Difference between revisions of "Cardio-oncology"

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[[File:Cardio-oncology.png|alt=Cardio-oncology|thumb|Cardio-oncology]]
 
[[File:Cardio-oncology.png|alt=Cardio-oncology|thumb|Cardio-oncology]]
Cardio-oncology is an evolving field in [[cardiology]] that deals with the effects of [[cancer]], and treatments such as [[radiation therapy]] and [[chemotherapy]] for cancer [[patients]] with cancer and [[cancer]] survivors.
+
Cardio-oncology is an evolving field in [[cardiology]] that provides cardiac care for cancer patients and its survivors. It deals with early detection , reducing the adverse cardiovascular side effects , treating and preventing the cardiovascular effects of [[cancer]] therapies , such as [[radiation therapy|radiation]] [[chemotherapy]] ,  newly emerged targeted molecular therapy and [[Immunotherapy]]
 +
 
 +
Heart disease and cancer are the two main causes of mortality globally, accounting for 46.1% of deaths worldwide.1-2 <br />Due to current advancement in  cancer treatment,  there has been decrease in mortality in cancer patients. However, the cancer therapy-related cardiovascular complications, in particular chemo-therapy and radiation therapy-induced cardio toxicities are a major cause of morbidity and mortality in people living with or surviving cancer.
 +
 
 +
All chemotherapeutic agents and radiation therapy target tumor cells but also result in collateral damage to other normal tissues including the cardiovascular system.
 +
 
 +
The most recent ESC guideline broadly divides the cardiovascular complications of cancer therapy into nine major categories( 3) . The cardiac complications encompass myocardial dysfunction and congestive heart failure( CHF)  , coronary artery disease, valvular heart disease, arrhythmias, and pericardial diseases. The vascular complications would include arterial hypertension, thromboembolic event, peripheral vascular disease and stroke, and pulmonary hypertension
 +
 
 +
 
 +
'''Cardiovascular complications of Radiation Therapy'''
 +
 
 +
Radiation therapy to the chest has improved  survival in patients with Hodgkin lymphoma, early-stage breast cancer, and other thoracic malignancies .  With higher survival rates with radiation therapy, cardiovascular disease has emerged as the most common nonmalignant cause of death in patients treated with chest radiation therapy, accounting for 25% of deaths in survivors of Hodgkin lymphoma. Thoracic irradiation, especially to the left side  damages all cells, including those of the pericardium, myocardium, valves, coronary vasculature and conduction system, with clinical disease usually presenting two to three decades after treatment.
 +
 
 +
They can present as Chronic or constrictive pericarditis ,Radiation-induced cardiomyopathy, mixed regurgitation and stenosis of predominantly left sided valves,sinus node dysfunction, fascicular ,  bundle branch blocks, and complete heart block. Coronary artery disease (CAD) occurs earlier and with increased incidence in patients treated with radiation therapy. Coronary artery lesions are typically ostial, long, smooth, and concentric and have a higher fibrotic content than typical atherosclerotic lesions. In-stent restenosis rates with bare metal stents are significantly higher in patients with radiation-induced CAD. In patients with radiation-induced CAD, native vessels, including the left internal mammary artery, may be rendered unusable for bypass. The postoperative course,  after coronary artery bypass surgery may be complicated by radiation-induced lung injury (pleural effusion, prolonged ventilation) and a higher incidence of atrial fibrillation.
 +
 
 +
Acute pericarditis is the most common early manifestation of radio toxicity; however, it is now less common (incidence of 2.5%) because of changes in shielding, divided dosing, and lower cumulative doses
 +
 
 +
Traditional cardiovascular risk factors, such as smoking, dyslipidemia, diabetes and hypertension, should be aggressively managed because of the increased risk for coronary artery disease in patients with a history of chest radiation therapy.
 +
 
 +
There is no consensus on cardiac testing in asymptomatic patients after chest radiation. Baseline cardiac evaluation that includes echocardiography is reasonable, and several organizations have recommended starting stress echocardiography at 5 to 10 years after completion of therapy or at age 30 years, whichever comes first.
 +
 
