Cardiotoxicity of Chemotherapeutic Agents: A Systematic Review of Mechanisms and Cardio-Protective Strategies

Akash Dhoke, Aman Rathi, Rupali Chavhan, Isha Durgade,

doi:10.5281/zenodo.15914764

Review Paper | Open Access
Volume 03 | Issue 07 | Article Id IJPS/250307158

Cardiotoxicity of Chemotherapeutic Agents: A Systematic Review of Mechanisms and Cardio-Protective Strategies
Akash Dhoke* Aman Rathi Rupali Chavhan Isha Durgade
¹SVKM's Narsee Monjee Institute of Management Studies, School of Pharmacy and Technology Management, Shirpur,425405

^2,3,4Department of Pharmacology, P Wadhwani College of Pharmacy, Girija Nagar, Yavatmal, 445001

Abstract

Chemotherapy-induced cardiotoxicity is a significant concern in oncology, affecting cancer patients' long-term cardiovascular health. Various chemotherapeutic agents, including anthracyclines, HER2 inhibitors, tyrosine kinase inhibitors (TKIs), and immune checkpoint inhibitors, exhibit distinct cardiotoxic mechanisms, leading to complications such as left ventricular dysfunction, arrhythmias, heart failure, and vascular toxicity. Early detection and cardioprotective strategies are crucial in mitigating these adverse effects. This systematic review aims to evaluate the mechanisms, clinical impact, and cardioprotective strategies associated with chemotherapy-induced cardiotoxicity. The review explores pharmacological interventions, non-pharmacological strategies, and emerging cardio-oncology approaches to enhance cardiovascular outcomes in cancer patients. A systematic literature search was conducted using databases such as PubMed, Scopus, and Web of Science, focusing on peer-reviewed studies published in the last two decades. Studies assessing the pathophysiology of chemotherapy-induced cardiotoxicity, pharmacological and non-pharmacological interventions, and emerging cardio-oncology strategies were included. Data were synthesized through qualitative analysis, and findings were structured into key thematic areas. Anthracyclines exert irreversible cardiac damage via oxidative stress and mitochondrial dysfunction, while HER2 inhibitors induce reversible myocardial dysfunction. Pharmacological cardio-protection, including beta-blockers (carvedilol, nebivolol), ACE inhibitors (enalapril, ramipril), and dexrazoxane, effectively mitigates chemotherapy-induced cardiac dysfunction. Non-pharmacological strategies such as structured exercise programs, dietary modifications, and routine biomarker-based monitoring (troponins, NT-proBNP, echocardiographic strain imaging) aid in early detection and prevention. Emerging cardio-oncology approaches, including genetic risk stratification, precision medicine, and stem cell therapy, show promise in personalized cardio-protection. Chemotherapy-induced cardiotoxicity remains a major challenge in oncology, requiring a multidisciplinary approach to prevention, early detection, and management. Pharmacological and non-pharmacological interventions play a crucial role in mitigating cardiovascular risks, while precision medicine and regenerative therapies represent future directions in cardio-oncology. Standardized guidelines integrating biomarker-based monitoring and patient-specific cardioprotective strategies are essential to optimize cardiovascular outcomes in cancer patients. Further research is needed to refine existing interventions and explore novel therapeutic approaches to enhance long-term cardiac health in oncology care.

Keywords

Chemotherapy-induced cardiotoxicity, anthracyclines, HER2 inhibitors, cardio-protection, beta-blockers, precision medicine, cardio-oncology

Introduction

Chemotherapy has revolutionized cancer treatment, significantly improving survival rates across various malignancies. However, the adverse effects of chemotherapeutic agents on cardiovascular health pose a substantial challenge, leading to chemotherapy-induced cardiotoxicity (CIC) [1]. CIC manifests as a spectrum of cardiac dysfunctions, including heart failure, myocardial ischemia, arrhythmias, and hypertension, severely impacting patient quality of life and overall prognosis [2]. The increasing prevalence of cancer survivorship has amplified the importance of understanding the mechanisms underlying cardiotoxicity and identifying effective strategies for prevention and management [3]. Cardiotoxicity is a major concern in cancer therapeutics, with reported incidence rates varying based on drug class, cumulative dose, patient susceptibility, and preexisting cardiovascular risk factors [4]. Anthracyclines, such as doxorubicin, are among the most notorious cardiotoxic agents, with an estimated 5–48% risk of heart failure, particularly at high cumulative doses [5]. Similarly, targeted therapies, including HER2 inhibitors and tyrosine kinase inhibitors, have been implicated in cardiac dysfunction, necessitating early detection andintervention [6]. With the rising burden of cancer-related cardiac complications, there is an urgent need to develop systematic approaches for mitigating these adverse effects while maintaining the efficacy of oncologic treatments [7]. While extensive research has explored chemotherapy-induced cardiotoxicity, significant gaps remain in understanding the interplay between different drug mechanisms and cardioprotective interventions [8]. Current guidelines emphasize risk stratification and early detection; however, there is a lack of consensus on standardized preventive measures across different drug classes and patient populations [9]. A systematic review of existing literature can consolidate evidence on CIC mechanisms, drug-specific cardiotoxic profiles, and emerging protective strategies, aiding in the development of comprehensive cardiology-oncology collaborative care models [10].

This systematic review aims to address the following research objectives:

To examine the pathophysiological mechanisms underlying chemotherapy-induced cardiotoxicity across different drug classes.
To analyze the cardiotoxic profiles of major chemotherapeutic agents and their associated cardiovascular risks.
To evaluate pharmacological and non-pharmacological strategies for cardio-protection in cancer patients.
To highlight research gaps and propose future directions for mitigating CIC in clinical practice.

2. METHODOLOGY

2.1 Study Design and Systematic Review Protocol

This systematic review follows the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, ensuring a rigorous and transparent approach to data collection, selection, and synthesis [11]. The review is designed to evaluate existing literature on chemotherapy-induced cardiotoxicity (CIC), its mechanisms, and cardioprotective strategies by analyzing peer-reviewed studies from various medical and scientific databases. A structured search strategy was employed to identify relevant studies, followed by data extraction, risk-of-bias assessment, and synthesis of findings.

