Victoria Vinje-Jakobsen

• Gynnild, Mari Nordbø; Mecinaj, Albulena; Wethal, Torgeir; Jakobsen, Even Olav; Vinje-Jakobsen, Victoria & Heck, Siri Lagethon [Vis alle 12 forfattere av denne artikkelen] (2026). Sacubitril/Valsartan and Right Ventricular and Diastolic Function During Breast Cancer Therapy. JACC: CardioOncology. 8(4), s. 436–436. doi: 10.1016/j.jaccao.2026.06.002. Fulltekst i vitenarkiv
• Gynnild, Mari Nordbø; Holtrop, Joris; Hageman, Steven H J; Vinje, Victoria; Dorresteijn, Jannick A N & Visseren, Frank L J [Vis alle 10 forfattere av denne artikkelen] (2025). External validation of the systematic coronary risk evaluation 2 (SCORE2) and SCORE2-older persons in cancer patients. European Journal of Preventive Cardiology (EJPC). ISSN 2047-4873. doi: 10.1093/eurjpc/zwaf356. Fulltekst i vitenarkiv Vis sammendrag

  Aims The 2022 European Society of Cardiology cardio-oncology guidelines recommend cardiovascular disease (CVD) risk stratification for cancer patients and suggest using SCORE2 and SCORE2-OP. However, these models have not been validated or specifically adapted for cancer populations. Our aim was to refine the SCORE2 and SCORE2-OP models to accurately predict 10-year fatal and non-fatal CVD risk in cancer patients. Methods and results We included 1622 patients from the HUNT3 study (2006–08) who were diagnosed with cancer within 4 years after their enrolment and followed until 2023 linked to national registries. The primary outcome was a composite of myocardial infarction (MI), stroke, or CVD mortality. Model performance was assessed using Harrel’s C-statistic and calibration curves. Both models were recalibrated by applying a multiplicative adjustment factor based on expected–observed (E/O) ratios. The most prevalent cancers were gastrointestinal (23%), prostate (17%), and breast (14%). Mean age was 65.2 years, 52% were female. During a median follow-up of 8.8 years [inter-quartile range 1.9–12.6], 252 CVD events (39% MI, 36% stroke, 25% CVD deaths) and 708 non-CVD deaths occurred. SCORE2 initially underestimated CVD risk (E/O ratio for men and women: 0.91 and 0.63, respectively) but showed adequate agreement after recalibration. C-statistics for SCORE2 was 0.693 [95% confidence interval (CI) 0.643–0.743], and 0.730 (95% CI 0.676–0.784) after excluding those not surviving the first 2 years. For SCORE2-OP, the C-statistics were 0.586 (95% CI 0.529–0.643) and 0.648 (95% CI 0.577–0.720). Conclusion SCORE2 underestimated CVD risk in cancer patients. After recalibration, the model may serve as a valuable tool for risk stratification in cancer patients.

• Gynnild, Mari Nordbø; Vinje-Jakobsen, Victoria; Holtrop, Joris; Hageman, Steven H.J.; Holte, Espen & Gulati, Geeta [Vis alle 14 forfattere av denne artikkelen] (2025). Prognostic Performance of a Modified HFA-ICOS Tool for Prediction of Cardiovascular Complications in Cancer Patients. JACC: Advances. 4(12). doi: 10.1016/j.jacadv.2025.102344. Fulltekst i vitenarkiv Vis sammendrag