 +
 
 +
'''Cardiovascular complications of cancer therapy'''
 +
 
 +
Chemotherapy may result in many types of cardiovascular toxicity ( '''''INSERT''' '''TABLE''''') . Two broad categories of chemotherapeutic cardiac injury have been defined based on severity: type I, which is marked by dose-dependent cardiac dysfunction with irreversible ultrastructural necrosis, and type II, which is not dose dependent and is often reversible.
 +
 
 +
 
 +
Type I injury is associated with the use of anthracyclines, such as doxorubicin, daunorubicin, and epirubicin. Daunorubicin was the first anthracycline with cardiotoxicity being reported half a century ago , in the original study, of the 19 children of solid tumors or acute leukemia who received daunorubicin ( 4)The discovery and application of other anthracycline chemotherapies and the demonstration of dose-dependent probability of CHF in the 1970s  were perhaps the first event to foster partnership between oncologists and cardiologists.(5,6)
 +
 
 +
Acute anthracycline toxicity, which can present as heart block, arrhythmias, heart failure, myocarditis, and pericarditis, occurs in less than 1% of patients and may be reversible. Chronic progressive anthracycline toxicity usually presents as dilated cardiomyopathy and is most closely linked with the use of doxorubicin. Chronic progressive toxicity has an early onset (within 1 year of treatment) in 1.6% to 2% of patients and a late onset (after 1 year) in up to 5% of patients. Late-onset chronic progressive toxicity is related to total cumulative dose. In patients with a cumulative anthracycline dose of 550 mg/m2, the incidence of heart failure is up to 26%, and toxicity may not become clinically evident until 10 to 20 years after treatment. Factors associated with increased risk for anthracycline toxicity include concomitant use of cyclophosphamide, trastuzumab, or paclitaxel; previous chest irradiation; and female sex.  Concomitant dexrazoxane reduces the risk for doxorubicin toxicity.
 +
 
 +
Type II injury is more commonly associated with molecularly targeted therapy, such as trastuzumab. Overexpression of human epidermal growth factor receptor 2 (HER2/ErbB2) in breast cancer is a poor prognostic indicator, Trastuzumab (Herceptin), a humanized anti-HER2 monoclonal antibody targeting the extracellular domain of this receptor,dramatically changes the survival in HER2 positive breast cancer.These receptor (ErbB2/ ErbB4) are also expressed in cardiomyocytes and play a protective role against myocardial stress.The binding of anticancer drugs to HER2 receptor may disrupt this cardioprotective pathway and result in cardiotoxicity toxicity results in left ventricular systolic dysfunction, with symptoms of heart failure in 3% to 7% of patients. It is more common in patients older than 50 years or with concomitant anthracycline use. Patients who demonstrate normalization of left ventricular function after discontinuation of trastuzumab may receive additional therapy.
 +
 
 +
 
 +
Alkylating agents including nitrogen mustards (i.e., cyclophosphamide and ifosfamide) and the platinum-containing molecule, cisplatin, are the oldest class of anticancer agents. cyclophosphamide-induced cardiotoxicity include pericardial effusions, myocarditis, pericarditis, and heart failure which is irreversible in 25% of cases at a doses of  ≥ 1.55 g/m2/day.In addition to vascular events such as deep vein thrombosis and pulmonary embolism, cisplatin treatment is also associated with both acute and late-onset cardiotoxicity. Acute myocardial infarction, angina pectoris, and cerebrovascular ischemia are relatively uncommon, occurring in ~2% of patients. Likely pathophysiology is multifactorial including procoagulant and direct endothelial toxic effects, as well as hypersensitivity reactions occurring during treatment.
 +
 
 +
Antimetabolites and antimicrotubule agents related cardiotoxicity .In cancer patients treated using 5-fluorouracil (5-FU) containing regimen, cardiac symptoms generally occur early during the drug infusion.The pathogenic mechanism of cardiovascular toxicity associated with 5-FU is not completely understood; however, coronary thrombosis, arteritis, and vasospasm have been proposed as possible explanations.
 +
 