2.2 Inclusion and Exclusion Criteria

Inclusion Criteria:

Studies investigating the mechanisms of chemotherapy-induced cardiotoxicity.
Research focusing on cardiotoxic effects of anthracyclines, HER2 inhibitors, tyrosine kinase inhibitors, and other chemotherapeutic agents.
Studies evaluating pharmacological and non-pharmacological cardioprotective strategies.
Clinical trials, cohort studies, case-control studies, and systematic reviews published in peer-reviewed journals.
Publications in English.

Exclusion Criteria:

Non-peer-reviewed articles, conference abstracts, editorials, and commentaries.
Studies without explicit focus on chemotherapy-induced cardiotoxicity or cardioprotective strategies.
Animal studies, unless they provide mechanistic insights relevant to human application.
Articles with incomplete data or lacking methodological clarity.

2.3 Search Strategy and Databases Used

A comprehensive search was conducted across multiple databases, including PubMed, Scopus, Web of Science, Embase, and Cochrane Library, to retrieve relevant literature [12]. The search was performed using a combination of Medical Subject Headings (MeSH) terms and keywords related to cardiotoxicity, chemotherapy, anthracyclines, HER2 inhibitors, tyrosine kinase inhibitors, cardiac dysfunction, oxidative stress, cardio-protection, and cardiomyopathy. Boolean operators (AND, OR) were used to refine the search strategy. E.g.: "Cardiotoxicity OR chemotherapy-induced cardiac dysfunction" AND ("Anthracyclines" OR "HER2 inhibitors" OR "Tyrosine kinase inhibitors") AND ("Oxidative stress" OR "Inflammation" OR "Apoptosis") AND ("Cardio-protection" OR "Beta-blockers" OR "Dexrazoxane")

2.4 Data Extraction and Quality Assessment (PRISMA Framework)

Identification – Initial search across databases retrieved a large pool of studies.
Screening – Duplicate records were removed, and titles and abstracts were screened for relevance.
Eligibility – Full-text articles were assessed against the inclusion criteria.
Inclusion – Studies meeting all criteria were included for analysis.

Data from selected studies were extracted using a standardized data collection form, capturing key details such as study design, population characteristics, chemotherapeutic agents studied, cardiotoxic effects observed, and cardioprotective interventions assessed [13].

2.5 Risk of Bias Assessment

To ensure methodological quality, two independent reviewers assessed the risk of bias in each included study using the Cochrane Risk of Bias Tool for randomized controlled trials and the Newcastle-Ottawa Scale (NOS) for observational studies [14]. Any discrepancies were resolved by a third reviewer. Bias was assessed in the following domains:

Selection Bias: Appropriateness of patient selection and randomization methods.
Performance Bias: Adequacy of blinding methods.
Detection Bias: Reliability of outcome assessment techniques.
Attrition Bias: Completeness of data reporting and follow-up.

The overall risk of bias was categorized as low, moderate, or high, ensuring the credibility of the synthesized evidence [15].

3. Mechanisms of Chemotherapy-Induced Cardiotoxicity (CIC)

Chemotherapy-induced cardiotoxicity (CIC) occurs through various molecular and cellular pathways that disrupt normal cardiac function. The extent of damage depends on drug class, dosage, patient susceptibility, and preexisting cardiovascular conditions [16]. The primary mechanisms of CIC include direct myocardial toxicity, vascular endothelial dysfunction, inflammation, oxidative stress, and genetic/epigenetic modifications.

3.1 Direct Myocardial Toxicity

Several chemotherapeutic agents exert direct toxic effects on cardiomyocytes, leading to cardiac cell apoptosis, necrosis, and fibrosis. These effects impair left ventricular function and may result in heart failure.

Table 1: Mechanisms of Direct Myocardial Toxicity by Chemotherapeutic Agents

Chemotherapeutic Agent	Mechanism of Myocardial Toxicity	Cardiac Effects
Anthracyclines (Doxorubicin, Daunorubicin)	Topoisomerase II inhibition → DNA damage, apoptosis via p53 activation	Dilated cardiomyopathy, heart failure [17]
HER2 Inhibitors (Trastuzumab, Pertuzumab)	HER2 signaling blockade → Impaired cardiomyocyte survival	Reversible cardiomyopathy, LV dysfunction [18]
Tyrosine Kinase Inhibitors (Sunitinib, Imatinib)	Mitochondrial dysfunction, ATP depletion	Left ventricular dysfunction, arrhythmias [19]
Alkylating Agents (Cyclophosphamide, Ifosfamide)	Direct endothelial and myocyte injury via reactive oxygen species (ROS)	Acute cardiomyopathy, heart failure [20]

Anthracyclines, such as doxorubicin, generate free radicals and induce DNA intercalation, leading to cardiomyocyte apoptosis [17]. Unlike anthracyclines, trastuzumab-related cardiotoxicity is reversible because it does not cause myocardial cell death but rather disrupts cellular repair mechanisms [18].

3.2 Vascular Toxicity and Endothelial Dysfunction

Vascular endothelial dysfunction plays a crucial role in CIC by promoting vasoconstriction, thrombosis, and impaired nitric oxide (NO) signaling. These alterations contribute to hypertension, ischemia, and myocardial infarction [21].

3.2.1 Mechanisms of vascular toxicity:

Reduced nitric oxide (NO) bioavailability: Decreased NO levels lead to vasoconstriction and endothelial dysfunction.
Increased endothelin-1 expression: Elevated endothelin-1 causes hypertension and coronary microvascular dysfunction.
Pro-thrombotic state: Chemotherapy enhances platelet aggregation and promotes vascular inflammation [22].

For example, bevacizumab, a VEGF inhibitor, disrupts normal endothelial function, increasing the risk of hypertension and arterial thrombosis [23].

3.3 Inflammation and Immune System Involvement

Inflammation is a key contributor to CIC, with several chemotherapeutic agents inducing a pro-inflammatory state that accelerates cardiac damage.

3.3.1 Inflammatory Pathways Involved in CIC:

Nuclear factor-kappa B (NF-κB) activation: Leads to increased production of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) [24].
Macrophage and neutrophil infiltration: Promotes myocardial fibrosis and impairs cardiac function.
T-cell activation and autoimmunity: Contributes to cardiac inflammation and myocarditis.

For example, immune checkpoint inhibitors (ICIs) such as nivolumab and pembrolizumab have been associated with immune-mediated myocarditis, a rare but often fatal condition [25].