  Background The 2022 European Society of Cardiology Cardio-oncology Guidelines recommend the Heart Failure Association and International Cardio-Oncology Society risk stratification tool to predict cardiovascular disease (CVD) risk in cancer patients. Developed from expert consensus rather than mathematical derivation, its quantitative prognostic value in unselected cancer populations remains uncertain. Objectives The objective of the study was to assess the prognostic utility of a modified Heart Failure Association and International Cardio-Oncology Society tool, excluding biomarkers and imaging, in predicting CVD complications in cancer patients, thereby providing a quantitative correlate to an expert consensus-based method. Methods We included 2,290 cancer patients from the third follow-up of the Trøndelag Health study, diagnosed within 4 years of participation, and followed through 2023. Cancer therapy details were obtained from the Norwegian Cancer Registry. The primary outcome was a composite of myocardial infarction, heart failure hospitalization, stroke, or CVD mortality, identified via national registries. Results The mean age was 65.8 years; 48% were female. The most common cancers were gastrointestinal (23%), prostate (19%), and breast (12%). The median follow-up was 6.9 years. The modified tool classified 28% as low-, 35% moderate-, 34% high-, and 3% very high-risk. CVD incidence rose across categories: 7%, 21%, 29%, and 37% (P < 0.001). The C-statistic was 0.696 (95% CI: 0.674-0.718), and 0.746 (95% CI: 0.676-0.812) among anthracycline-treated patients. Within the low-to-moderate group, event rates ranged from 6% to 8% (0-1 points) to 24% to 27% (3-4 points). Conclusions The tool stratifies CVD risk in cancer patients and may guide tailored follow-up and cardioprotection. Heterogeneity within moderate-risk patients highlights the need for refinement to improve individualized assessment.

• Chadwick, Jessica; Berry, Colin; Carpenter, Meredith A.; Gulati, Geeta; Heck, Siri Lagethon & Hinterberg, Michael A. [Vis alle 18 forfattere av denne artikkelen] (2025). Utilization of Proteomic Measures for Early Detection of Drug Benefits and Adverse Effects. Journal of clinical pharmacology. ISSN 0091-2700. 65(11), s. 1460–1473. doi: 10.1002/jcph.70077. Fulltekst i vitenarkiv Vis sammendrag

  Recognition of benefits and adverse effects of therapies in earlier clinical trial phases could improve the safety, efficiency, and cost of clinical trials. Using four clinical trials representing a diverse set of diseases and drug classes (EXSCEL: exenatide/GLP‐1 RA, SUGAR‐DM‐HF: empagliflozin/SGLT2i, PRADA: epirubicin/anthracycline, and AMPLE: abatacept/immunomodulator and adalimumab/TNF inhibitor), we hypothesized that previously validated proteomic measures for cardiometabolic outcomes could enable the detection of beneficial and adverse drug effects in fewer participants over a shorter follow‐up period. Changes in SomaSignal TM proteomic tests over time in response to treatment were assessed in the EXSCEL (baseline vs 1 year; once‐weekly exenatide (EQW) (n) = 1812 vs control (n) = 1787), SUGAR‐DM‐HF (baseline vs 12 weeks and 36 weeks; empagliflozin (n) = 45 vs control (n) = 52), AMPLE (baseline vs 85 days and 1 year; abatacept (n) = 210, adalimumab (n) = 222), and PRADA (baseline vs 7–10 days and 3 months, n = 120) trial. Improvement of cardiovascular risk and cardiometabolic traits with EQW was detectable within 1 year ( P = .002) in sample sizes significantly smaller than the original study. Cardio‐ and kidney‐protective ( P = .06, P = .037) effects of empagliflozin were detectable within 36 weeks in a small sample size (n ∼ 50). Abatacept and adalimumab treatment demonstrated significant improvements in cardiovascular risk ( P ≤ .001, P ≤ .001) and cardiorespiratory fitness ( P ≤ .001, P ≤ .001) within 85 days. In contrast, anthracycline treatment led to significant increases in heart failure mortality risk ( P ≤ 0.001) and cardiovascular risk ( P = .004) after the first cycle of chemotherapy treatment. These findings provide preliminary evidence that proteomics may provide a powerful tool for optimizing drug pipelines by predicting the effects of novel therapeutics in smaller, shorter trials.

• Mecinaj, Albulena; Vinje, Victoria; Ngo, Doan T. M.; Sverdlov, Aaron L. & Myhre, Peder Langeland (2025). The SARAH trial: more evidence on the role of neurohormonal blockers in prevention of anthracycline-induced cardiotoxicity. Heart Failure Reviews. ISSN 1382-4147. 30(3), s. 627–631. doi: 10.1007/s10741-025-10495-1. Fulltekst i vitenarkiv Vis sammendrag

  This mini-review highlights the results of the SARAH trial, which evaluated the efficacy of sacubitril/valsartan in preventing subclinical cardiac dysfunction in patients undergoing anthracycline-based chemotherapy. The trial demonstrated a significant reduction in GLS decline in the treatment group compared to placebo. The findings are discussed in context with other trials investigating neurohormonal blockade for the prevention of cancer therapy-related cardiac dysfunction.

