecular drugs you have the
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egfr thyrosin kyese Inhibitors such as
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otin atin they target egfr mutation
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positive non-s small cell lung cancer
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you have ALK inhibitor in non small cell
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lung cancer you have
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vegfr thyrosin KY inhibitor I describ
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the VFR monoclonal antibody Bas
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cab and here you have the tyosin kyes
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inhibitor vegfr such as
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suntin axitinib sfin they are used to
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treat renal coloral thyroid
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neuroendocrine and hypocellular Cancers
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you have imatinib the famous one that
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targets the tyrosin kyese resulting from
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the BCR abl Fusion Gene of the
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Philadelphia chromos
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in CML this one BCR a kise you have RAF
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and Mac inhibitor kise Inhibitors in
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metastatic Mel melanoma you have Bruton
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tyrosin kise Inhibitors that are used in
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CL and and some bell lymphoma you have
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the CD kyes 46 inhibitor that are used
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in some metastatic breast cancer that
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are hormone positive her to negative and
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have the proteasome Inhibitors the names
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of which end in
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Meb and those are used to treat multiple
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Myoma all targeted therapies especially
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vegf receptor antibodies and Inhibitors
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may cause hypertension very frequently
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because of their vascular toxicity heart
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failure because of their myocardial cell
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toxicity heart failure and
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cardiomyopathy in about 1 to 10% and
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over 10 10% with
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VF targeted therapy and over 10% with
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her two targeted therapy then you have
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arterial thrombosis including m in about
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1 to 10% that's a big proportion and you
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have Venus thrombosis and Venus
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thromboembolism also many of those kise
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Inhibitors may increase a fib risk and
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prolong QT so you have remember those
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big five type of side effects with those
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Target therapy hyper tension heart
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failure arar thrombi Venus thrombi and
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aib also you have QT prolongation you
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get also skin problems and impaired
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wound healing because of their effect on
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skin cell growth now the fourth type of
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systemic cancer therapy is immunotherapy
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and this mainly consists of immune check
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points inhibitor also CTI cell therapy
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and immunomodulators use in multiple
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Myoma
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and I'll describe here briefly the
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immune checkpoint Inhibitors those are
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antibodies so their names end in mb as
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well so those are antibodies that Target
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physiological immune
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breaks so those are Inhibitors of
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Inhibitors of the immune system
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therefore those are promoter activators
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of the immune systems and let me show
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you those breaks of the immune system
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you have the pd1 protein and pdl1
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protein expressed on cancer cells those