 +
Multitargeted tyrosine kinase inhibitors and anti–vascular endothelial growth factor antibodies are increasingly being used as targeted molecular therapy. Unfortunately, despite their “selective” action they can still cause cardiovascular complications such as arterial hypertension (HTN), QT interval prolongation, CHF, cardiomyopathy, stroke, acute myocardial infarction, thromboembolic events and cardiovascular deaths. Sunitinib, pazopanib, and especially vandetanib prolong the QT and therefore increase the risk of Torsades de pointes (TdP), a form of lethal arrhythmia. These drugs should only be used cautiously in the presence of a history of QT prolongation or concomitant antiarrhythmic treatments, bradycardia, or electrolyte abnormalities, while in such conditions vandetanib should be completely avoided. . Of the tyrosine kinase inhibitors, sunitinib has been most frequently associated with cardiotoxicity, with up to a 50% incidence of new or worsened hypertension and up to a 15% incidence of decreased left ventricular ejection fraction (LVEF). These effects may be reversible with early recognition. . The anti–vascular endothelial growth factor antibody bevacizumab is associated with significant but reversible hypertension
 +
 
 +
 
 +
Malignancy accounts for 13% to 23% of pericardial effusions and may be the first presentation of the disease. Lung, breast, and esophageal cancers; melanoma; lymphoma; and leukemia are the most common malignancies that cause pericardial effusions.Cardiac tamponade results when the pericardial fluid pressure impairs filling of one or both ventricles, leading to decreased cardiac output.
 +
 
 +
'''Immunotherapy'''
 +
 
 +
Immune checkpoints  prevent the immune system from attacking normal tissues (self), but immunotherapy can take advantage of this by inhibiting the checkpoints  and allowing the immune system to be more aggressive and so attack cancer cells.
 +
 
 +
Antibodies that block these checkpoints  release the brakes on the immune system and allow it to aggressively attack the tumor. To date, development of these agents has focused on two major targets: Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and the programmed cell death protein-1 (PD-1) pathway. Immune checkpoint inhibition has demonstrated superb efficacy in a variety of malignancies that have historically conferred a poor prognosis. Side effects are related to resultant autoimmunity from the less-regulated immune system. Though rare, immune-mediated cardiac toxicity has been observed in patients enrolled in large clinical trials and in individual case reports. In accordance with preclinical data, autoimmune myocarditis has been reported with both anti-CTLA4 and anti-PD-1 therapies
 +
 
 +
 
 +
'''Monitoring'''
 +
 
 +
In patients preparing to receive chemotherapy associated with known cardiotoxicity, an electrocardiogram should be obtained at baseline. Baseline evaluation of LVEF (with echocardiography or multigated acquisition scanning) is important if the associated cardiotoxicity includes left ventricular dysfunction and heart failure. It is reasonable to repeat echocardiography at a total cumulative anthracycline dose of 300 mg/m2 and before each dose in patients with pre-existent left ventricular dysfunction or those receiving higher cumulative doses. European guidelines suggest that patients receiving trastuzumab should undergo repeat echocardiography every 3 months. In general, cardiovascular consultation should be obtained in asymptomatic patients who demonstrate a decline in LVEF of 10% or more or in patients with symptoms of heart failure associated with a decline in LVEF of 5% or more to a level below 55%. Three-dimensional echocardiographic evaluation of left ventricular volumes may be more accurate in detecting small changes.
 +
 
 +
In patients with clinical signs or symptoms of cardiac dysfunction, cardiac biomarkers (such as troponin and N-terminal proB-type natriuretic peptide) along with imaging techniques (such as echocardiographically derived global longitudinal strain) may be helpful in identifying early toxicity and guiding individual therapy. At present, treatment of patients with chemotherapy-induced heart failure follows standard paradigms.
 +
 
 +
Surveillance with baseline N-terminal proB-type natriuretic peptide measurement and LVEF assessment at baseline, 1 month, and every 3 months thereafter has been advocated for patients taking sunitinib.
 +
 
 +
Traditional cardiovascular risk factors, such as smoking, dyslipidemia, diabetes and hypertension, should be aggressively managed. Exercise and heart healthy diet recommended 
 +
 
 +
Despite significant understanding of the molecular and pathophysiologic mechanisms behind the cardiovascular toxicity of cancer therapy, there is still lack of evidence-based approach for the monitoring and management of patients. 
 +
 
 +
 
 +
'''Multi-disciplinary approaches toward individualized cardio-oncology care'''
 +
 