• Omland, Torbjørn; Heck, Siri Lagethon; Holte, Espen; Mecinaj, Albulena; Gynnild, Mari Nordbø & Fagerland, Morten [Vis alle 13 forfattere av denne artikkelen] (2025). Sacubitril/Valsartan and Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy: The PRADA II Randomized Clinical Trial. Circulation. ISSN 0009-7322. 152(16), s. 1136–1145. doi: 10.1161/circulationaha.125.076616. Fulltekst i vitenarkiv Vis sammendrag

  Background: Anthracycline- and trastuzumab-associated cardiotoxicity may lead to cardiac dysfunction and dose reduction or halt in potentially life-saving adjuvant cancer therapy. Whether angiotensin receptor neprilysin inhibitors can prevent cancer therapy-related cardiac dysfunction and injury remains to be established. Methods: PRADA II was a randomized, parallel-group, placebo-controlled, double-blind multicenter trial conducted at 4 academic medical centers in Norway that evaluated the cardioprotective effect of sacubitril-valsartan vs. placebo administered concomitantly with anthracycline-containing breast cancer therapy and continued for 18 months. The target dose was 97/103 mg b.i.d. The primary outcome was change in left ventricular ejection fraction by cardiovascular magnetic resonance from prior to initiation of chemotherapy to 18 months after. Secondary outcomes included change in echocardiographic global longitudinal strain, circulating cardiac troponins, and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Results: In total, 138 women (mean (±SD) age: 54.0 ± 9.4 years) were randomized. The overall decline in left ventricular ejection fraction from baseline to 18 months was 2.2 percentage points (95% confidence interval [CI], 1.1 to 3.3) in the placebo group and 1.1 percentage points (95% CI, -0.01 to 2.2) in the sacubitril-valsartan group. The between-group difference was 1.1 percentage points (95% CI, -0.4 to 2.7; P=0.16). Left ventricular global longitudinal strain was normal and remained stable in the sacubitril-valsartan group throughout the study (change from baseline to 18 months -0.32 [95% CI, -0.80 to 0.15]). In contrast, there was a progressive decline in the placebo group (change from baseline to 18 months 0.53 [95% CI, 0.05 to 1.00]). The between-group difference was -0.85 (95% CI, -1.52 to -0.18). The mean increases in NT-proBNP and cardiac troponin I concentrations from baseline to 18 months were greater in the placebo than in the sacubitril-valsartan group (log difference 0.303 (95% CI 0.0547 to 0.552) for NT-proBNP and 0.534 (95% CI 0.114 to 0.954) for cardiac troponin I). Conclusions: Anthracycline-based treatment for early breast cancer is associated with a reduction in left ventricular ejection fraction that was not significantly attenuated by sacubitril-valsartan.

Se alle arbeider i NVA

• Vinje-Jakobsen, Victoria; Gynnild, Mari Nordbø; Mecinaj, Albulena; Wisløff, Torbjørn; Holte, Espen & Wethal, Torgeir [Vis alle 13 forfattere av denne artikkelen] (2026). The effect of sacubitril/valsartan on functional disability and skeletal muscle injury during breast cancer therapy: insights from the PRADA II trial. Fulltekst i vitenarkiv Vis sammendrag