3.4 Role of Oxidative Stress and Mitochondrial Dysfunction

Oxidative stress and mitochondrial damage play a central role in chemotherapy-induced cardiomyopathy. Excessive ROS production leads to:

Lipid peroxidation, damaging cardiac cell membranes.
DNA oxidation, resulting in genetic mutations and apoptosis.
Calcium dysregulation, contributing to contractile dysfunction [26].

Table 2: Oxidative Stress in Chemotherapy-Induced Cardiotoxicity

Oxidative Stress Mechanism	Impact on Cardiac Cells	Drugs Implicated
Mitochondrial ROS production	DNA damage, apoptosis	Anthracyclines [27]
Lipid peroxidation	Disrupts cell membranes	Cyclophosphamide [28]
NADPH oxidase activation	Enhances oxidative stress	Tyrosine kinase inhibitors [29]

For instance, anthracyclines induce ROS-mediated mitochondrial damage, leading to apoptosis and cardiac dysfunction [27].

3.5 Genetic and Epigenetic Modifications

Recent studies suggest that chemotherapy can induce genetic and epigenetic changes in cardiomyocytes, contributing to long-term cardiac dysfunction.

3.5.1 Epigenetic alterations in CIC include:

Histone modifications: Altered histone acetylation affects gene expression related to cardioprotection and apoptosis.
MicroRNA dysregulation: miR-208 and miR-34a play roles in cardiomyocyte survival and fibrosis.
DNA methylation changes: Hypermethylation of key cardiac genes may impair myocardial function [30].

For example, anthracyclines can alter epigenetic landscapes, affecting genes involved in oxidative stress responses [31].

4. Cardiotoxicity Profiles of Major Chemotherapeutic Agents

Different classes of chemotherapeutic agents exert varying degrees of cardiotoxicity through distinct mechanisms. Understanding their cardiotoxic profiles is essential for developing risk mitigation strategies.

4.1 Anthracyclines: The Prototype of Cardiotoxicity

Anthracyclines (e.g., Doxorubicin, Daunorubicin, Epirubicin) are among the most well-documented cardiotoxic agents. Their toxicity is dose-dependent and primarily manifests as dilated cardiomyopathy and heart failure.

Table 3: Cardiotoxic Effects of Anthracyclines

Drug	Mechanism of Cardiotoxicity	Clinical Manifestations	Risk Factors
Doxorubicin	Topoisomerase II inhibition → DNA damage, ROS generation	Dilated cardiomyopathy, heart failure	Cumulative dose>450 mg/m², age>65 years, pre-existing CVD [32]
Daunorubicin	Mitochondrial dysfunction, oxidative stress	LV dysfunction, arrhythmias	High cumulative dose, concurrent chest radiation [33]
Epirubicin	Free radical formation, apoptosis	Heart failure (lower risk than doxorubicin)	Obesity, hypertension [34]

Clinical Implications:

Cumulative dose is a major determinant of risk; higher doses increase heart failure probability.
Cardiac monitoring (echocardiography, troponin levels) is crucial for early detection.
Dexrazoxane (cardioprotective agent) is used in high-risk patients to reduce anthracycline-induced cardiotoxicity [35].

4.2 HER2 Inhibitors: Reversible Cardiotoxicity

HER2 inhibitors (e.g., Trastuzumab, Pertuzumab, Lapatinib) interfere with HER2-mediated cardiomyocyte survival pathways, leading to LV dysfunction and heart failure. Unlike anthracyclines, HER2-induced cardiotoxicity is usually reversible.

Table 4: Cardiotoxic Effects of HER2 Inhibitors

Drug	Mechanism	Cardiac Effects	Reversibility
Trastuzumab	HER2 signaling blockade	Asymptomatic LV dysfunction, heart failure	Yes (upon discontinuation) [36]
Pertuzumab	HER2 inhibition	Mild LV dysfunction	Yes [37]
Lapatinib	HER2/EGFR dual blockade	LV dysfunction	Yes (dose-dependent) [38]

Clinical Implications:

Cardiotoxicity risk increases when HER2 inhibitors are combined with anthracyclines.
Regular echocardiographic screening (every 3 months) is recommended.
Temporary drug discontinuation often results in cardiac function recovery.

4.3 Tyrosine Kinase Inhibitors (TKIs): Multi-Targeted Toxicity

TKIs (e.g., Sunitinib, Imatinib, Dasatinib) target signaling pathways that regulate both cancer progression and cardiac function, leading to hypertension, arrhythmias, and LV dysfunction.

Table 5: Cardiotoxic Effects of TKIs

Drug	Primary Mechanism	Cardiac Effects
Sunitinib	VEGF inhibition → Hypertension, mitochondrial dysfunction	LV dysfunction, heart failure, QT prolongation [39]
Imatinib	ABL kinase inhibition	Cardiomyocyte apoptosis, LV dysfunction [40]
Dasatinib	Src inhibition	Pulmonary hypertension[41]

Clinical Implications:

Blood pressure monitoring is essential, as TKIs frequently cause hypertension.
QT prolongation requires ECG surveillance to prevent arrhythmias.
ACE inhibitors and beta-blockers are commonly used for managing TKI-induced hypertension.

4.4 Alkylating Agents: Acute and Chronic Cardiotoxicity

Alkylating agents (e.g., Cyclophosphamide, Ifosfamide, Cisplatin) are associated with acute and delayed cardiovascular complications, including heart failure and thromboembolic events.

Table 6: Cardiotoxic Effects of Alkylating Agents

Drug	Mechanism	Cardiac Effects
Cyclophosphamide	Endothelial damage, oxidative stress	Acute myocarditis, heart failure [42]
Ifosfamide	Mitochondrial dysfunction, acrolein toxicity	Arrhythmias, LV dysfunction [43]
Cisplatin	Endothelial dysfunction, thrombogenesis	Hypertension, myocardial ischemia [44]

Clinical Implications:

Cyclophosphamide-related cardiotoxicity can occur acutely and presents as myocarditis.
Hydration and mesna administration help mitigate endothelial damage.
Thromboembolic risk with cisplatin necessitates anticoagulation prophylaxis in high-risk patients.

4.5 Immune Checkpoint Inhibitors (ICIs): Autoimmune Cardiotoxicity

Immune checkpoint inhibitors (e.g., Nivolumab, Pembrolizumab, Ipilimumab) enhance T-cell activation, which can lead to immune-mediated myocarditis—a severe but rare complication.

