2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T8f8,Hypertension and valvular heart disease, both associated with left ventricular (LV) pressure overload, increase the risk of anthracycline cardiotoxicity. While epidemiologically established, the underlying mechanisms remain unclear, precluding identification of therapeutic targets. Two-month-old Yucatan pigs (males and females) underwent aortic banding to induce LV pressure overload or no operation. After 4 months, animals received a low-risk cumulative dose of doxorubicin (5 weekly 1 mg/kg intravenous injections) or vehicle, generating four groups: (i) healthy controls (no LV overload, no doxorubicin), (ii) Dox (doxorubicin, no LV overload), (iii) Banding (B: LV overload, no doxorubicin), and (iv) B + Dox (LV overload plus doxorubicin). Cardiac function, structure, and metabolism were assessed over 8 months by cardiac magnetic resonance, magnetic resonance spectroscopy, and hybrid positron emission tomography/computed tomography. At study end, proteomics and mitochondrial structure and function were analysed. Complementary in vivo and ex vivo studies examined the mechanistic role of energetic imbalance. LV overload increased LV mass (P < .0001) and ejection fraction (P = .0081), with compensatory metabolic changes (drop in phosphocreatine (P = .022)). Low-risk Dox alone altered myocardial metabolism (increased glucose uptake, P = .014) but preserved cardiac function. In pigs with pre-existing LV pressure overload, doxorubicin increased mortality (P < .0001 vs all other groups), reduced left ventricular ejection fraction (LVEF) (P < .0001), increased fibrosis, and impaired mitochondrial respiration (P = .032). In HL-1 cardiomyocytes, reducing energy demand with mavacamten rescued cell viability under combined doxorubicin and hypertrophic stress. LV pressure overload increases myocardial susceptibility to anthracycline cardiotoxicity by inducing a high-energy-demand state. Anthracycline treatment, even at a low-risk dose, disrupts compensatory mechanisms in the pressure-overloaded heart, rapidly leading to cardiac dysfunction and heart failure. Preventive strategies targeting this metabolic vulnerability are urgently needed for patients with extant LV pressure overload (e.g. hypertension or valvular heart disease) who are undergoing anthracycline therapy.31:Tb93,Abstract Background and Aims Hypertension and valvular heart disease, both associated with left ventricular (LV) pressure overload, increase the risk of anthracycline cardiotoxicity. While epidemiologically established, the underlying mechanisms remain unclear, precluding identification of therapeutic targets. Methods Two-month-old Yucatan pigs (males and females) underwent aortic banding to induce LV pressure overload or no operation. After 4 months, animals received a low-risk cumulative dose of doxorubicin (5 weekly 1 mg/kg intravenous injections) or vehicle, generating four groups: (i) healthy controls (no LV overload, no doxorubicin), (ii) Dox (doxorubicin, no LV overload), (iii) Banding (B: LV overload, no doxorubicin), and (iv) B + Dox (LV overload plus doxorubicin). Cardiac function, structure, and metabolism were assessed over 8 months by cardiac magnetic resonance, magnetic resonance spectroscopy, and hybrid positron emission tomography/computed tomography. At study end, proteomics and mitochondrial structure and function were analysed. Complementary in vivo and ex vivo studies examined the mechanistic role of energetic imbalance. Results LV overload increased LV mass (P < .0001) and ejection fraction (P = .0081), with compensatory metabolic changes (drop in phosphocreatine (P = .022)). Low-risk Dox alone altered myocardial metabolism (increased glucose uptake, P = .014) but preserved cardiac function. In pigs with pre-existing LV pressure overload, doxorubicin increased mortality (P < .0001 vs all other groups), reduced left ventricular ejection fraction (LVEF) (P < .0001), increased fibrosis, and impaired mitochondrial respiration (P = .032). In HL-1 cardiomyocytes, reducing energy demand with mavacamten rescued cell viability under combined doxorubicin and hypertrophic stress. Conclusions LV pressure overload increases myocardial susceptibility to anthracycline cardiotoxicity by inducing a high-energy-demand state. Anthracycline treatment, even at a low-risk dose, disrupts compensatory mechanisms in the pressure-overloaded heart, rapidly leading to cardiac dysfunction and heart failure. Preventive strategies targeting this metabolic vulnerability are urgently needed for patients with extant LV pressure overload (e.g. hypertension or valvular heart disease) who are undergoing anthracycline therapy. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Cardiac Myosin Inhibitor: modality Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Cardiac Myosin Inhibitor (modality). Clinician-written summaries and actionable practice insights. 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NT-proBNP ≥50% reduction had the lowest NNT (1.7); peak VO₂ improvement was not statistically significant (P=0.1). Improvements in symptom burden (71% vs. 53%), septal e' (51% vs. 26%), and NT-proBNP (63% vs. 5%) all favored aficamten.","limitations":"- Peak VO₂ improvement (≥0.5 mL/kg/min) did not reach statistical significance (P=0.1), raising questions about exercise capacity benefit.\n- This is a responder analysis—a post-hoc analytical approach—which may be subject to outcome selection bias.