 +
Cardio-oncology  is an integrative and translational medicine between cardiologists and oncologists focusing on the diagnosis, prevention, and management of cardiovascular complications associated with the development and treatment of malignancy.
 +
 
 +
Clear communication among a large multidisciplinary team '''(Fig. 1)''' including cardiologists, oncologists, imaging specialists, clinical pharmacologists, the patient, and their family is essential for many life-modifying decisions, and this often requires periodic reconsideration during a course of therapy. Adding to the complexity is the fact that many decisions must be based on limited evidence, and in the context of rapidly evolving cancer therapeutics, experience and expert opinion become increasingly important.
 +
 
 +
 
 +
Cardio-oncology care should include primary prevention of cardiovascular complications in “high risk” patients with aggressive risk factor modifications and ongoing monitoring early toxicities, effective treatment of complications that have already developed and active prevention of worsening complications, pre-operative assessment of cardiovascular risks for cancer surgeries, and investigation of possible cardiac invasion from malignancy.
 +
 
 +
 
 +
references
 +
 
 +
#Weir, H. K. et al. Heart Disease and Cancer Deaths-Trends and Projections in the United States, 1969–2020. ''Prev. Chronic. Dis.'' 13, e157 (2016)
 +
#American Cancer Society. Cancer Facts & Figures 2017. American Cancer Society, (2017).
 +
#Zamorano, J. L. et al. 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: The Task Force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC). ''Eur. Heart. J.'' 37, 2768–2801 (2016).
 +
#Tan, C., Tasaka, H., Yu, K. P., Murphy, M. L. & Karnofsky, D. A. Daunomycin, an antitumor antibiotic, in the treatment of neoplastic disease: clinical evaluation with special reference to childhood leukemia. ''Cancer'' 20, 333–353 (1967).
 +
#Von Hoff, D. D. et al. Risk factors for doxorubicin-induced congestive heart failure. ''Ann. Intern. Med.'' 91, 710–717 (1979)
 +
#Von Hoff, D. D., Rozencweig, M., Layard, M., Slavik, M. & Muggia, F. M. Daunomycin-induced cardiotoxicity effects in children and adults: a review of 110 cases. ''Am. J. Med.'' 62, 200–208 (1977).
  
 
==Topics in cardio oncology==
 
==Topics in cardio oncology==
Line 12: Line 92:
 
*[[Thromboembolic disease]].
 
*[[Thromboembolic disease]].
 
*[[Peripheral vascular disease]] and [[stroke]].
 
*[[Peripheral vascular disease]] and [[stroke]].
 +
*Acute [[chemotherapy]] treatment side effects
 +
*[[Imaging]] and [[cardio toxicity]]
  
 
==Cardio-oncology case series==
 
==Cardio-oncology case series==
Line 29: Line 111:
  
 
==External links==
 
==External links==
 +
 
*[https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-16/Cardio-oncology-principles-and-organisational-issues Cardio-oncology principles and organisational-issues]
 
*[https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-16/Cardio-oncology-principles-and-organisational-issues Cardio-oncology principles and organisational-issues]
 
*[https://www.acc.org/clinical-topics/cardio-oncology#sort=%40fcommonsortdate90022%20descending American College of Cardiology - Cardio-oncology section]
 
*[https://www.acc.org/clinical-topics/cardio-oncology#sort=%40fcommonsortdate90022%20descending American College of Cardiology - Cardio-oncology section]

Revision as of 20:59, 14 January 2020

Cardio-oncology
Cardio-oncology

Cardio-oncology is an evolving field in cardiology that provides cardiac care for cancer patients and its survivors. It deals with early detection , reducing the adverse cardiovascular side effects , treating and preventing the cardiovascular effects of cancer therapies , such as radiation , chemotherapy , newly emerged targeted molecular therapy and Immunotherapy.

Heart disease and cancer are the two main causes of mortality globally, accounting for 46.1% of deaths worldwide.1-2
Due to current advancement in cancer treatment, there has been decrease in mortality in cancer patients. However, the cancer therapy-related cardiovascular complications, in particular chemo-therapy and radiation therapy-induced cardio toxicities are a major cause of morbidity and mortality in people living with or surviving cancer.

All chemotherapeutic agents and radiation therapy target tumor cells but also result in collateral damage to other normal tissues including the cardiovascular system.

