ABSTRACT

AIM: Expected 1-year survival is essential to risk stratification of patients with heart failure (HF); however, little is known about the 1-year prognosis of patients with HF and cancer. Thus, the objective was to investigate the 1-year prognosis following new-onset HF stratified by cancer status in patients with breast-, gastrointestinal-, or lung cancer.

METHODS AND RESULTS: All Danish patients with new-onset HF from 2000-2018 were included. Cancer status was categorized as history of cancer (no cancer-related contact within five years of HF diagnosis), non-active cancer (curative intended procedure administered) and active cancer. Standardized 1-year all-cause mortality was reported using G-computation. Age-stratified 1-year all-cause mortality was estimated using the Kaplan-Meier estimator. In total, 193 359 patients with HF were included, 7.3% had either a breast-, gastrointestinal or lung cancer diagnosis. Patients with cancer were older and more comorbid than patients without cancer. Standardized 1-year all-cause mortalities (95% confidence intervals) were 24.6% (23.0%-26.2%), 27.1% (25.5%-28.6%), and 29.9% (25.9%-34.0%) for history of breast-, gastrointestinal-, and lung cancer, which was comparable to patients with non-active cancers. For active breast-, gastrointestinal-, and lung cancer, standardized 1-year all-cause mortalities were 36.2% (33.8%-38.6%), 49.0% (47.2%-50.9%), and 61.6% (59.7%-63.5%), respectively. One-year all-cause mortality increased incrementally with age, except for active lung cancer.

CONCLUSION: Standardized 1-year all-cause mortality were comparable for patients with history of cancer and non-active cancer regardless cancer type, but varied comprehensively for active cancers. Prognostic impact of age was limited for active lung cancer. Thus, granular stratification of cancer is necessary for optimized management of new-onset HF. This article is protected by copyright. All rights reserved.

PMID:37534618 | DOI:10.1002/ejhf.2984

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PubMed articles on: Cardio-Oncology

Cancer Therapy-Related Cardiotoxicity: A Comprehensive Retrospective Analysis at Najran Cancer Center, Saudi Arabia

Cureus. 2023 Jul 2;15(7):e41287. doi: 10.7759/cureus.41287. eCollection 2023 Jul.

ABSTRACT

Background Cardiotoxicity, produced as an adverse effect of anticancer therapy, is a common issue during cancer treatment. Acute coronary syndrome, myocarditis, arrhythmias, or heart failure can all be symptoms of this issue. Little is known about its occurrence among Saudi Arabian cancer patients. This study aims to investigate factors linked to anticancer therapy-related cardiotoxicity. Methods A retrospective study was conducted from April 2020 to May 2022 at the King Khalid Hospital, Najran, Saudi Arabia. The study included adult cancer patients receiving anticancer therapy, regardless of their cardiovascular disease history. Univariate analysis was used to investigate factors associated with the occurrence of cardiotoxicity related to anticancer therapy. Results Of 78 patients receiving anticancer therapy, cardiotoxicity occurred in 12 (15.4%) patients. The mean age was 56.5 ± 13.4 years, with 33.3% aged over 65 years. Comorbidities included hypertension (44; 56.4%), diabetes (41; 52.6%), dyslipidemia (13; 16.7%), smoking (16; 20.5%), heart disease (6; 7.7%), trastuzumab use (9; 11.5%), and chronic kidney disease (2; 2.6%). The most common cancers were breast cancer and gastrointestinal cancer (27.6% each). Monoclonal anticancer agents 35 (46.1%) and alkylating agents 29 (38.2%) were commonly used chemotherapies. Cardiac protective agents were used in 16 (21.1%) of patients, with angiotensin-converting enzyme (ACE) inhibitors 15 (19.7%) and statins (13; 17.1%) being the most prescribed. Baseline ejection fraction (EF) was normal in 69 (90.8%) of cases. The follow-up duration was 1.93 ± 1.90 years. A drop in EF occurred in five (6.6%) of cases. Dyslipidemia (OR: 0.12; 95% CI: 0.03-0.47, p=0.002), previous heart disease (OR: 0.14; 95% CI: 0.02-0.81, p=0.029), and impaired baseline EF (p=0.029) were associated with increased risk of cardiotoxicity. Statin (OR: 0.22; 95% CI: 0.05 to 0.84, p=0.028) and antiplatelet agents (OR: 0.19; 95% CI: 0.03 to 1.01, p=0.051) were protective agents against cardiac toxicity. Conclusion Effective anti-cancer therapy may be accompanied by an increased risk of cardiotoxicity. In this study, a history of prior heart disease, dyslipidemia, low baseline ejection fraction, and the administration of multiple anticancer therapy agents was associated with cardiotoxicity. Proactive management strategies aimed at mitigating the potential cardiotoxic effects of anti-cancer therapies are crucial.