  Background: Anthracycline therapy induces dose-dependent cardiotoxicity and systemic adverse effects, including functional disability. While sacubitril/valsartan attenuates early subclinical myocardial injury during breast cancer therapy, its impact on functional capacity and skeletal muscle injury remains unknown. Purpose: To evaluate whether sacubitril/valsartan attenuates anthracycline-induced decline in functional capacity and skeletal muscle injury compared to placebo. Methods: PRADA II was a randomised, double-blind, placebo-controlled multicentre trial including 138 women with early breast cancer receiving (neo)adjuvant anthracycline therapy±trastuzumab. Participants were randomised prior to anthracycline initiation to sacubitril/valsartan or placebo for 18 months. The predefined primary outcome of this substudy was change in maximal handgrip strength from baseline to 18 months. Secondary outcomes included changes in 6-minute walk distance and circulating creatine kinase (CK) and myoglobin concentrations. Assessments were performed at baseline, post-anthracycline (Visit 2), and at 18 months (Visit 3). Changes were analysed using generalised linear mixed models, and a two-sided alpha level of 0.05 was applied to the primary outcome of this predefined substudy. Results: Maximal handgrip strength declined in both groups from baseline to Visit 2, with partial recovery at Visit 3 in the sacubitril/valsartan group and continued decline in the placebo group. No significant between-group difference was observed in handgrip strength (between-group change from baseline to Visit 3: -0.3 kg, 95% CI -1.5 to 0.8, p=0.57). However, a greater decline from baseline to Visit 2 was observed with sacubitril/valsartan than placebo, corresponding to a between-group difference of -1.8 kg, 95% CI -3.0 to -0.6. 6-minute walk distance increased from baseline to both follow-up timepoints in the sacubitril/valsartan group, and a transient reduction was observed in the placebo group from baseline to Visit 2. Between-group changes did not differ at Visit 2 (8.8 m, 95% CI -19.3 to 36.9) or Visit 3 (13.6 m, 95% CI -13.3 to 40.5). CK and myoglobin were numerically higher in the placebo group from baseline to Visit 3, however, the confidence intervals for between-group differences included the null value (CK geometric mean ratio 1.17, 95% CI 0.94 to 1.45; myoglobin 1.10, 95% CI 0.98 to 1.23). Temporal changes by randomisation group are shown in Figure 1. Conclusions: Sacubitril/valsartan did not significantly attenuate anthracycline-related decline in functional capacity assessed by maximal handgrip strength and 6-minute walk distance or changes in biomarkers of skeletal muscle injury. These findings suggest a neutral effect of sacubitril/valsartan on functional capacity, without challenging its potential cardioprotective role during anthracycline therapy.

• Vinje-Jakobsen, Victoria; Orstad, Eivind Bjørkan; Gulati, Geeta; Nerdrum, Tone; Iqbal, Naveed & Schirmer, Henrik [Vis alle 9 forfattere av denne artikkelen] (2026). Incidence and severity of cancer-therapy-related cardiac dysfunction during contemporary breast cancer therapy in a real-world cohort. Fulltekst i vitenarkiv Vis sammendrag

  Background: Cancer therapy-related cardiac dysfunction (CTRCD) is a well-known complication in breast cancer patients exposed to anthracyclines and Human Epidermal Growth Factor Receptor 2 (HER2) targeted therapy. However, the incidence of CTRCD in unselected contemporary breast cancer populations treated according to current standard-of-care regimens remains incompletely investigated. Purpose: To determine the incidence of CTRCD in women receiving (neo-)adjuvant breast cancer therapy in a real-world setting. Methods: In this prospective observational study, women scheduled for (neo-)adjuvant breast cancer therapy were included. Participants were categorized into three treatment regimen groups: 1) anthracycline therapy only, 2) HER2-targeted therapy only, and 3) sequential treatment with anthracycline therapy followed by HER2-targeted therapy. The primary endpoint was the incidence of CTRCD, defined according to the echocardiographic criteria included in the 2022 ESC Cardio-Oncology Guidelines (Figure 1), from baseline to 12 months after completion of scheduled therapy. Echocardiography was assessed at baseline, after completion of scheduled therapy, and 12 months thereafter. In addition, echocardiography was performed every 3 months during HER2-targeted therapy and when clinically indicated. Results: In total, 515 women were included (median age: 53 years (IQR 45,64)). During follow-up, 123 (24%) developed CTRCD. Of these, 78% were classified as mild, 19% moderate, and 2% severe. The highest incidence of CTRCD was observed among participants receiving sequential anthracycline therapy (EC90 x 4) and HER2-targeted therapy (Table 1). This regimen also had the highest incidence of moderate and severe CTRCD (13%), compared with 4% in the anthracycline-only group and 1% in the HER2-only group. Overall, severe CTRCD was observed in 0.6% of all study participants. The cumulative incidence of the worst observed severity of CTRCD during follow-up, overall and by treatment regimen, is summarized in Table 1. Conclusion: In this real-world breast cancer cohort, nearly one in four women developed CTRCD during follow-up; however, most cases were categorised as mild. Moderate and severe cardiac dysfunction were primarily observed in patients receiving sequential anthracycline and HER2-targeted therapy. Severe CTRCD was rare in the overall study population.