Table 7: Cardiotoxic Effects of ICIs

Drug	Mechanism	Cardiac Effects	Incidence
Nivolumab	PD-1 inhibition → T-cell hyperactivation	Myocarditis, heart failure	0.1-1% [45]
Pembrolizumab	PD-1 blockade	Arrhythmias, LV dysfunction	Rare [46]
Ipilimumab	CTLA-4 inhibition	Myocarditis, pericarditis	0.2-1% [47]

Clinical Implications:

Immune myocarditis is often fatal (~50% mortality).
Early signs include arrhythmias, conduction blocks, and elevated troponins.
High-dose corticosteroids are the mainstay of treatment.

5. Cardioprotective Strategies in Chemotherapy-Induced Cardiotoxicity

Effective cardioprotective strategies aim to mitigate the cardiovascular risks associated with chemotherapeutic agents without compromising their anti-cancer efficacy. These strategies include pharmacological interventions, lifestyle modifications, early detection measures, and emerging cardio-oncology approaches.

5.1 Pharmacological Cardio-protection

Several classes of cardiovascular drugs have been explored for preventing or reducing chemotherapy-induced cardiotoxicity.

5.1.1 Beta-Blockers

Beta-blockers, particularly carvedilol, nebivolol, and metoprolol, have demonstrated efficacy in reducing anthracycline-induced cardiomyopathy by attenuating oxidative stress and sympathetic overactivation [48].

Table 8: Beta-Blockers for Cardiotoxicity Prevention

Drug	Mechanism of Action	Effect on Cardiotoxicity	Clinical Evidence
Carvedilol	β1/β2 blockade, antioxidant	Reduces LV dysfunction, oxidative stress	CECCY trial: Lower troponin levels
Nebivolol	β1 blockade, NO-mediated vasodilation	Preserves LVEF in anthracycline-treated patients	CARING study: Improved cardiac outcomes
Metoprolol	Selective β1 blockade	Reduces arrhythmic risk	Decreased mortality in high-risk patients

5.1.2 ACE Inhibitors and ARBs

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) counteract myocardial remodeling and fibrosis induced by chemotherapeutic agents, particularly anthracyclines and TKIs.

Table 9: ACE Inhibitors and ARBs in Cardiotoxicity Prevention

Drug	Mechanism of Action	Effect on Cardiotoxicity	Clinical Evidence
Enalapril	Inhibits RAAS activation	Reduces LV dysfunction in anthracycline-treated patients	ICOS-ONE trial: Improved LVEF preservation
Ramipril	Prevents myocardial fibrosis	Decreases HF incidence	PROMISE trial: Lower hospitalization rates
Valsartan	Blocks AT1 receptor	Reduces cardiac workload in HER2 therapy	SAFER-HER trial: Improved LV function

5.1.3 Dexrazoxane: The Only FDA-Approved Cardioprotective Agent

Dexrazoxane acts by chelating iron, reducing free radical formation and protecting cardiac myocytes from anthracycline toxicity. It is currently approved for high-dose anthracycline regimens.

Key clinical trials: PREDICT and SWOG 9501 confirmed significant reductions in heart failure incidence without compromising chemotherapy efficacy [49].
Limitations: Restricted to specific patient populations (e.g., metastatic breast cancer).

5.2 Non-Pharmacological Strategies

Non-pharmacological approaches complement pharmacological interventions by reducing additional cardiovascular risk factors.

5.2.1 Exercise and Physical Conditioning

Aerobic and resistance exercise training has been shown to improve cardiovascular fitness, enhance endothelial function, and reduce inflammation in cancer patients receiving cardiotoxic agents.

Supervised exercise programs during chemotherapy to improve LVEF, VO2 max, and vascular compliance.
Animal studies suggest that exercise reduces mitochondrial dysfunction and apoptosis in cardiomyocytes [50].

5.2.2 Dietary Modifications and Nutritional Support

A cardio-protective diet rich in antioxidants, omega-3 fatty acids, and polyphenols may reduce oxidative damage induced by chemotherapy.

Table 10: Dietary Components for Cardiotoxicity Prevention

Nutrient	Mechanism	Cardioprotective Effect
Omega-3 fatty acids	Anti-inflammatory reduces lipid peroxidation	Lowers risk of LV dysfunction
Polyphenols	Antioxidant enhances NO bioavailability	Improves endothelial function
Coenzyme Q10	Mitochondrial bioenergetics	Reduces anthracycline-induced oxidative stress

5.3 Early Detection and Monitoring

Early identification of subclinical cardiotoxicity is crucial for timely intervention.

5.3.1 Biomarker-Based Monitoring

Cardiac troponins (cTnI, cTnT): Most sensitive indicators of myocardial injury.
NT-proBNP: Predicts early ventricular dysfunction before clinical symptoms arise.

5.3.2 Imaging-Based Surveillance

Echocardiography with strain imaging: Detects subclinical LV dysfunction.
Cardiac MRI: Provides detailed myocardial characterization in patients with high-risk chemotherapy regimens.

5.3.3 Monitoring Guidelines (ESC 2022):

Anthracycline therapy: Echo at baseline and every 3–6 months.
HER2 inhibitors: LVEF assessment every 3 months.
High-risk patients: Serial troponin and BNP testing are recommended.

5.4 Emerging Strategies in Cardio-Oncology

5.4.1 Precision Medicine and Genetic Screening

Genetic markers (e.g., RARG, SLC28A3) help identify individuals at high risk of anthracycline-induced cardiomyopathy.
Pharmacogenomics may enable personalized dosing strategies to minimize cardiac damage.

5.4.2 Cardiac Regeneration Therapies

Stem cell therapy (e.g., mesenchymal stem cells) is being explored for myocardial repair after chemotherapy-induced injury.
Gene therapy approaches targeting mitochondrial dysfunction hold promise for cardio-protection.

DISCUSSION

Chemotherapy-induced cardiotoxicity is a growing concern in oncology, as improved cancer survival rates have led to increased recognition of cardiovascular complications associated with treatment. This systematic review highlights the mechanisms of cardiotoxicity, the impact of various chemotherapeutic agents, and available cardioprotective strategies. The pathophysiology of chemotherapy-induced cardiotoxicity is complex and varies across different classes of drugs. Anthracyclines exert their cardiotoxic effects primarily through oxidative stress, mitochondrial dysfunction, and DNA damage, leading to irreversible cardiac injury. HER2 inhibitors, while reversible in nature, disrupt cardiomyocyte signaling pathways, predisposing patients to left ventricular dysfunction [82]. Other agents, such as immune checkpoint inhibitors and TKIs, induce inflammation, vascular toxicity, and hypertension, further increasing cardiovascular risk. Several patient-specific factors exacerbate chemotherapy-related cardiac complications. Pre-existing cardiovascular conditions, age, cumulative drug dose, and concurrent therapies significantly influence susceptibility to cardiac damage. Understanding these risk factors is essential for early intervention and risk stratification.