PMID:37533611 | PMC:PMC10393428 | DOI:10.7759/cureus.41287

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PubMed articles on: Cardio-Oncology

The protective effect of thiolutin on doxorubicin-induced H9c2 cardiomyocyte injury

J Toxicol Sci. 2023;48(8):469-479. doi: 10.2131/jts.48.469.

ABSTRACT

The use of doxorubicin (DOX) may contribute to cardiotoxicity, limiting its clinical application. Thiolutin (THL) has been found to exert protective roles in various biological activities, while its effects on DOX-induced cardiotoxicity are still uncovered. Cell counting kit 8 assay was utilized to detect cell viability and half maximal inhibitory concentration of THL in H9c2 cardiomyocytes. The level of lactate dehydrogenase (LDH), adenosine triphosphate (ATP), interleukin (IL)-18 and IL-1 beta (IL-1β) were measured using the corresponding detection kits, and flow cytometry determined cell apoptosis rate. The reactive oxygen species (ROS) accumulation was evaluated by utilizing immunofluorescence or flow cytometry assay. The protein levels of NLR family Pyrin domain 3 (NLRP3), pro-Caspase1, cleaved-Caspase1, gasdermin D (GSDMD) and cleaved-GSDMD (GSDMD-N) in H9c2 cells were detected by immunoblotting assay. The treatment of THL reduced H9c2 cell viability in a gradient-dependent manner. THL treatment reversed the DOX-induced inhibition of proliferation, decrease of ATP, up-regulation of LDH, IL-18, IL-1β and production of ROS, activation of NLRP3 and inflammasome-mediated pyroptosis in H9c2 cells. Additionally, NLRP3 knockdown abolished the effects of THL in DOX-treated H9c2 cells remarkably. This investigation proved that THL notably ameliorated DOX-induced apoptosis, oxidative stress, and pyroptosis in H9c2 cardiomyocytes. Besides, THL effectively inactivated DOX-induced NLRP3 inflammasome in H9c2 cells. These findings revealed a promising drug to assist DOX in its anti-cancer effects and protect the heart of patients.

PMID:37532580 | DOI:10.2131/jts.48.469

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PubMed articles on: Cardio-Oncology

Non-coding RNAs, cancer treatment and cardiotoxicity: A triad of new hope

Cancer Treat Res Commun. 2023 Jul 28;36:100750. doi: 10.1016/j.ctarc.2023.100750. Online ahead of print.

ABSTRACT

The global health landscape has experienced a shift towards non-communicable diseases, with cardiovascular diseases and cancer as leading causes of mortality. Although advancements in healthcare have led to an increase in life expectancy, they have concurrently resulted in a greater burden of chronic health conditions. Unintended consequences of anticancer therapies on various tissues, particularly the cardiovascular system, contribute to elevated morbidity and mortality rates that are not directly attributable to cancer. Consequently, the field of cardio-oncology has emerged to address the prevalence of CVD in cancer survivors and the cardiovascular toxicity associated with cancer therapies. Non-coding RNAs (ncRNAs) have been found to play a crucial role in early diagnosis, prognosis, and therapeutics within the realm of cardio-oncology. This comprehensive review evaluates the risk assessment of cancer survivors concerning the acquisition of adverse cardiovascular consequences, investigates the association of ncRNAs with CVD in patients undergoing cancer treatment, and delves into the role of ncRNAs in the diagnosis, treatment, and prevention of CVD in patients with a history of anti-cancer therapy. A thorough understanding of the pathogenesis of cancer therapy-related cardiovascular disease and the involvement of ncRNAs in cardio-oncology will enable healthcare professionals to provide anticancer treatment with minimized cardiovascular side effects, thereby improving patient outcomes. Ultimately, this comprehensive analysis aims to provide valuable insights into the complex interplay between cancer and cardiovascular diseases, facilitating the development of more effective diagnostic, therapeutic, and preventive strategies in the burgeoning field of cardio-oncology.

PMID:37531735 | DOI:10.1016/j.ctarc.2023.100750

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PubMed articles on: Cardio-Oncology

Cardiorenal Syndrome: A Literature Review

Cureus. 2023 Jul 1;15(7):e41252. doi: 10.7759/cureus.41252. eCollection 2023 Jul.