• Vinje-Jakobsen, Victoria; Orstad, Eivind Bjørkan; Gulati, Geeta; Caliskan, Gulser; Nerdrum, Tone & Iqbal, Naveed [Vis alle 10 forfattere av denne artikkelen] (2026). Rationale, design and baseline characteristics of the cardio-oncology registry (CARE) study: a prospective, observational study of cardiotoxic effects during breast cancer therapy. European Heart Journal, Supplement. ISSN 1520-765X. 28(Supplement_8). doi: 10.1093/eurheartjsupp/suag097.103. Fulltekst i vitenarkiv Vis sammendrag

  Background: Anthracycline and Human Epidermal Growth Factor Receptor 2 (HER2) targeted therapy may induce cancer therapy-related cardiac dysfunction (CTRCD). Current guidelines recommend risk stratification using the Heart Failure Association–International Cardio-Oncology Society (HFA-ICOS) risk assessment tool. However, data on the incidence of CTRCD in contemporary breast cancer populations treated according to current standard-of-care regimens remain limited. Moreover, the actual cardiovascular risk associated with the HFA-ICOS risk categories in breast cancer treatment remains uncertain. Real-world evaluation of whether this consensus-based stratification appropriately separates patients according to subsequent CTRCD risk has been highlighted as a key research priority. Purpose: Overall, the study aims to determine the incidence of CTRCD and to evaluate cardiovascular risk stratification using the HFA-ICOS tool and its association with subsequent CTRCD. Methods: CARE is a prospective observational study including women scheduled for (neo)adjuvant anthracycline therapy and/or HER2-targeted therapy. Echocardiography, using standard and novel echocardiographic parameters, and circulating cardiac biomarkers were assessed at baseline (visit 1), after completion of scheduled therapy (visit 2), and 12 months after completion of scheduled therapy (visit 3). Participants were categorized into three treatment regimen groups: 1) Anthracycline therapy only, 2) HER2-targeted therapy only, and 3) HER2-targeted therapy sequentially to anthracyclines (Figure 1). The primary outcome is incidence of CTRCD. Secondary outcomes include HFA-ICOS risk stratification in relation to subsequent CTRCD. Results: In total, 515 women (median age (Q1,Q3): 53 (45,64) years) were included. Overall, 335 (63%) participants received anthracycline therapy only, 100 (15%) received HER2-targeted therapy only, and 80 (19%) received anthracycline therapy followed by HER2-targeted therapy. Baseline cardiovascular risk factors included hypertension in 20%, current smoking in 13%, diabetes in 7%, and a history of heart disease in 7.6%, while 3.5% had received previous anti-cancer treatment (Table 1). Conclusion: The CARE study is a large prospective observational cardio-oncology study evaluating the incidence of CTRCD after contemporary breast cancer therapy regimens. With systematic echocardiographic and biomarker assessment, the study will provide important insights into the incidence of CTRCD, the performance of the HFA-ICOS risk stratification tool and follow-up strategies in routine cardio-oncology care.Table 1Baseline Characteristics CARE  Figure 1Consort Diagram

• Gynnild, Mari Nordbø; Gulati, Geeta; Mecinaj, Albulena; Wethal, Torgeir; Holte, Espen & Vinje-Jakobsen, Victoria [Vis alle 11 forfattere av denne artikkelen] (2026). Baseline and early changes in cardiac biomarkers as predictors of global longitudinal strain deterioration during breast cancer therapy: a PRADAII substudy. Fulltekst i vitenarkiv Vis sammendrag

