{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T18:00:55Z","timestamp":1780941655151,"version":"3.54.1"},"reference-count":60,"publisher":"Public Library of Science (PLoS)","issue":"6","license":[{"start":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T00:00:00Z","timestamp":1780876800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["INCT\/FAPESP - 2025\/27076-4"],"award-info":[{"award-number":["INCT\/FAPESP - 2025\/27076-4"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","award":["INCT - 408940\/2024-7 and 442643\/2020-9"],"award-info":[{"award-number":["INCT - 408940\/2024-7 and 442643\/2020-9"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Zerbini Foundation"},{"name":"Foxconn Brazil","award":["Omics in Cardiovascular Medicine Grant"],"award-info":[{"award-number":["Omics in Cardiovascular Medicine Grant"]}]}],"content-domain":{"domain":["www.plosntds.org"],"crossmark-restriction":false},"short-container-title":["PLoS Negl Trop Dis"],"abstract":"<jats:sec id=\"sec001\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Chronic Chagas cardiomyopathy (CCC) remains a major cause of heart failure (HF)\u2013related mortality in Latin America and is increasingly recognized as a global health concern. Prognostic models developed in non-Chagas populations often perform poorly in CCC, highlighting the need for etiology-specific risk stratification.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec002\">\n                    <jats:title>Methodology\/principal findings<\/jats:title>\n                    <jats:p>\n                      We applied high-throughput plasma proteomics to evaluate 2-year mortality risk in CCC compared with other HF etiologies. Baseline plasma from 1,212 adults with heart failure with reduced ejection fraction (HFrEF; LVEF &lt;50%) was analyzed to quantify 734 circulating proteins. CCC was confirmed in 191 participants (16%) by dual\n                      <jats:italic>Trypanosoma cruzi<\/jats:italic>\n                      serology. Two-year mortality was higher in CCC than in the overall HF cohort (26% vs. 16%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.01). Feature-selection methods identified a nine-protein panel (P9: C1QA, CCL4, REN, EGLN1, COL9A1, GP1BA, ITM2A, CNPY2, NT-proBNP) that improved risk classification compared with NT-proBNP alone, increasing F1-macro by 20% (0.674 vs. 0.560) and integrated time-dependent discrimination for 2-year mortality (iAUC) by 6%. Performance gains varied by HF etiology. Improvements were greatest in hypertensive (+40%) and ischemic (+21%) HF, whereas in CCC the P9 panel underperformed NT-proBNP alone (\u221216%), suggesting distinct underlying disease biology. External validation in the UK Biobank confirmed generalizability: compared with NT-proBNP, P9 improved F1-macro by 18% and iAUC by 7.4%, reaching an F1-macro of 0.612 in the highest-risk tertile. Pathway enrichment identified 14 CCC-specific pathways, mainly related to fibrosis, integrin signaling, immune dysregulation, and impaired protein trafficking. Exploratory analyses also highlighted potential pathway-linked therapeutic targets consistent with distinct CCC mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"sec003\">\n                    <jats:title>Conclusions\/significance<\/jats:title>\n                    <jats:p>The P9 proteomic panel improved mortality risk prediction beyond NT-proBNP and the MAGGIC clinical score across most HF etiologies and showed consistent performance in an independent population-based cohort. In contrast, in CCC P9 underperformed NT-proBNP alone, highlighting the distinct biological features of this disease. These findings underscore the limitations of universal biomarker models in CCC and support the need for etiology-specific risk stratification strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1371\/journal.pntd.0014370","type":"journal-article","created":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T17:33:57Z","timestamp":1780940037000},"page":"e0014370","update-policy":"https:\/\/doi.org\/10.1371\/journal.pntd.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["Plasma proteomics improves risk prediction in heart failure and reveals unique biology in chronic chagas cardiomyopathy"],"prefix":"10.1371","volume":"20","author":[{"given":"Jos\u00e9 S. 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