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link to their receptors on the t- cells
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and inhibit the t- cell response so
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blocking them will activate the t- cell
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response you have also the ctla4 on the
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dritic cells that links to the ctla4
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receptor on the t- cell those are the
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three types of immune checkpoints and
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Inhibitors will block any one of those
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three
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because they activate the immune system
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they may cause autoimmune reaction
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affecting not only the cancer cells but
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also normal organ cells most commonly
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and to various degree of severity the
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following four systems the skin the
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gastrointestinal tract the endocrine
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system or the liver those are the four
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most commonly involved but they are
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frequently mildly involved when involved
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and they are frequently well tolerated
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and side effects are relatively mild
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about 10 to 20% of patients treated with
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ICI experience more severe side effects
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in those four systems skin GI tract or
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more rarely in severe cases they
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experience autoimmune reaction in the
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lung such as pneumonitis the neurologic
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system such as gamare or aseptic menitis
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the muscles such as myositis or
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importantly for us the heart myocarditis
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in 1 to 2% of patients and up to 3% in
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those receiving a combination of
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ICI myocarditis is unlikely to occur in
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the absence of other more common
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autoimmune manifestation such as
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particularly myositis dermatitis and
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Colitis there is some correlation
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between Cancer response and side effects
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meaning patients who experience severe
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side effects with ICI generally have a
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great cancer response because that tells
00:14:04
us that well they've had a very strong
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activation of the immune system which
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destroyed cancer cells and destroyed
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some normal organ
00:14:13
cells severe side effects including
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myocarditis warrant treatment
00:14:18
Interruption but the drug remains at its
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Target for several months and its
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immunologic efficacy persists even after
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Interruption partly through immune
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memory so even when you stop the drug
00:14:32
because of side effect you can feel some
00:14:35
comfort in knowing that the drug will
00:14:37
continue to act and will continue to
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inhibit cancer cell and the patient may
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still have some good response even if
00:14:45
you stopped it even corticosteroid that
00:14:48
are used to treat severe side effect may
00:14:51
not diminish the cancer
00:14:54
response being antibodies ICI names end
00:14:57
in mb and they are administered
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intravenously these are examples of
00:15:01
immune checkpoint inhibitor a famous One
00:15:04
pmab Kuda which targets pd1 neolab which
00:15:09
targets pd1 as well you have UAB which
00:15:13
targets ctla4 and durvalumab which
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targets
00:15:17
pdl1 they are mainly and traditionally
00:15:19
used in unresectable or metastatic nonm
00:15:23
cell lung cancer renal cell and otal
00:15:26
carcinoma head and neck cancer metast
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itic GI malignancy such as colon
00:15:31
esophagal you have melanoma lymphoma
00:15:33
hypocellular cancer but importantly
00:15:36
recently their use has been
00:15:38
expanded to receptable tumors as adant
00:15:42
or neoadjuvant therapy such as non small
00:15:44
cell lung cancer ular carcinoma and
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melanoma now with any of those four
00:15:53