  Background: Cardiac biomarkers are recommended for risk stratification before and during potentially cardiotoxic cancer therapy, but the prognostic value of baseline levels and early changes for subsequent left ventricular (LV) dysfunction remains unclear. Objectives: To evaluate whether baseline and early changes in high-sensitivity cardiac troponins (hs-cTnI, hs-cTnT) and N-terminal pro–B-type natriuretic peptide (NT-proBNP) predict changes in global longitudinal strain (GLS) over 18 months. Methods: In the randomized PRADAII, 138 women treated with anthracyclines (±trastuzumab) received sacubitril/valsartan or placebo and underwent serial biomarker sampling and cardiac imaging at baseline, post-anthracycline, and 18 months. Longitudinal changes in GLS and left ventricular ejection fraction (LVEF) were analyzed using adjusted linear mixed models, including exploratory analyses of combined, persistent, and peak biomarker elevations. Results: Mean age was 54.0±9.4 years. At baseline, no patients had hs-cTnI values above the sex-specific 99th percentile, 6 (4%) had hs-cTnT >99th percentile, and 16 (12%) had NT-proBNP >125 ng/L. Mean baseline GLS was −19.5±2.1% and CMR- and echocardiography-derived LVEF was 60.3±4.8% and 58.3±6.2%, respectively. GLS declined modestly over follow-up, with less deterioration in the sacubitril/valsartan group than in the placebo group (ΔΔ −1.26, 95% CI −2.19 to −0.33). Both hs-cTnI and hs-cTnT increased markedly after anthracycline therapy, with 16.7% and 71.7% exceeding the sex-specific 99th percentile at peak, whereas NT-proBNP showed modest changes with wide inter-individual variability. Transient and persistent troponin elevation occurred in 60.1% and 11.6%, respectively; corresponding NT-proBNP elevations in 5.1% and 7.3%, and combined troponin and NT-proBNP elevation in 9.4%. Baseline biomarker levels were not associated with GLS deterioration, and no biomarker–treatment interactions were observed (all p for interaction >0.27). Early post-anthracycline changes in hs-cTnI, hs-cTnT, or NT-proBNP were not predictive of subsequent GLS decline, nor were peak or persistent elevations (Table 1, Figure 1). No significant associations were observed between baseline or early biomarker levels and changes in LVEF assessed by echocardiography or CMR. Conclusions: In our breast cancer cohort with preserved baseline LV function, baseline levels and early changes in hs-cTnI, hs-cTnT, and NT-proBNP were not associated with subsequent deterioration in GLS over 18 months. Larger studies including higher-risk patients and clinical endpoints are needed to clarify the role of cardiac biomarkers in individualized cardiotoxicity risk stratification.

• Gynnild, Mari Nordbø; Gulati, Geeta; Mecinaj, Albulena; Wethal, Torgeir; Holte, Espen & Vinje-Jakobsen, Victoria [Vis alle 11 forfattere av denne artikkelen] (2026). Baseline and early changes in cardiac biomarkers as predictors of global longitudinal strain deterioration during breast cancer therapy: a PRADAII substudy. European Heart Journal, Supplement. ISSN 1520-765X. 28(Supplement_8). doi: 10.1093/eurheartjsupp/suag097.089. Fulltekst i vitenarkiv Vis sammendrag