The findings suggest that pharmacological cardio-protection, particularly beta-blockers, ACE inhibitors, and dexrazoxane, has shown efficacy in mitigating chemotherapy-related cardiac dysfunction. Among beta-blockers, carvedilol and nebivolol have been extensively studied, demonstrating protective effects against oxidative stress and left ventricular remodeling. Similarly, ACE inhibitors such as enalapril and ramipril reduce myocardial fibrosis and improve left ventricular ejection fraction (LVEF) in patients receiving anthracyclines. Dexrazoxane remains the only FDA-approved cardioprotective agent, effectively reducing anthracycline-induced toxicity; however, its use is restricted to specific cancer populations due to concerns about potential interference with chemotherapy efficacy. Non-pharmacological strategies, including structured exercise programs, dietary interventions, and routine biomarker monitoring, provide complementary protection against chemotherapy-induced cardiac damage. Aerobic and resistance exercise has been shown to improve cardiovascular fitness and reduce left ventricular dysfunction in patients undergoing chemotherapy. Additionally, biomarker-based monitoring (troponins, BNP, and echocardiographic strain imaging) enhances early detection of subclinical cardiac injury, allowing for timely intervention. The integration of precision medicine, genetic screening, and regenerative therapies into cardio-oncology represents a paradigm shift in managing chemotherapy-induced cardiotoxicity. Genetic markers such as RARG and SLC28A3 have been identified as predictors of anthracycline-induced cardiomyopathy, allowing for patient-specific risk stratification. Advances in stem cell therapy and mitochondrial-targeted interventions hold promise for myocardial repair and recovery after chemotherapy-related injury. Despite these advancements, challenges remain in implementing standardized cardioprotective protocols. Variability in clinical guidelines, limited accessibility to early cardiac screening tools, and concerns about drug interactions necessitate further research and real-world clinical trials to establish universally accepted cardioprotective strategies.

CONCLUSION

Chemotherapy-induced cardiotoxicity is a critical challenge in oncology, requiring a multidisciplinary approach for effective prevention, early detection, and management. This systematic review highlights the complex mechanisms of cardiotoxicity across different chemotherapeutic agents and underscores the importance of both pharmacological and non-pharmacological cardioprotective strategies.

Mechanisms of cardiotoxicity vary by drug class, with anthracyclines causing irreversible damage through oxidative stress, HER2 inhibitors inducing reversible dysfunction, and TKIs leading to vascular toxicity.
Pharmacological cardio-protection (beta-blockers, ACE inhibitors, dexrazoxane) has demonstrated efficacy in mitigating cardiac damage, particularly in high-risk patients.
Non-pharmacological strategies such as exercise, dietary modifications, and routine cardiac monitoring play an essential role in maintaining cardiovascular health during chemotherapy.
Emerging approaches in cardio-oncology, including precision medicine, genetic risk stratification, and regenerative therapies, offer potential avenues for personalized cardio-protection.

To ensure optimal patient outcomes, future research should focus on developing standardized cardio-oncology guidelines, incorporating advanced biomarker-based monitoring, and evaluating long-term cardiovascular outcomes in cancer survivors. A collaborative effort between oncologists, cardiologists, and researchers is essential to address this growing concern and improve the quality of life for cancer patients undergoing chemotherapy.