types of systemic cancer therapy you may
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get cancer related cardiac dysfunction
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we call it CTR
00:16:01
CD and there are those five major
00:16:05
cardiovascular side effects one heart
00:16:08
failure cardiopathy two arterial
00:16:10
thrombosis slmi three ven thrombosis
00:16:14
four hypertension and five aib and you
00:16:16
have a six one which is QT prolongation
00:16:19
a various drug will cause some or many
00:16:23
of those in a various percent now when
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we see a patient with a planned systemic
00:16:29
cancer therapy how do you assess his
00:16:32
risk before cancer therapy with all
00:16:35
cancer therapy particularly the ones
00:16:37
known to cause LV
00:16:39
dysfunction we have to always evaluate
00:16:42
the patient before cancer therapy and we
00:16:45
classify his risk based on the following
00:16:48
criteria cancer therapy is considered
00:16:51
high risk if at basine the the patient
00:16:54
has any of those four clinical heart
00:16:57
failure or s valvular disease stenotic
00:17:01
or regurgitant or based on EF less than
00:17:04
50% or prior major CAD history such as a
00:17:08
major type 1 mi or prior PCI or
00:17:13
cabbage cancer therapy is considered
00:17:16
moderate risk if you have borine LV
00:17:18
dysfunction with the F of 50 to
00:17:20
54% or low GLS Global longitudinal
00:17:24
strain on Echo or elevated baseline
00:17:27
troponin or NP or you have aib or a
00:17:32
history of
00:17:33
aib now with this classification it's
00:17:36
important to know that a high risk does
00:17:39
not preclude cancer therapy but it
00:17:42
warrants cardiac heart failure
00:17:44
optimization CAD risk factors and
00:17:47
symptom optimization and closer
00:17:50
surveillance during therapy and possibly
00:17:54
optimization with ACE inhibitor and beta
00:17:57
blocker therapy
00:17:59
even a Bas LF of 30 to 50% is generally
00:18:03
not prohibitive of initiating
00:18:05
cardiotoxic therapies under Clos
00:18:07
surveillance you may even initiate the
00:18:10
most toxic one which is intrac cyclin
00:18:12
under Clos surveillance and a and beta
00:18:16
blocker therapy EF less than 30% is
00:18:19
generally prohibitive of intrac cycling
00:18:22
therapy based on the ASE guidelines EF
00:18:26
less than 30% may be prohibited of her
00:18:29
two Inhibitors and other cancer targeted
00:18:33
therapy such as VF Inhibitors but not
00:18:36
always particularly if no other cancer
00:18:39
treatment is
00:18:42
possible and those are charts from the
00:18:44
ESC guidelines that provide a more
00:18:47
detailed evaluation of high risk and
00:18:51
moderate risk factors I sum them up for
00:18:54
you in those four for the highrisk and
00:18:58
three for the moderate risk but those
00:19:02
charts are more detailed for example
00:19:04
even patient with a combination of CKD
00:19:06
diabetes and smoking is a moderate risk
00:19:09
patient patient over the age of 80 is a
00:19:12
moderate to high risk patient they also
00:19:15
provide tables classifying the risk of
00:19:17
the patient depending on the therapy
00:19:18
intrac cycl versus her two therapy
00:19:21
versus vegf therapies but again it's
00:19:24
easier for me to wrap my head against
00:19:26
those summarized criteria
00:19:30
prior CAD history type 1 mi PCI or
00:19:34
cabbage or CAD symptoms are considered
00:19:37
high risk for all cancer therapy that
00:19:39
can cause car dysfunction but
00:19:41
particularly cancer therapy associated
00:19:43
with vascular toxicity such as the
00:19:45
targeted
00:19:47
therapy such as VF antibodies inhibitor
00:19:51
and other kise Inhibitors and thyren
00:19:54
kyes Inhibitors other targeted therapies
00:19:58
and also fop pyamid such as 5fu which
00:20:01
can cause coronary vasospasm and OAS
00:20:04
coronary thrombosis particularly in
00:20:06
patient with a prior CAD history and
00:20:09
this is from the ESC guidelines
00:20:12
highlighting the fact that even if you
00:20:14
have high cardiac risk that doesn't mean
00:20:17
that we should withhold cancer therapy
00:20:20
identifying prior cardiovascular disease
00:20:23
should not automatically be a reason to
00:20:24
withhold cancer therapy but considered
00:20:27
an opportunity to to optimize
00:20:29
cardiovascular risk prior to and during
00:20:31
treatment risk benefit discussions
00:20:33
should include the patients and
00:20:35
oncologists and they give a class one
00:20:37
for this now after having described how
00:20:40
to classify the patient risk before
00:20:43
therapy this is the most important slide
00:20:46
this is how we defined cardiac toxicity
00:20:50
under therapy so with all cancer
00:20:53
therapies including chemotherapy and
00:20:55
targeted therapies ESC defines
00:20:58
significant ific car toxicity as the
00:21:00
following you have severe ctrcd which is
00:21:03
again cancer therapy related car
00:21:05
dysfunction you have moderate CCD and
00:21:08
Mild C rcd you need to know that slide
00:21:11
very well any cardiologist need to know
00:21:13
that so severe CCD is clinically severe
00:21:17
heart failure meaning heart failure that
00:21:19
requires
00:21:21
hospitalization or Worse heart failure
00:21:24
with shock usually with an EF decline to
00:21:28
less than
00:21:29
40% or you may have the asymptomatic
00:21:32
severe CCD where you get an EF reduction
00:21:35
to less than
00:21:36
40% without clinically severe heart
00:21:40
failure now moderate CCD is defined as
00:21:45
clinically moderate ctrcd where you get
00:21:47
clinical heart failure that requires
00:21:50
outpatient diuretic treatment and heart
00:21:53
failure therapy but does not require
00:21:55
inpatient hospitalization unlike severe
00:21:58
symptomatic
00:22:00
ctrcd or you can have for moderate ctrcd
00:22:04
an EF decline of more than 10% to an EF
00:22:08
of 40 to 49% not below 40% or an EF