The most recent ESC guideline broadly divides the cardiovascular complications of cancer therapy into nine major categories( 3) . The cardiac complications encompass myocardial dysfunction and congestive heart failure( CHF) , coronary artery disease, valvular heart disease, arrhythmias, and pericardial diseases. The vascular complications would include arterial hypertension, thromboembolic event, peripheral vascular disease and stroke, and pulmonary hypertension


Cardiovascular complications of Radiation Therapy

Radiation therapy to the chest has improved survival in patients with Hodgkin lymphoma, early-stage breast cancer, and other thoracic malignancies . With higher survival rates with radiation therapy, cardiovascular disease has emerged as the most common nonmalignant cause of death in patients treated with chest radiation therapy, accounting for 25% of deaths in survivors of Hodgkin lymphoma. Thoracic irradiation, especially to the left side damages all cells, including those of the pericardium, myocardium, valves, coronary vasculature and conduction system, with clinical disease usually presenting two to three decades after treatment.

They can present as Chronic or constrictive pericarditis ,Radiation-induced cardiomyopathy, mixed regurgitation and stenosis of predominantly left sided valves,sinus node dysfunction, fascicular , bundle branch blocks, and complete heart block. Coronary artery disease (CAD) occurs earlier and with increased incidence in patients treated with radiation therapy. Coronary artery lesions are typically ostial, long, smooth, and concentric and have a higher fibrotic content than typical atherosclerotic lesions. In-stent restenosis rates with bare metal stents are significantly higher in patients with radiation-induced CAD. In patients with radiation-induced CAD, native vessels, including the left internal mammary artery, may be rendered unusable for bypass. The postoperative course, after coronary artery bypass surgery may be complicated by radiation-induced lung injury (pleural effusion, prolonged ventilation) and a higher incidence of atrial fibrillation.

Acute pericarditis is the most common early manifestation of radio toxicity; however, it is now less common (incidence of 2.5%) because of changes in shielding, divided dosing, and lower cumulative doses

Traditional cardiovascular risk factors, such as smoking, dyslipidemia, diabetes and hypertension, should be aggressively managed because of the increased risk for coronary artery disease in patients with a history of chest radiation therapy.

There is no consensus on cardiac testing in asymptomatic patients after chest radiation. Baseline cardiac evaluation that includes echocardiography is reasonable, and several organizations have recommended starting stress echocardiography at 5 to 10 years after completion of therapy or at age 30 years, whichever comes first.


Cardiovascular complications of cancer therapy

Chemotherapy may result in many types of cardiovascular toxicity ( INSERT TABLE) . Two broad categories of chemotherapeutic cardiac injury have been defined based on severity: type I, which is marked by dose-dependent cardiac dysfunction with irreversible ultrastructural necrosis, and type II, which is not dose dependent and is often reversible.


Type I injury is associated with the use of anthracyclines, such as doxorubicin, daunorubicin, and epirubicin. Daunorubicin was the first anthracycline with cardiotoxicity being reported half a century ago , in the original study, of the 19 children of solid tumors or acute leukemia who received daunorubicin ( 4)The discovery and application of other anthracycline chemotherapies and the demonstration of dose-dependent probability of CHF in the 1970s were perhaps the first event to foster partnership between oncologists and cardiologists.(5,6)

Acute anthracycline toxicity, which can present as heart block, arrhythmias, heart failure, myocarditis, and pericarditis, occurs in less than 1% of patients and may be reversible. Chronic progressive anthracycline toxicity usually presents as dilated cardiomyopathy and is most closely linked with the use of doxorubicin. Chronic progressive toxicity has an early onset (within 1 year of treatment) in 1.6% to 2% of patients and a late onset (after 1 year) in up to 5% of patients. Late-onset chronic progressive toxicity is related to total cumulative dose. In patients with a cumulative anthracycline dose of 550 mg/m2, the incidence of heart failure is up to 26%, and toxicity may not become clinically evident until 10 to 20 years after treatment. Factors associated with increased risk for anthracycline toxicity include concomitant use of cyclophosphamide, trastuzumab, or paclitaxel; previous chest irradiation; and female sex. Concomitant dexrazoxane reduces the risk for doxorubicin toxicity.