REFERENCES

Mir A, Badi Y, Bugazia S, Nourelden AZ, Fathallah AH, Ragab KM, et al. Efficacy and safety of cardioprotective drugs in chemotherapy-induced cardiotoxicity: an updated systematic review&network meta-analysis. Cardio-Oncology. 2023;9(1):1–34.
Koutsoukis A, Ntalianis A, Repasos E, Kastritis E, Dimopoulos MA, Paraskevaidis I. Cardio-oncology: a focus on cardiotoxicity. Eur Cardiol. 2018;13(1):64–9.
Curigliano G, Cardinale D, Suter T, et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO Clinical Practice Guidelines. Ann Oncol. 2012;23(Suppl 7):vii155–66.
Zamorano JL, Lancellotti P, Rodriguez Muñoz D, et al. 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines. Eur Heart J. 2016;37(36):2768–801.
Plana JC, Galderisi M, Barac A, et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2014;15(10):1063–93.
Cardinale D, Colombo A, Lamantia G, et al. Anthracycline-induced cardiomyopathy: clinical relevance and response to pharmacologic therapy. J Am Coll Cardiol. 2010;55(3):213–20.
Kalam K, Marwick TH. Role of cardioprotective therapy for prevention of cardiotoxicity with chemotherapy: a systematic review and meta-analysis. Eur J Cancer. 2013;49(13):2900–9.
Lipshultz SE, Cochran TR, Franco VI, Miller TL. Treatment-related cardiotoxicity in survivors of childhood cancer. Nat Rev Clin Oncol. 2013;10(12):697–710.
Yeh ETH, Tong AT, Lenihan DJ, et al. Cardiovascular complications of cancer therapy: diagnosis, pathogenesis, and management. Circulation. 2004;109(25):3122–31.
Sawaya H, Sebag IA, Plana JC, et al. Early detection and prediction of cardiotoxicity in chemotherapy-treated patients. Am J Cardiol. 2011;107(9):1375–80.
Cardinale D, Sandri MT, Colombo A, et al. Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation. 2004;109(22):2749–54.
Jones RL, Swanton C, Ewer MS. Anthracycline cardiotoxicity. Expert Opin Drug Saf. 2006;5(6):791–809.
Swain SM, Whaley FS, Ewer MS. Congestive heart failure in patients treated with doxorubicin: a retrospective analysis of three trials. Cancer. 2003;97(11):2869–79.
Lotrionte M, Biondi-Zoccai G, Abbate A, et al. Review and meta-analysis of incidence and clinical predictors of anthracycline cardiotoxicity. Am J Cardiol. 2013;112(12):1980–4.
Chavez-MacGregor M, Zhang N, Buchholz TA, et al. Trastuzumab-related cardiotoxicity among older patients with breast cancer. J Clin Oncol. 2013;31(33):4222–8.
Chen MH, Kerkela R, Force T. Mechanisms of cardiac dysfunction associated with tyrosine kinase inhibitor cancer therapeutics. Circulation. 2008;118(1):84–95.
Ky B, Vejpongsa P, Yeh ET, et al. Emerging paradigms in cardiomyopathies associated with cancer therapies. Circ Res. 2013;113(6):754–64.
Ewer MS, Ewer SM. Cardiotoxicity of anticancer treatments: what the cardiologist needs to know. Nat Rev Cardiol. 2010;7(10):564–75.
Lenihan DJ, Cardinale DM. Late cardiac effects of cancer treatment. J Clin Oncol. 2012;30(30):3657–64.
Pai VB, Nahata MC. Cardiotoxicity of chemotherapeutic agents: incidence, treatment and prevention. Drug Saf. 2000;22(4):263–302.
Jain D. Cardiotoxicity of doxorubicin and other anthracycline derivatives. J Nucl Cardiol. 2000;7(1):53–62.
Moudgil R, Yeh ET. Mechanisms of cardiotoxicity of cancer chemotherapeutic agents: cardiomyopathy and beyond. Can J Cardiol. 2016;32(7):863–70.
Sawaya H, Sebag IA, Plana JC, et al. Assessment of echocardiography and biomarkers for the extended prediction of cardiotoxicity in patients treated with anthracyclines, taxanes, and trastuzumab. Circ Cardiovasc Imaging. 2012;5(5):596–603.
Kerkelä R, Grazette L, Yacobi R, et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med. 2006;12(8):908–16.
Ewer MS, Lippman SM. Type II chemotherapy-related cardiac dysfunction: time to recognize a new entity. J Clin Oncol. 2005;23(13):2900–2.
Neilan TG, Coelho-Filho OR, Shah RV, et al. Myocardial extracellular volume by cardiovascular magnetic resonance imaging in patients treated with anthracycline-based chemotherapy. Circ Cardiovasc Imaging. 2013;6(6):900–7.
Thavendiranathan P, Poulin F, Lim KD, et al. Use of myocardial strain imaging to assess early cardiac injury in patients during and after cancer therapy. J Am Coll Cardiol. 2014;63(25 Pt A):2751–68.
Jassal DS, Han SY, Hans C, et al. Utility of echocardiography for monitoring chemotherapy-related cardiotoxicity. Clin Med Insights Cardiol. 2009;3:47–59.
Curigliano G, Lenihan D, Fradley M, et al. Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations. Ann Oncol. 2020;31(2):171–90.
Lyon AR, Dent S, Stanway S, et al. Baseline cardiovascular risk assessment in cancer patients planned for targeted therapies: a position statement and new risk assessment tools from the cardio-oncology study group of the heart failure association of the European Society of Cardiology. Eur J Heart Fail. 2020;22(11):1945–60.
Herrmann J, Yang EH, Iliescu CA, et al. Vascular toxicities of cancer therapies: the old and the new—an evolving avenue. Circulation. 2016;133(13):1272–89.
Demissei BG, Hubbard RA, Zhang L, et al. Changes in cardiovascular biomarkers with anthracycline and trastuzumab treatment and associations with cardiac dysfunction. J Am Coll Cardiol. 2020;76(11):1245–56.
Armenian SH, Lacchetti C, Barac A, et al. Prevention and monitoring of cardiac dysfunction in survivors of adult cancers: American Society of Clinical Oncology clinical practice guideline. J Clin Oncol. 2017;35(8):893–911.
Virani SA, Dent S. Prevention of chemotherapy-induced heart failure: is it ready for prime time? J Am Coll Cardiol. 2016;68(9):971–3.
Zamorano JL, Lancellotti P, Muñoz DR, et al. ESC Position Paper on cancer treatments and cardiovascular toxicity. Eur Heart J. 2016;37(36):2768–801.
Moslehi J. Cardiovascular toxic effects of targeted cancer therapies. N Engl J Med. 2016;375(15):1457–67.
Minotti G, Menna P, Salvatorelli E, Cairo G, Gianni L. Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity. Pharmacol Rev. 2004;56(2):185–229.
Curigliano G, Lenihan D, Fradley M, Ganatra S, Barac A, Blaes A, et al. Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations. Ann Oncol. 2020;31(2):171–90.
Michel L, Rassaf T, Totzeck M. Cardiotoxicity from immune checkpoint inhibitors. Int J Cardiol Heart Vasc. 2019;25:100420.
Armenian SH, Lacchetti C, Barac A, Carver J, Constine LS, Denduluri N, et al. Prevention and monitoring of cardiac dysfunction in survivors of adult cancers: ASCO Clinical Practice Guideline. J Clin Oncol. 2017;35(8):893–911.
Herrmann J. Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia. Nat Rev Cardiol. 2020;17(8):474–502.
Zafar A, Harbeck B, Finkelmeier F, Müller OJ, Pizarro C, Goßmann A, et al. Multimodal imaging in cardio-oncology: cardiovascular toxicity of cancer therapy. J Clin Med. 2020;9(11):3582.
Lancellotti P, Suter TM, López-Fernández T, Galderisi M, Lyon AR, Van der Meer P, et al. Cardio-oncology care in Europe: a survey of the European Society of Cardiology Council of Cardio-Oncology. Eur J Heart Fail. 2022;24(1):147–53.
Pudil R, Mueller C, ?elutkien? J, Henriksen PA, Lenihan DJ, Dent S, et al. Role of serum biomarkers in cancer patients receiving cardiotoxic cancer therapies: a position statement from the Cardio-Oncology Study Group of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2020;22(11):1966–83.
Michel L, Rassaf T. Cardiotoxicity of immune checkpoint inhibitors: an update. Front Cardiovasc Med. 2021;8:713102.
Herrmann J, Yang EH, Iliescu CA, Cilingiroglu M, Charitakis K, Hakeem A, et al. Vascular toxicities of cancer therapies: the old and the new—an evolving avenue. Circulation. 2016;133(13):1272–89.
Lyon AR, López-Fernández T, Couch LS, Asteggiano R, Aznar MC, Bergler-Klein J, et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), European Society for Therapeutic Radiology and Oncology (ESTRO), and International Cardio-Oncology Society (IC-OS). Eur Heart J. 2022;43(41):4229–361.
Hamo CE, Bloom MW, Cardinale D, Ky B, Nohria A, Baer L, et al. Cancer therapy–related cardiac dysfunction and heart failure: Part 2—prevention, treatment, guidelines, and future directions. Circ Heart Fail. 2022;15(1):e008971.
D’Errico MP, Grimaldi L, Petruzzelli MF, et al. Radiation-induced cardiotoxicity. Anticancer Res. 2017;37(10):5355–64.
Xu R, Pujara AC, Golzar H, Yang EH. Immune checkpoint inhibitor-associated cardiotoxicity: current understanding on its mechanism, diagnosis and management. Front Cardiovasc Med. 2022;9:857083.