\n- The 36-week follow-up limits conclusions about long-term durability of response.","practice_takeaway":"For patients with symptomatic nHCM (a condition with no currently approved therapy), aficamten produced broad multi-domain improvements, with an NNT as low as 1.7 for NT-proBNP reduction. Clinicians should weigh these results as supporting evidence for aficamten as a disease-modifying option in nHCM, pending regulatory approval."}},{"doi":"10.1001/jamacardio.2026.1730","pmid":"42307914","title":"Exercise Performance With Aficamten vs Metoprolol in Obstructive Hypertrophic Cardiomyopathy","journal_title":"JAMA Cardiology","journal_issn":"2380-6583","published_at":"2026-06-17T00:00:00.000Z","url":"https://doi.org/10.1001/jamacardio.2026.1730","source_score":33,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-17T13:33:00.840Z","updated_at":"2026-08-17T13:33:00.840Z","tags":[{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"condition","value":"Obstructive Hypertrophic Cardiomyopathy","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"generic","value":"aficamten","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"generic","value":"metoprolol","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"modality","value":"Beta Blocker","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"modality","value":"Cardiac Myosin Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"sample_size","value":"n=175","value_numeric":175},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"warning","value":"Brand name for aficamten (e.g., Zafgen/Cytokinetics investigational name) is not yet established as a proprietary marketed name; no brand tag applied.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"warning","value":"Level of evidence assigned as 2 (secondary analysis of a phase 3 RCT); the primary MAPLE-HCM trial results are referenced but not fully reproduced here.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"warning","value":"The full text provided is largely the CPET Manual of Operating Procedures for the MAPLE-HCM trial, not the final published results paper; clinical outcome data are drawn from the abstract and results sections only. Some granular subgroup and safety data may not be fully captured.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.1730","tag_type":"warning","value":"The trial excluded patients with atrial fibrillation and those with mandatory indications for beta-blockers, which may limit the applicability of the first-line therapy conclusion to broader oHCM populations.","value_numeric":null}],"summaries":{"what_studied":"This prespecified secondary analysis of the MAPLE-HCM phase 3 RCT compared aficamten monotherapy (5–20 mg daily) vs metoprolol (50–200 mg daily) across 16 cardiopulmonary exercise test (CPET) measures in 175 adults with symptomatic obstructive HCM (oHCM) over 24 weeks at 71 international sites.","key_result":"Aficamten outperformed metoprolol across multiple exercise phases: VE/VCO2 slope improved by −2.8 (95% CI −4.0 to −1.5, P<.001), anaerobic threshold by +76 mL/min (95% CI 41–111, P<.001), peak workload by +8 W (95% CI 3–13, P=.003), and circulatory power by +819 mm Hg × mL/min per kg (95% CI 569–1070, P<.001). Large pVO2 gains (≥3.0 mL/kg/min) were far more common with aficamten (20.5% vs 3.7%; OR 6.8); large pVO2 losses were far more common with metoprolol (20.7% vs 2.4%; OR 10.6).","limitations":"- This is a secondary analysis of a trial that excluded patients with atrial fibrillation or contraindications to β-blockers, limiting generalizability to those subgroups.\n- Active-comparator design means results reflect superiority over metoprolol, not placebo; absolute benefit vs no therapy is not established.\n- Patients with a medical indication for β-blockers were excluded, potentially selecting a population less likely to benefit from metoprolol.","practice_takeaway":"Aficamten monotherapy produced broad, consistent exercise improvements over metoprolol in symptomatic oHCM, supporting its consideration as first-line therapy rather than β-blockers. Clinicians should note that metoprolol was associated with large drops in pVO2 in roughly 1 in 5 patients—a meaningful safety signal for exercise tolerance."}},{"doi":"10.1161/jaha.125.045994","pmid":"42037447","title":"Mavacamten in Obstructive Hypertrophic Cardiomyopathy: National Insights on Access and Safety Profile From Real‐World Data","journal_title":"Journal of the American Heart Association","journal_issn":"2047-9980","published_at":"2026-04-27T00:00:00.000Z","url":"https://doi.org/10.1161/jaha.125.045994","source_score":9,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-07T13:26:46.320Z","updated_at":"2026-06-07T13:26:46.320Z","tags":[{"paper_doi":"10.1161/jaha.125.045994","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"brand","value":"Camzyos","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"condition","value":"Acute Heart Failure","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"condition","value":"Atrial Fibrillation","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"condition","value":"Left Ventricular Systolic Dysfunction","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"condition","value":"Obstructive Hypertrophic Cardiomyopathy","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"generic","value":"mavacamten","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"modality","value":"Cardiac