Type II injury is more commonly associated with molecularly targeted therapy, such as trastuzumab. Overexpression of human epidermal growth factor receptor 2 (HER2/ErbB2) in breast cancer is a poor prognostic indicator, Trastuzumab (Herceptin), a humanized anti-HER2 monoclonal antibody targeting the extracellular domain of this receptor,dramatically changes the survival in HER2 positive breast cancer.These receptor (ErbB2/ ErbB4) are also expressed in cardiomyocytes and play a protective role against myocardial stress.The binding of anticancer drugs to HER2 receptor may disrupt this cardioprotective pathway and result in cardiotoxicity toxicity results in left ventricular systolic dysfunction, with symptoms of heart failure in 3% to 7% of patients. It is more common in patients older than 50 years or with concomitant anthracycline use. Patients who demonstrate normalization of left ventricular function after discontinuation of trastuzumab may receive additional therapy.


Alkylating agents including nitrogen mustards (i.e., cyclophosphamide and ifosfamide) and the platinum-containing molecule, cisplatin, are the oldest class of anticancer agents. cyclophosphamide-induced cardiotoxicity include pericardial effusions, myocarditis, pericarditis, and heart failure which is irreversible in 25% of cases at a doses of  ≥ 1.55 g/m2/day.In addition to vascular events such as deep vein thrombosis and pulmonary embolism, cisplatin treatment is also associated with both acute and late-onset cardiotoxicity. Acute myocardial infarction, angina pectoris, and cerebrovascular ischemia are relatively uncommon, occurring in ~2% of patients. Likely pathophysiology is multifactorial including procoagulant and direct endothelial toxic effects, as well as hypersensitivity reactions occurring during treatment.

Antimetabolites and antimicrotubule agents related cardiotoxicity .In cancer patients treated using 5-fluorouracil (5-FU) containing regimen, cardiac symptoms generally occur early during the drug infusion.The pathogenic mechanism of cardiovascular toxicity associated with 5-FU is not completely understood; however, coronary thrombosis, arteritis, and vasospasm have been proposed as possible explanations.

Multitargeted tyrosine kinase inhibitors and anti–vascular endothelial growth factor antibodies are increasingly being used as targeted molecular therapy. Unfortunately, despite their “selective” action they can still cause cardiovascular complications such as arterial hypertension (HTN), QT interval prolongation, CHF, cardiomyopathy, stroke, acute myocardial infarction, thromboembolic events and cardiovascular deaths. Sunitinib, pazopanib, and especially vandetanib prolong the QT and therefore increase the risk of Torsades de pointes (TdP), a form of lethal arrhythmia. These drugs should only be used cautiously in the presence of a history of QT prolongation or concomitant antiarrhythmic treatments, bradycardia, or electrolyte abnormalities, while in such conditions vandetanib should be completely avoided. . Of the tyrosine kinase inhibitors, sunitinib has been most frequently associated with cardiotoxicity, with up to a 50% incidence of new or worsened hypertension and up to a 15% incidence of decreased left ventricular ejection fraction (LVEF). These effects may be reversible with early recognition. . The anti–vascular endothelial growth factor antibody bevacizumab is associated with significant but reversible hypertension


Malignancy accounts for 13% to 23% of pericardial effusions and may be the first presentation of the disease. Lung, breast, and esophageal cancers; melanoma; lymphoma; and leukemia are the most common malignancies that cause pericardial effusions.Cardiac tamponade results when the pericardial fluid pressure impairs filling of one or both ventricles, leading to decreased cardiac output.

Immunotherapy

Immune checkpoints prevent the immune system from attacking normal tissues (self), but immunotherapy can take advantage of this by inhibiting the checkpoints and allowing the immune system to be more aggressive and so attack cancer cells.