Reference

Mir A, Badi Y, Bugazia S, Nourelden AZ, Fathallah AH, Ragab KM, et al. Efficacy and safety of cardioprotective drugs in chemotherapy-induced cardiotoxicity: an updated systematic review&network meta-analysis. Cardio-Oncology. 2023;9(1):1–34.
Koutsoukis A, Ntalianis A, Repasos E, Kastritis E, Dimopoulos MA, Paraskevaidis I. Cardio-oncology: a focus on cardiotoxicity. Eur Cardiol. 2018;13(1):64–9.
Curigliano G, Cardinale D, Suter T, et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO Clinical Practice Guidelines. Ann Oncol. 2012;23(Suppl 7):vii155–66.
Zamorano JL, Lancellotti P, Rodriguez Muñoz D, et al. 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines. Eur Heart J. 2016;37(36):2768–801.
Plana JC, Galderisi M, Barac A, et al. Expert consensus for multimodality imaging evaluation of adult patients during and after cancer therapy: a report from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2014;15(10):1063–93.
Cardinale D, Colombo A, Lamantia G, et al. Anthracycline-induced cardiomyopathy: clinical relevance and response to pharmacologic therapy. J Am Coll Cardiol. 2010;55(3):213–20.
Kalam K, Marwick TH. Role of cardioprotective therapy for prevention of cardiotoxicity with chemotherapy: a systematic review and meta-analysis. Eur J Cancer. 2013;49(13):2900–9.
Lipshultz SE, Cochran TR, Franco VI, Miller TL. Treatment-related cardiotoxicity in survivors of childhood cancer. Nat Rev Clin Oncol. 2013;10(12):697–710.
Yeh ETH, Tong AT, Lenihan DJ, et al. Cardiovascular complications of cancer therapy: diagnosis, pathogenesis, and management. Circulation. 2004;109(25):3122–31.
Sawaya H, Sebag IA, Plana JC, et al. Early detection and prediction of cardiotoxicity in chemotherapy-treated patients. Am J Cardiol. 2011;107(9):1375–80.
Cardinale D, Sandri MT, Colombo A, et al. Prognostic value of troponin I in cardiac risk stratification of cancer patients undergoing high-dose chemotherapy. Circulation. 2004;109(22):2749–54.
Jones RL, Swanton C, Ewer MS. Anthracycline cardiotoxicity. Expert Opin Drug Saf. 2006;5(6):791–809.
Swain SM, Whaley FS, Ewer MS. Congestive heart failure in patients treated with doxorubicin: a retrospective analysis of three trials. Cancer. 2003;97(11):2869–79.
Lotrionte M, Biondi-Zoccai G, Abbate A, et al. Review and meta-analysis of incidence and clinical predictors of anthracycline cardiotoxicity. Am J Cardiol. 2013;112(12):1980–4.
Chavez-MacGregor M, Zhang N, Buchholz TA, et al. Trastuzumab-related cardiotoxicity among older patients with breast cancer. J Clin Oncol. 2013;31(33):4222–8.
Chen MH, Kerkela R, Force T. Mechanisms of cardiac dysfunction associated with tyrosine kinase inhibitor cancer therapeutics. Circulation. 2008;118(1):84–95.
Ky B, Vejpongsa P, Yeh ET, et al. Emerging paradigms in cardiomyopathies associated with cancer therapies. Circ Res. 2013;113(6):754–64.
Ewer MS, Ewer SM. Cardiotoxicity of anticancer treatments: what the cardiologist needs to know. Nat Rev Cardiol. 2010;7(10):564–75.
Lenihan DJ, Cardinale DM. Late cardiac effects of cancer treatment. J Clin Oncol. 2012;30(30):3657–64.
Pai VB, Nahata MC. Cardiotoxicity of chemotherapeutic agents: incidence, treatment and prevention. Drug Saf. 2000;22(4):263–302.
Jain D. Cardiotoxicity of doxorubicin and other anthracycline derivatives. J Nucl Cardiol. 2000;7(1):53–62.
Moudgil R, Yeh ET. Mechanisms of cardiotoxicity of cancer chemotherapeutic agents: cardiomyopathy and beyond. Can J Cardiol. 2016;32(7):863–70.
Sawaya H, Sebag IA, Plana JC, et al. Assessment of echocardiography and biomarkers for the extended prediction of cardiotoxicity in patients treated with anthracyclines, taxanes, and trastuzumab. Circ Cardiovasc Imaging. 2012;5(5):596–603.
Kerkelä R, Grazette L, Yacobi R, et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med. 2006;12(8):908–16.
Ewer MS, Lippman SM. Type II chemotherapy-related cardiac dysfunction: time to recognize a new entity. J Clin Oncol. 2005;23(13):2900–2.
Neilan TG, Coelho-Filho OR, Shah RV, et al. Myocardial extracellular volume by cardiovascular magnetic resonance imaging in patients treated with anthracycline-based chemotherapy. Circ Cardiovasc Imaging. 2013;6(6):900–7.
Thavendiranathan P, Poulin F, Lim KD, et al. Use of myocardial strain imaging to assess early cardiac injury in patients during and after cancer therapy. J Am Coll Cardiol. 2014;63(25 Pt A):2751–68.
Jassal DS, Han SY, Hans C, et al. Utility of echocardiography for monitoring chemotherapy-related cardiotoxicity. Clin Med Insights Cardiol. 2009;3:47–59.
Curigliano G, Lenihan D, Fradley M, et al. Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations. Ann Oncol. 2020;31(2):171–90.
Lyon AR, Dent S, Stanway S, et al. Baseline cardiovascular risk assessment in cancer patients planned for targeted therapies: a position statement and new risk assessment tools from the cardio-oncology study group of the heart failure association of the European Society of Cardiology. Eur J Heart Fail. 2020;22(11):1945–60.
Herrmann J, Yang EH, Iliescu CA, et al. Vascular toxicities of cancer therapies: the old and the new—an evolving avenue. Circulation. 2016;133(13):1272–89.
Demissei BG, Hubbard RA, Zhang L, et al. Changes in cardiovascular biomarkers with anthracycline and trastuzumab treatment and associations with cardiac dysfunction. J Am Coll Cardiol. 2020;76(11):1245–56.
Armenian SH, Lacchetti C, Barac A, et al. Prevention and monitoring of cardiac dysfunction in survivors of adult cancers: American Society of Clinical Oncology clinical practice guideline. J Clin Oncol. 2017;35(8):893–911.
Virani SA, Dent S. Prevention of chemotherapy-induced heart failure: is it ready for prime time? J Am Coll Cardiol. 2016;68(9):971–3.
Zamorano JL, Lancellotti P, Muñoz DR, et al. ESC Position Paper on cancer treatments and cardiovascular toxicity. Eur Heart J. 2016;37(36):2768–801.
Moslehi J. Cardiovascular toxic effects of targeted cancer therapies. N Engl J Med. 2016;375(15):1457–67.
Minotti G, Menna P, Salvatorelli E, Cairo G, Gianni L. Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity. Pharmacol Rev. 2004;56(2):185–229.
Curigliano G, Lenihan D, Fradley M, Ganatra S, Barac A, Blaes A, et al. Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations. Ann Oncol. 2020;31(2):171–90.
Michel L, Rassaf T, Totzeck M. Cardiotoxicity from immune checkpoint inhibitors. Int J Cardiol Heart Vasc. 2019;25:100420.
Armenian SH, Lacchetti C, Barac A, Carver J, Constine LS, Denduluri N, et al. Prevention and monitoring of cardiac dysfunction in survivors of adult cancers: ASCO Clinical Practice Guideline. J Clin Oncol. 2017;35(8):893–911.
Herrmann J. Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia. Nat Rev Cardiol. 2020;17(8):474–502.
Zafar A, Harbeck B, Finkelmeier F, Müller OJ, Pizarro C, Goßmann A, et al. Multimodal imaging in cardio-oncology: cardiovascular toxicity of cancer therapy. J Clin Med. 2020;9(11):3582.
Lancellotti P, Suter TM, López-Fernández T, Galderisi M, Lyon AR, Van der Meer P, et al. Cardio-oncology care in Europe: a survey of the European Society of Cardiology Council of Cardio-Oncology. Eur J Heart Fail. 2022;24(1):147–53.
Pudil R, Mueller C, ?elutkien? J, Henriksen PA, Lenihan DJ, Dent S, et al. Role of serum biomarkers in cancer patients receiving cardiotoxic cancer therapies: a position statement from the Cardio-Oncology Study Group of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2020;22(11):1966–83.
Michel L, Rassaf T. Cardiotoxicity of immune checkpoint inhibitors: an update. Front Cardiovasc Med. 2021;8:713102.
Herrmann J, Yang EH, Iliescu CA, Cilingiroglu M, Charitakis K, Hakeem A, et al. Vascular toxicities of cancer therapies: the old and the new—an evolving avenue. Circulation. 2016;133(13):1272–89.
Lyon AR, López-Fernández T, Couch LS, Asteggiano R, Aznar MC, Bergler-Klein J, et al. 2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), European Society for Therapeutic Radiology and Oncology (ESTRO), and International Cardio-Oncology Society (IC-OS). Eur Heart J. 2022;43(41):4229–361.
Hamo CE, Bloom MW, Cardinale D, Ky B, Nohria A, Baer L, et al. Cancer therapy–related cardiac dysfunction and heart failure: Part 2—prevention, treatment, guidelines, and future directions. Circ Heart Fail. 2022;15(1):e008971.
D’Errico MP, Grimaldi L, Petruzzelli MF, et al. Radiation-induced cardiotoxicity. Anticancer Res. 2017;37(10):5355–64.
Xu R, Pujara AC, Golzar H, Yang EH. Immune checkpoint inhibitor-associated cardiotoxicity: current understanding on its mechanism, diagnosis and management. Front Cardiovasc Med. 2022;9:857083.