ABSTRACT

Cardiorenal syndrome (CRS) is a condition characterized by the intricate two-way relationship between the heart and kidneys, which can lead to acute or chronic dysfunction in these organs. The interplay between cardiorenal connectors and both hemodynamic and non-hemodynamic factors is crucial to understanding this syndrome. The clinical importance of these interactions is evident in the changes observed in hemodynamic factors, neurohormonal markers, and inflammatory processes. Identifying and understanding biomarkers associated with CRS is valuable for early detection and enabling intervention before significant organ dysfunction occurs. This comprehensive review focuses on the clinical significance of biomarkers in the diagnosis, prognosis, and management of CRS. Finally, it highlights the necessity for further advancements in managing this condition.

PMID:37529809 | PMC:PMC10389294 | DOI:10.7759/cureus.41252

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PubMed articles on: Cardio-Oncology

Anthracycline induced left ventricular dysfunction in AML: A focus on the molecularly defined future of cardio-oncology

Leuk Res. 2023 Jul 29;133:107366. doi: 10.1016/j.leukres.2023.107366. Online ahead of print.

NO ABSTRACT

PMID:37531679 | DOI:10.1016/j.leukres.2023.107366

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PubMed articles on: Cardio-Oncology

Diagnostic Value of Three-Dimensional Speckle Tracking Imaging Strain Parameters for Detection of Cancer Chemotherapy-Related Cardiac Dysfunction: A Meta-Analysis

Arq Bras Cardiol. 2023 Jul;120(8):e20220370. doi: 10.36660/abc.20220370.

ABSTRACT

BACKGROUND: Chemotherapeutic agents (e.g., anthracyclines, trastuzumab) commonly used for treating malignant tumors have been demonstrated to have cardiotoxic effects, which is associated with poor prognosis. Three-dimensional echocardiography has been used to predict cancer chemotherapy-induced cardiac dysfunction.

OBJECTIVES: Evaluation of the diagnostic performance of strain parameters, global area strain (GAS), longitudinal strain (GLS), circumferential strain (GCS), and radial strain (GRS) by meta-analysis.

METHODS: Relevant studies were searched from the Embase, PubMed, and Web of Science databases. Statistical analysis was performed using Stata 12. The summary receiver operating characteristic curve, sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), and corresponding 95% confidence interval for the four strain parameters were pooled. P<0.05

RESULTS: Nine studies involving 650 participants were included. GAS and GLS showed significant diagnostic advantages over GCS and GRS. For GAS, the sensitivity was 0.85 (0.70, 0.93) and specificity was 0.82(0.78, 0.86) with PLR of 4.76 (3.55, 6.39) and NLR of 0.18 (0.09, 0.39) and an area under the curve (AUC) of 0.85 (0.82, 0.88). For GLS, the sensitivity was 0.81 (0.74, 0.86) and specificity was 0.81(0.68, 0.90) with PLR of 4.35(2.42, 7.80) and NLR of 0.23 (0.17, 0.33) and an AUC of 0.85 (0.82, 0.88). The GCS showed a sensitivity of 0.63 and a specificity of 0.79 with an AUC of 0.77. The GRS showed a sensitivity of 0.74 and a specificity of 0.66 with an AUC of 0.73.

CONCLUSION: 3D-STI strain parameters GAS and GLS showed good performance in detecting early cardiac dysfunction in patients with tumors receiving chemotherapy.

PMID:37531470 | DOI:10.36660/abc.20220370

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PubMed articles on: Cardio-Oncology

Late-onset cardiotoxicity in patients with HER2-positive metastatic breast cancer receiving trastuzumab-based therapy

J Oncol Pharm Pract. 2023 Aug 1:10781552231193149. doi: 10.1177/10781552231193149. Online ahead of print.

ABSTRACT

INTRODUCTION: Patients with human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (MBC) typically receive long-term trastuzumab treatment for several years. The aim of our study is to identify the incidence and characterize late-onset cardiotoxicity in patients with HER2-positive MBC receiving trastuzumab-based therapy.

METHODS: We retrospectively reviewed charts of HER2-positive MBC patients who received >1 year of trastuzumab-based therapy at the Massachusetts General Hospital Cancer Center over three-year period. The primary endpoint was development of trastuzumab-induced cardiotoxicity (TIC). Secondary endpoints included time to TIC development, incidence/duration of trastuzumab interruption due to TIC, incidence of permanent discontinuation of trastuzumab due to TIC, clinic visit, or hospitalization due to TIC.