Antibodies that block these checkpoints release the brakes on the immune system and allow it to aggressively attack the tumor. To date, development of these agents has focused on two major targets: Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and the programmed cell death protein-1 (PD-1) pathway. Immune checkpoint inhibition has demonstrated superb efficacy in a variety of malignancies that have historically conferred a poor prognosis. Side effects are related to resultant autoimmunity from the less-regulated immune system. Though rare, immune-mediated cardiac toxicity has been observed in patients enrolled in large clinical trials and in individual case reports. In accordance with preclinical data, autoimmune myocarditis has been reported with both anti-CTLA4 and anti-PD-1 therapies


Monitoring

In patients preparing to receive chemotherapy associated with known cardiotoxicity, an electrocardiogram should be obtained at baseline. Baseline evaluation of LVEF (with echocardiography or multigated acquisition scanning) is important if the associated cardiotoxicity includes left ventricular dysfunction and heart failure. It is reasonable to repeat echocardiography at a total cumulative anthracycline dose of 300 mg/m2 and before each dose in patients with pre-existent left ventricular dysfunction or those receiving higher cumulative doses. European guidelines suggest that patients receiving trastuzumab should undergo repeat echocardiography every 3 months. In general, cardiovascular consultation should be obtained in asymptomatic patients who demonstrate a decline in LVEF of 10% or more or in patients with symptoms of heart failure associated with a decline in LVEF of 5% or more to a level below 55%. Three-dimensional echocardiographic evaluation of left ventricular volumes may be more accurate in detecting small changes.

In patients with clinical signs or symptoms of cardiac dysfunction, cardiac biomarkers (such as troponin and N-terminal proB-type natriuretic peptide) along with imaging techniques (such as echocardiographically derived global longitudinal strain) may be helpful in identifying early toxicity and guiding individual therapy. At present, treatment of patients with chemotherapy-induced heart failure follows standard paradigms.

Surveillance with baseline N-terminal proB-type natriuretic peptide measurement and LVEF assessment at baseline, 1 month, and every 3 months thereafter has been advocated for patients taking sunitinib.

Traditional cardiovascular risk factors, such as smoking, dyslipidemia, diabetes and hypertension, should be aggressively managed. Exercise and heart healthy diet recommended

Despite significant understanding of the molecular and pathophysiologic mechanisms behind the cardiovascular toxicity of cancer therapy, there is still lack of evidence-based approach for the monitoring and management of patients.


Multi-disciplinary approaches toward individualized cardio-oncology care

Cardio-oncology is an integrative and translational medicine between cardiologists and oncologists focusing on the diagnosis, prevention, and management of cardiovascular complications associated with the development and treatment of malignancy.

Clear communication among a large multidisciplinary team (Fig. 1) including cardiologists, oncologists, imaging specialists, clinical pharmacologists, the patient, and their family is essential for many life-modifying decisions, and this often requires periodic reconsideration during a course of therapy. Adding to the complexity is the fact that many decisions must be based on limited evidence, and in the context of rapidly evolving cancer therapeutics, experience and expert opinion become increasingly important.


Cardio-oncology care should include primary prevention of cardiovascular complications in “high risk” patients with aggressive risk factor modifications and ongoing monitoring early toxicities, effective treatment of complications that have already developed and active prevention of worsening complications, pre-operative assessment of cardiovascular risks for cancer surgeries, and investigation of possible cardiac invasion from malignancy.


references

  1. Weir, H. K. et al. Heart Disease and Cancer Deaths-Trends and Projections in the United States, 1969–2020. Prev. Chronic. Dis. 13, e157 (2016)
  2. American Cancer Society. Cancer Facts & Figures 2017. American Cancer Society, (2017).
  3. Zamorano, J. L. et al. 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: The Task Force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC). Eur. Heart. J. 37, 2768–2801 (2016).
  4. Tan, C., Tasaka, H., Yu, K. P., Murphy, M. L. & Karnofsky, D. A. Daunomycin, an antitumor antibiotic, in the treatment of neoplastic disease: clinical evaluation with special reference to childhood leukemia. Cancer 20, 333–353 (1967).
  5. Von Hoff, D. D. et al. Risk factors for doxorubicin-induced congestive heart failure. Ann. Intern. Med. 91, 710–717 (1979)
  6. Von Hoff, D. D., Rozencweig, M., Layard, M., Slavik, M. & Muggia, F. M. Daunomycin-induced cardiotoxicity effects in children and adults: a review of 110 cases. Am. J. Med. 62, 200–208 (1977).

Topics in cardio oncology

Cardio-oncology case series

Cardio-oncology journals

Cardio-oncology on Medpage

Resources in cardio-oncology

External links


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