Akash Dhoke

Corresponding author

P Wadhwani College of Pharmacy, Girija Nagar, Yavatmal, 445001

Aman Rathi

Co-author

SVKM's Narsee Monjee Institute of Management Studies, School of Pharmacy and Technology Management, Shirpur,425405

Rupali Chavhan

Co-author

P Wadhwani College of Pharmacy, Girija Nagar, Yavatmal, 445001

Isha Durgade

Co-author

P Wadhwani College of Pharmacy, Girija Nagar, Yavatmal, 445001

Aman Rathi, Akash Dhoke, Rupali Chavhan, Isha Durgade, Cardiotoxicity of Chemotherapeutic Agents: A Systematic Review of Mechanisms and Cardio-Protective Strategies, Int. J. of Pharm. Sci., 2025, Vol 3, Issue 7, 2041-2054. https://doi.org/10.5281/zenodo.15914764

View Article

Cardiotoxicity of Chemotherapeutic Agents: A Systematic Review of Mechanisms and Cardio-Protective Strategies

Abstract

Keywords

Introduction

Reference

Akash Dhoke

Aman Rathi

Rupali Chavhan

Isha Durgade

More related articles

Breast Cancer...

A Review On Orodispersible Tablets...

Aegle Marmelos Linn: A Compressive Overview ...

View more

Formulation Development and Evaluation Of Wax Incorporated Floating Beads Of Dal...

Advancement In Nanoemulsion And Nanogels Technology For Topical Drug Delivery ...

A Comprehensive Review of Spinal Muscular Atrophy (Sma): Treatment Strategies ...

View more

Related Articles

Formulation And Evaluation Of Face Scrub In Modern Pharmaceutics: An Herbal Form...

Nanostructured Lipid Carrier (Nlc): A Cutting Edge Drug Delivery System...

Validation Of Neutraceuticals For Quality Assurance...

The Role of Functional Ingredients in the Creation of Vegan Gummy ...

Breast Cancer...

More related articles

Breast Cancer...

A Review On Orodispersible Tablets...

Aegle Marmelos Linn: A Compressive Overview ...

View more

Breast Cancer...

A Review On Orodispersible Tablets...

Aegle Marmelos Linn: A Compressive Overview ...

View more