00:22:13
decline less than 10% to ANF of 40 to
00:22:16
49% along with either a new decline of
00:22:20
GLS by more than 15% or a new rise in
00:22:24
kak biomarker stron or BNP so basically
00:22:28
moderate CCD is a clinically moderate
00:22:30
heart failure exacerbation that doesn't
00:22:33
require hospitalization but requires
00:22:36
titration of therapies or an EF decline
00:22:39
to 40 to
00:22:41
49% uh especially more than 10% to a 40
00:22:45
49% or less than 10% but with some other
00:22:49
features GLS or
00:22:51
biomarkers mild C rcd is no decline in
00:22:55
EF and no worsening of clinical heart
00:22:58
faer all you have in mild city rcd is a
00:23:02
decline of global longitudinal score by
00:23:05
more than 15% or a rise in KCT
00:23:08
biomarkers BNP and troponin without a
00:23:11
drop in EF to less than 50% and without
00:23:13
a new heart
00:23:15
failure so what to do when ctrcd happens
00:23:19
so if you get severe ctrcd whether
00:23:23
clinically severe heart failure or
00:23:25
asymptomatic severe EF reduction you
00:23:27
have to interrupt the cancer drug again
00:23:29
whether it's intrac cycl or whether it
00:23:32
is targeted therapies but you may
00:23:34
reinitiate it once clinical heart
00:23:37
failure resolves and EF normalizes even
00:23:41
if EF declined to less than 40% at some
00:23:45
point and even if severe heart failure
00:23:48
occur at some point the exception is if
00:23:51
you get severe clinical ctrcd with
00:23:54
severe clinical heart failure with entra
00:23:57
cyclines in that case you do need to
00:23:59
permanently discontinue inra cycling but
00:24:02
if you get asymptomatic or mildly
00:24:05
moderately symptomatic EF decline with
00:24:07
intra cycling less than 40% with
00:24:10
moderate heart failure not heart failure
00:24:12
requiring hospitalization you may still
00:24:15
reinitiate entra cyclings after recovery
00:24:18
of heart failure and
00:24:20
EF now if you get moderate
00:24:23
ctrcd in that case you temporarily
00:24:26
interrupt the drug until heart failure
00:24:28
resolves and EF normalizes usually that
00:24:31
takes one plus month with heart failure
00:24:35
therapy diuretics ACE inhibitor beta
00:24:38
blockers aldosterone antagonist the drug
00:24:41
may even be continued without
00:24:43
interruption during moderate
00:24:45
asymptomatic ctrcd meaning an EF of 40%
00:24:49
without clinical heart failure
00:24:52
especially with troab and targeted
00:24:54
therapy not with enty with entracing you
00:24:57
do need to interrupt the drug even
00:24:59
moderate asymptomatic
00:25:01
ctrcd this is what we call permissive
00:25:03
carot toxicity meaning continuing her
00:25:05
two antagonist and targeted therapy with
00:25:08
moderate asymptomatic
00:25:11
ctrcd now with mild ctrcd meaning in
00:25:14
impairment of global longitudinal score
00:25:17
or arising troponin and
00:25:20
BNP we monitor those we take those into
00:25:23
account we worry about a decline in GLS
00:25:27
because it does predict
00:25:29
EF Decline and clinical heart failure
00:25:32
however by itself a decline in GLS or a
00:25:36
rising biomarker does not warrant
00:25:38
Interruption of the drug you continue
00:25:39
the drug if the F remains more than 50%
00:25:42
GLS per se does not prompt halting or
00:25:45
changing chemotherapy or immune therapy
00:25:49
but it predicts future heart failure and
00:25:51
warrants closer monitoring of the
00:25:53
patient of EF and starting beta blocker
00:25:56
and Ace inhibitor AR therapy this
00:25:59
applies to both enty trastuzumab and
00:26:02
targeted
00:26:04
therapies same applies to the
00:26:06
measurement of troponin and BNP before
00:26:08
and during cancer therapy it does not
00:26:10
warrant Interruption of therapy but it
00:26:13
warrants closer monitoring and therapy
00:26:16
with beta blocker and Ace
00:26:19
ARB and here is a slide about preventive
00:26:21
ACE inhibitor and beta blockade most of
00:26:24
the data address patients receiving
00:26:26
intrac Ace and carv have both shown in
00:26:30
many small randomiz st a reduction of
00:26:32
intrac cycl toxicity mainly in
00:26:34
attenuation of EF decline GLS Decline
00:26:38
and tropon Rise in patient receiving
00:26:40
high doses of an enty or those with a
00:26:43
rise in tronent after
00:26:45
chemotherapy in a large metaanalysis of
00:26:48
randomized Trials cardio protection with
00:26:51
Ace and or beta blockers was associated
00:26:53
with a lesser decline in EF but not with
00:26:57
a red reduc risk of overt heart failure
00:27:00
that said there is evidence of benefit
00:27:02
with those therapies therefore per ESC
00:27:06
full heart failure therapy is
00:27:08
recommended for patient who develop
00:27:10
moderate or severe ctrcd whether
00:27:12
symptomatic with a clinical heart
00:27:14
failure or not with an isolated decline
00:27:16
of EF outside moderate or severe ctrcd
00:27:21
preventive acrb and beta blocker should
00:27:23
be considered for one primary prevention
00:27:26
in high risk pay s that you assess
00:27:29
before therapy that I describ meaning
00:27:32
underlying clinical heart failure F less
00:27:35
than 50% CAD or low
00:27:39
GLS so in those patients receiving entra
00:27:43
cycline and or her two therapies and or
00:27:45
targeted therapies with heart failure
00:27:47
risk we should give Ace and beta blocker
00:27:51
before initiating cancer therapies the
00:27:54
second group where you use preventive
00:27:56
acrb is like a describe patients who
00:27:59
while receiving therapy develop mild c
00:28:01
rcd meaning a decline of GLS or a rising
00:28:04
troponin BNP with ef remaining over
00:28:08
50% also Statin should be considered for
00:28:12
primary prevention in adult patients
00:28:14
with cancer at at high and very high CAD
00:28:18
toxicity risk such as patients with
00:28:21
underlying CAD who are receiving
00:28:23
therapies that have a cad risk like 5fu
00:28:28
or the targeted therapy such as VF
00:28:31
targeted therapy