RESULTS: Thirty-seven patients were included. Mean age was 56 years (range: 33-78 years, SD 9.5). Seven patients received prior doxorubicin and 14 patients received previous or concurrent breast irradiation. Mean duration of trastuzumab-based therapy was 57 months (range: 14-140 months, SD 39.3). Seven patients (18.9%) experienced TIC resulting in treatment interruption for two patients (28 and 78 days). The median time from starting trastuzumab therapy to TIC was 14 months (interquartile range: 11-29.5 months). The mean number of left ventricular ejection fraction (LVEF) assessment completed per year was 2.7 (range: 1.2-6.6, SD 1.1).

CONCLUSION: Cardiotoxicity occurred in a minority of patients with HER2-positive MBC receiving trastuzumab-based therapy for more than one year. LVEF reductions to below the institutional lower limit of normal and therapy modifications were uncommon.

PMID:37528623 | DOI:10.1177/10781552231193149

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PubMed articles on: Cardio-Oncology

Statins as preventive therapy for anthracycline cardiotoxicity: A meta-analysis of randomized controlled trials

Int J Cardiol. 2023 Jul 30:131219. doi: 10.1016/j.ijcard.2023.131219. Online ahead of print.

ABSTRACT

BACKGROUND: Cardiotoxicity occurs in 5-20% of cancer patients who receive anthracyclines. The aim of this study was to pool all the randomized controlled trials (RCTs) investigating the cardio-protective role of statins in patients treated with anthracyclines.

METHODS: PubMed and Scopus electronic databases were scanned for eligible studies up to May 3rd, 2023. A total of 5 RCTs with 808 patients were included. Efficacy endpoints were the rate of anthracycline-mediated cardiotoxicity, the incidence of hospitalization for heart failure (HF), left ventricular ejection fraction (LVEF) value after anthracycline treatment, and ∆LVEF calculated as the difference in LVEF before and after anthracycline therapy. Safety endpoints [i.e., the incidence of muscle pain and serious adverse events (SAE)] were also assessed.

RESULTS: On pooled analysis, the statin-treated group had a lower incidence of cardiotoxicity compared to the placebo group [risk ratio (RR) 0.52, 95% confidence Interval (CI) 0.33-0.83, P = 0.01; I2 = 0%], as well as higher mean LVEF [Mean difference (MD) 1.88, 95% CI 0.66-3.1, P < 0.01; I2 = 57.3%)] and a more favorable ∆LVEF during follow-up (MD 2.38, 95% CI -0.03 - +4.79, P = 0.05; I2 = 99%), despite no significant difference in terms of hospitalization for HF and rate of adverse events. Of note, severe heterogeneity affected the analyses for both LVEF and ΔLVEF.

CONCLUSIONS: The current meta-analysis of all RCTs conducted so far shows an overall beneficial effect of statins on the risk of anthracyclines induced cardiotoxicity and LVEF preservation. No difference was observed in the rate of HF hospitalization. . More powered RCTs are needed to fully investigate the impact of statins on prognosis in patients receiving anthracyclines therapy.

PMID:37527752 | DOI:10.1016/j.ijcard.2023.131219

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PubMed articles on: Cardio-Oncology

Role of hypoxia inducible factor/vascular endothelial growth factor/endothelial nitric oxide synthase signaling pathway in mediating the cardioprotective effect of dapagliflozin in cyclophosphamide-induced cardiotoxicity

Hum Exp Toxicol. 2023 Jan-Dec;42:9603271231193392. doi: 10.1177/09603271231193392.

ABSTRACT

BACKGROUND: Cyclophosphamide (CP) is a commonly used chemotherapeutic and immunosuppressive alkylating agent. However, cardiac adverse effects of CP interfere with its clinical benefit. Cardio-oncology research is currently an important issue and finding effective cardiopreserving agents is a critical need. For the first time, we aimed to detect if dapagliflozin (DAP) could ameliorate CP-induced cardiac injury and investigated the role of hypoxia inducible factor α (HIF1α)/vascular endothelial growth factor (VEGF)/endothelial nitric oxide synthase (eNOS) pathway.

METHODS: Forty male Wistar albino rats were included in the current model. Studied groups are: control group; CP-induced cardiotoxicity group; CP group treated with DAP; CP group treated with DAP and administered a nitric oxide synthase inhibitor; nitro-ω-L-arginine (L-NNA) before DAP to explore the role of eNOS.