Myosin Inhibitor","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"sample_size","value":"n=15145","value_numeric":15145},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"warning","value":"Age distribution of the study population is not explicitly reported; the 'adult' age group tag is inferred from the clinical context of HCM management.","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"warning","value":"Outcome follow-up duration is not explicitly stated in the abstract; the full observation window spans 2011–2023 but individual patient follow-up times may vary.","value_numeric":null},{"paper_doi":"10.1161/jaha.125.045994","tag_type":"warning","value":"The 1:3 propensity-score matching is weighted (not strictly 1:3 raw), so the effective control group size equals 502, not 1,475 unique patients — clinical interpretation should account for this weighting.","value_numeric":null}],"summaries":{"what_studied":"This observational multicenter study used TriNetX real-world data (2011–2023) to compare 502 propensity-matched obstructive HCM patients treated with mavacamten versus 502 matched controls (1:3 weighted), evaluating prescription access patterns and outcomes including acute heart failure, systolic dysfunction, cardiovascular hospitalization, new-onset AF, and all-cause mortality.","key_result":"Only 3.5% (509/15,145) of eligible patients received mavacamten; Black patients were 55% less likely to receive it than White patients (OR 0.45, 95% CI 0.33–0.63). Mavacamten patients with baseline AF (28% of recipients) had markedly worse outcomes: acute heart failure 7.8% vs. 3.6%, systolic dysfunction 12.8% vs. 6.4%, cardiovascular hospitalization 27.7% vs. 4.2%, and mortality 5% vs. 0% compared to those without AF.","limitations":"- Retrospective database design limits causal inference and may have unmeasured confounders.\n- TriNetX captures only patients within participating health systems, potentially missing those seen at safety-net or non-academic centers.\n- Drug dosing, echocardiographic parameters (e.g., LVEF at time of events), and socioeconomic variables are not granularly available in this dataset.","practice_takeaway":"Clinicians should be aware of a significant racial disparity in mavacamten access and take proactive steps to ensure equitable prescribing. Patients with preexisting AF starting mavacamten warrant heightened monitoring given substantially higher rates of heart failure, systolic dysfunction, hospitalization, and mortality."}},{"doi":"10.1056/nejmoa2601103","pmid":"41910394","title":"Mavacamten in Adolescents with Obstructive Hypertrophic Cardiomyopathy","journal_title":"New England Journal of Medicine","journal_issn":"0028-4793","published_at":"2026-03-29T00:00:00.000Z","url":"https://doi.org/10.1056/nejmoa2601103","source_score":380,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-26T13:44:46.560Z","updated_at":"2026-07-26T13:44:46.560Z","tags":[{"paper_doi":"10.1056/nejmoa2601103","tag_type":"age_group","value":"adolescent","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"brand","value":"Camzyos","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"category","value":"Medicine, General & Internal","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"condition","value":"Obstructive Hypertrophic Cardiomyopathy","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"generic","value":"mavacamten","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"modality","value":"Cardiac Myosin Inhibitor","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"sample_size","value":"n=44","value_numeric":44},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"study_design","value":"Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"warning","value":"Industry funding (Bristol Myers Squibb) is a potential source of bias.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"warning","value":"Sample size is very small (n=44), so serious adverse event rates should be interpreted cautiously — the trial is likely underpowered to detect rare safety signals.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"warning","value":"The brand name 'Camzyos' is inferred from known mavacamten branding; the paper itself does not explicitly state a brand name.","value_numeric":null},{"paper_doi":"10.1056/nejmoa2601103","tag_type":"warning","value":"The level of evidence is rated '2' as a Phase 3 RCT, but the small sample and single trial in this age group limit generalizability.","value_numeric":null}],"summaries":{"what_studied":"Phase 3 double-blind RCT evaluating mavacamten (cardiac myosin inhibitor) vs. placebo in 44 symptomatic adolescents aged 12–<18 years with NYHA class II–III obstructive hypertrophic cardiomyopathy over 28 weeks.","key_result":"Mavacamten reduced Valsalva LVOT gradient by –48.5 mmHg vs. –0.5 mmHg with placebo (difference –48.0 mmHg; 95% CI –67.7 to –28.3; P<0.001); no patient had LVEF drop below 50%, and no deaths occurred.","limitations":"Very small sample (n=44); short 28-week follow-up limits assessment of long-term safety and durability; trial funded by Bristol Myers Squibb (industry sponsor), introducing potential bias.","practice_takeaway":"Mavacamten produces a large, significant reduction in LVOT obstruction in adolescents with obstructive HCM and appears well-tolerated over 28 weeks — supporting its potential use as a pharmacologic alternative to surgery in this age group. Clinicians should monitor closely for LVEF reduction and arrhythmia events given the early-stage safety data."