  Abstract Background Cardiac biomarkers are recommended for risk stratification before and during potentially cardiotoxic cancer therapy, but the prognostic value of baseline levels and early changes for subsequent left ventricular (LV) dysfunction remains unclear. Objectives To evaluate wheter baseline and early changes in high-sensitivity cardiac troponins (hs-cTnI, hs-cTnT) and N-terminal pro–B-type natriuretic peptide (NT-proBNP) predict changes in global longitudinal strain (GLS) over 18 months. Methods In the randomized PRADAII, 138 women treated with anthracyclines (±trastuzumab) received sacubitril/valsartan or placebo and underwent serial biomarker sampling and cardiac imaging at baseline, post-anthracycline, and 18 months. Longitudinal changes in GLS and left ventricular ejection fraction (LVEF) were analyzed using adjusted linear mixed models, including exploratory analyses of combined, persistent, and peak biomarker elevations. Results Mean age was 54.0±9.4 years. At baseline, no patients had hs-cTnI values above the sex-specific 99th percentile, 6 (4%) had hs-cTnT &gt;99th percentile, and 16 (12%) had NT-proBNP &gt;125 ng/L. Mean baseline GLS was −19.5±2.1% and CMR- and echocardiography-derived LVEF was 60.3±4.8% and 58.3±6.2%, respectively. GLS declined modestly over follow-up, with less deterioration in the sacubitril/valsartan group than in the placebo group (ΔΔ −1.26, 95% CI −2.19 to −0.33). Both hs-cTnI and hs-cTnT increased markedly after anthracycline therapy, with 16.7% and 71.7% exceeding the sex-specific 99th percentile at peak, whereas NT-proBNP showed modest changes with wide inter-individual variability. Transient and persistent troponin elevation occurred in 60.1% and 11.6%, respectively; corresponding NT-proBNP elevations in 5.1% and 7.3%, and combined troponin and NT-proBNP elevation in 9.4%. Baseline biomarker levels were not associated with GLS deterioration, and no biomarker–treatment interactions were observed (all p for interaction &gt;0.27). Early post-anthracycline changes in hs-cTnI, hs-cTnT, or NT-proBNP were not predictive of subsequent GLS decline, nor were peak or persistent elevations (Table 1, Figure 1). No significant associations were observed between baseline or early biomarker levels and changes in LVEF assessed by echocardiography or CMR. Conclusions In our breast cancer cohort with preserved baseline LV function, baseline levels and early changes in hs-cTnI, hs-cTnT, and NT-proBNP were not associated with subsequent deterioration in GLS over 18 months. Larger studies including higher-risk patients and clinical endpoints are needed to clarify the role of cardiac biomarkers in individualized cardiotoxicity risk stratification.  

• Gynnild, Mari Nordbø; Holtrop, Joris; Hageman, Steven HJ; Vinje, Victoria; Dorresteijn, Jannick AN & Visseren, Frank [Vis alle 10 forfattere av denne artikkelen] (2024). External validation of the HFA-ICOS risk stratification tool for prediction of cardiovascular complications after cancer treatment. European Heart Journal, Supplement. ISSN 1520-765X. doi: 10.1093/eurheartj/ehae666.2693. Fulltekst i vitenarkiv
• Gynnild, Mari Nordbø; Holtrop, Joris; Hageman, Steven; Vinje, Victoria; Dorresteijn, Jannick & Visseren, Frank [Vis alle 10 forfattere av denne artikkelen] (2024). External validation of the Systematic COronary Risk Evaluation 2 (SCORE2) model in cancer patients. Fulltekst i vitenarkiv
• Gynnild, Mari Nordbø; Holtrop, Joris; Hageman, Steven; Vinje, Victoria; Dorresteijn, Jannick A.N. & Visseren, Frank [Vis alle 10 forfattere av denne artikkelen] (2024). External validation of the HFA-ICOS risk stratification tool for prediction of cardiovascular complications after cancer treatment. Fulltekst i vitenarkiv
• Gynnild, Mari Nordbø; Holtrop, Joris; Hageman, Steven HJ; Vinje, Victoria; Dorresteijn, Jannick AN & Visseren, Frank [Vis alle 10 forfattere av denne artikkelen] (2024). External validation of the Systematic COronary Risk Evaluation 2 (SCORE2) model in cancer patients. European Heart Journal, Supplement. ISSN 1520-765X. doi: 10.1093/eurheartj/ehae666.2692. Fulltekst i vitenarkiv
• Vinje, Victoria; Cao, Shu-qin; Heck, Siri Lagethon; Wisløff, Torbjørn; Klæboe, Lars Gunnar & Nilsen, Hilde Loge [Vis alle 9 forfattere av denne artikkelen] (2023). Rationale And Design Of The NARNIA Trial: The Effect Of NicotinAmide Riboside ON Myocardial And Skeletal Muscle Injury And Function In Patients With Metastatic Breast Cancer Receiving Anthracyclines. Fulltekst i vitenarkiv

Se alle arbeider i NVA