RESULTS: Our data revealed that CP could induce cardiac damage as manifested by significant increases in cardiac enzymes, blood pressure, malondialdehyde (MDA), tumor necrosis factor alpha (TNFα), HIF1α, sodium glucose co-transporter 2 (SGLT2) and cleaved caspase-3 levels with toxic histopathological changes. However, there are significant decreases in reduced glutathione (GSH), total antioxidant capacity (TAC), VEGF, and eNOS. On the opposite side, co-administration of DAP showed marked improvement of CP-induced cardiac damage that may be due to its ability to inhibit SGLT2, antioxidant, anti-inflammatory and anti-apoptotic properties. Results showed decreasing the cardioprotective effect of DAP on administration of L-NNA, reflecting the critical effect of eNOS in mediating such protection.

CONCLUSION: DAP could reduce CP cardiotoxicity based upon its ability to modulate SGLT2 and HIF1α/VEGF/eNOS signaling pathway.

PMID:37526264 | DOI:10.1177/09603271231193392

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PubMed articles on: Cardio-Oncology

Neopetroside-B alleviates doxorubicin-induced cardiotoxicity via mitochondrial protection

Biomed Pharmacother. 2023 Jul 29;165:115232. doi: 10.1016/j.biopha.2023.115232. Online ahead of print.

ABSTRACT

Doxorubicin, a member of the anthracycline family, is a widely prescribed anticancer chemotherapy drug. Unfortunately, cumulative doses of doxorubicin can cause mitochondrial dysfunction, leading to acute or chronic cardiotoxicity. This study demonstrated that Neopetroside-B (NPS-B) protects cardiomyocytes in the presence of doxorubicin. NPS-B improved mitochondrial function in cardiomyocytes by increasing ATP production and oxygen consumption rates. On the other hand, NPS-B negatively influenced cancer cell lines by increasing reactive oxygen species. We analyzed NPS-B-influenced metabolites (VIP > 1.0; AUC>0.7; p < 0.05) and proteins (FC > 2.0) and constructed metabolite-protein enrichment, which showed that NPS-B affected uracil metabolism and NAD-binding proteins (e.g., aldehyde dehydrogenase and glutathione reductase) in cardiomyocytes. However, for the cancer cells, NPS-B decreased the NAD+/NADH balance, impairing cell viability. In a xenograft mouse model treated with doxorubicin, NPS-B reduced cardiac fibrosis and improved cardiac function. NPS-B may be a beneficial intervention to reducing doxorubicin-induced cardiotoxicity with anticancer effects.

PMID:37523986 | DOI:10.1016/j.biopha.2023.115232

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PubMed articles on: Cardio-Oncology

Cardio-oncology today: digest of the first European clinical guidelines (2022)

Kardiologiia. 2023 Jul 28;63(7):3-15. doi: 10.18087/cardio.2023.7.n2445.

ABSTRACT

Over the past few decades, due to the extensive implementation of cancer screening programs, up-to-date early diagnostic methods, and effective combinations of antitumor therapy, it has become possible to significantly improve survival of cancer patients. At the same time, despite the effective treatment of malignancies, most patient face adverse and often life-threatening effects of specific treatment on the heart and blood vessels. All this resulted in active development of a new field in cardiology, cardio-oncology. In recent years, based on the experience of leading experts, data from large studies, and meta-analyses, both international and Russian Consensuses, conciliation documents, have been formed and published. These documents regulate principal methodological approaches to management and control of the cardiovascular conditions in cancer patients. Finally, 2022 was marked by issuing the first official European Guidelines on Cardio-Oncology in the history of medicine. This article highlights the most relevant, in our opinion, positions of these guidelines as well as controversial and unresolved issues.

PMID:37522822 | DOI:10.18087/cardio.2023.7.n2445

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PubMed articles on: Cardio-Oncology

Editorial: Case reports in cardio-oncology: 2022

Front Cardiovasc Med. 2023 Jul 13;10:1235015. doi: 10.3389/fcvm.2023.1235015. eCollection 2023.

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PMID:37522080 | PMC:PMC10374430 | DOI:10.3389/fcvm.2023.1235015

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PubMed articles on: Cardio-Oncology

Reduction of Doxorubicin-Induced Cardiotoxicity by Co-Administration of Smart Liposomal Doxorubicin and Free Quercetin: In Vitro and In Vivo Studies

Pharmaceutics. 2023 Jul 11;15(7):1920. doi: 10.3390/pharmaceutics15071920.