}},{"doi":"10.1093/eurheartj/ehaf1060","pmid":"41528064","title":"Anthracycline cardiotoxicity: role of metabolic vulnerability induced by cardiac pressure overload","journal_title":"European Heart Journal","journal_issn":"0195-668X","published_at":"2026-01-13T00:00:00.000Z","url":"https://doi.org/10.1093/eurheartj/ehaf1060","source_score":163,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-01-18","doi":"10.1093/eurheartj/ehaf1060","days":"14","issn":"0195-668X","rank":"3","field":"Clinical Medicine","score":"163","category":"Cardiac & Cardiovascular Systems","categories":["Cardiac & Cardiovascular Systems"],"_categories":["Cardiac & Cardiovascular Systems"]},"pubmed":{"doi":"10.1093/eurheartj/ehaf1060","title":"Anthracycline cardiotoxicity: role of metabolic vulnerability induced by cardiac pressure overload.","journal":"European heart journal","methods":"","results":"LV overload increased LV mass (P < .0001) and ejection fraction (P = .0081), with compensatory metabolic changes (drop in phosphocreatine (P = .022)). Low-risk Dox alone altered myocardial metabolism (increased glucose uptake, P = .014) but preserved cardiac function. In pigs with pre-existing LV pressure overload, doxorubicin increased mortality (P < .0001 vs all other groups), reduced left ventricular ejection fraction (LVEF) (P < .0001), increased fibrosis, and impaired mitochondrial respiration (P = .032). In HL-1 cardiomyocytes, reducing energy demand with mavacamten rescued cell viability under combined doxorubicin and hypertrophic stress.","abstract":"$30","keywords":["Anthracyclines","Cardiooncology","Heart failure","MR spectroscopy"],"pubmed_id":"41528064","conclusions":"","publication_date":"2026-01-13T00:00:00"},"crossref":{"DOI":"10.1093/eurheartj/ehaf1060","URL":"https://doi.org/10.1093/eurheartj/ehaf1060","ISSN":["0195-668X","1522-9645"],"link":[{"URL":"https://academic.oup.com/eurheartj/advance-article-pdf/doi/10.1093/eurheartj/ehaf1060/66394973/ehaf1060.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https://academic.oup.com/eurheartj/advance-article-pdf/doi/10.1093/eurheartj/ehaf1060/66394973/ehaf1060.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Anthracycline cardiotoxicity: role of 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Cardiotoxicity","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"generic","value":"doxorubicin","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"generic","value":"mavacamten","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"modality","value":"Anthracycline Chemotherapy","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"modality","value":"Cardiac Myosin Inhibitor","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"study_design","value":"Preclinical Animal Study","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"warning","value":"Design classification uses a non‑standard clinical label.","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"warning","value":"Preclinical large‑animal and cell‑line data; no human outcomes are reported.","value_numeric":null},{"paper_doi":"10.1093/eurheartj/ehaf1060","tag_type":"warning","value":"Sample size and event counts are not provided in the abstract.","value_numeric":null}],"summaries":{"what_studied":"A preclinical large-animal model tested whether left ventricular (LV) pressure overload heightens susceptibility to anthracycline cardiotoxicity. Two-month-old Yucatan pigs underwent aortic banding or no operation; after 4 months they received low-dose doxorubicin (5 weekly 1 mg/kg IV) or vehicle, with multimodal imaging over up to 8 months and end-of-study proteomics/mitochondrial assays, plus HL-1 cardiomyocyte experiments modulating energy demand.","key_result":"LV pressure overload alone increased LV mass (P<.0001) and ejection fraction (P=.0081) with a drop in phosphocreatine (P=.022). Low-risk doxorubicin alone increased myocardial glucose uptake (P=.014) without functional loss; combined with pressure overload it increased mortality (P<.0001 vs all other groups), reduced LVEF (P<.0001), increased fibrosis, and impaired mitochondrial respiration (P=.032). Reducing energy demand with mavacamten rescued viability in HL-1 cells under combined doxorubicin and hypertrophic stress.","limitations":"Findings derive from a pig model and HL-1 cardiomyocytes rather than patients, limiting direct generalizability. The abstract does not report sample size or event counts, constraining effect-size interpretation.","practice_takeaway":"Preclinical data show that pre-existing LV pressure overload creates a metabolic vulnerability that makes the heart susceptible to anthracycline injury even at low cumulative doses. For patients with hypertension or valvular disease who need anthracyclines, consider them high risk and prioritize close cardiotoxicity surveillance; preventive therapies remain unproven in humans."}}],"initialOffset":5,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"modality","value":"Cardiac Myosin Inhibitor"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Modalities","href":"/hub/tag/modality"},{"name":"Cardiac Myosin Inhibitor"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"modality","hub_tag_value":"Cardiac Myosin Inhibitor"}}}]]

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