{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T13:24:57Z","timestamp":1791465897043,"version":"4.3.4"},"reference-count":59,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2019,7,10]],"date-time":"2019-07-10T00:00:00Z","timestamp":1562716800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Cancer is a systemic catabolic condition affecting skeletal muscle and fat. We aimed to determine whether cardiac atrophy occurs in this condition and assess its association with cardiac function, symptoms, and clinical outcomes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Treatment na\u00efve metastatic non\u2010small cell lung cancer patients (<jats:italic>n<\/jats:italic> = 50) were assessed prior to and 4 months after commencement of carboplatin\u2010based palliative chemotherapy. Methods included echocardiography for left ventricular mass (LVM) and LV function [LV ejection fraction, global longitudinal strain (GLS), diastolic function], computed tomography to quantify skeletal muscle and total adipose tissue, Eastern Cooperative Oncology Group Performance Status (ECOG\u2010PS), validated questionnaires for dyspnoea and fatigue, plasma biomarkers, tumour response to therapy, and overall survival.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>During 112 \u00b1 6 days, the median change in LVM was \u22128.9% [95% confidence interval (95% CI) \u221210.8 to \u22124.8, <jats:italic>P<\/jats:italic> &lt; 0.001]. Quartiles of LVM loss were \u221220.1%, \u221212.9%, \u22124.8%, and +5.5%. Losses of muscle, adipose tissue, and LVM were frequently concurrent; LVM loss &gt; median value was associated with loss of skeletal muscle [odds ratio (OR) = 4.5, 95% CI: 1.4\u201314.8, P=0.01] and loss of total adipose tissue (OR = 10.0, 95% CI: 2.7\u201336.7, <jats:italic>P<\/jats:italic> &lt; 0.001). LVM loss was associated with decreased GLS (OR = 6.6, 95% CI: 1.9\u201322.7, P=0.003) but not with LV ejection fraction or diastolic function. In the population overall, plasma levels of C\u2010reactive protein (P=0.008), high sensitivity troponin T (hs\u2010TnT) (P=0.03), and galectin\u20103 (P=0.02) increased over time, while N\u2010terminal pro B\u2010type natriuretic peptide and hs\u2010cTnI did not change over time. C\u2010reactive protein was the only biomarker associated with LVM loss but at the univariate level only. Independent predictors of LVM loss were prior weight loss (adjusted OR = 10.2, 95% CI: 2.2\u201346.9, P=0.003) and tumour progression (adjusted OR = 14.6, 95% CI: 1.4\u2013153.9, P=0.02). LVM loss was associated with exacerbations of fatigue (OR = 6.6, 95% CI: 1.9\u201322.7, P=0.003), dyspnoea (OR = 9.3, 95% CI: 2.4\u201335.8, P&lt;0.001), and deterioration of performance status (OR = 4.8, 95% CI: 1.3\u201318.3,P=0.02). Patients with concurrent loss of LVM, skeletal muscle, and fat were more likely to deteriorate in all three symptom domains and to have reduced survival (P=0.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Intense LVM atrophy is associated with non\u2010small cell lung cancer\u2010induced cachexia. Loss of LVM was associated with emerging alterations of GLS, indicating subtle changes in left ventricular function. Longer term studies are needed to assess the full scope of cardiac atrophy and its impact. LVM atrophy arises in conjunction with losses of fat and skeletal muscle and is temporally associated with meaningful declines in performance status, worsening of fatigue, and dyspnoea, as well as poorer tumour response and decreased survival. The specific contribution of LVM atrophy to these outcomes requires further study.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.12451","type":"journal-article","created":{"date-parts":[[2019,7,11]],"date-time":"2019-07-11T02:19:06Z","timestamp":1562811546000},"page":"1070-1082","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Rapid atrophy of cardiac left ventricular mass in patients with non\u2010small cell carcinoma of the lung"],"prefix":"10.1002","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9509-7030","authenticated-orcid":false,"given":"Seyyed Mohammad Reza","family":"Kazemi\u2010Bajestani","sequence":"first","affiliation":[{"name":"Department of Oncology, Division of Palliative Care Medicine University of Alberta  Edmonton Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald","family":"Becher","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Cardiology Alberta Cardiovascular and Stroke Research Centre  Edmonton Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles","family":"Butts","sequence":"additional","affiliation":[{"name":"Department of Oncology, Division of Medical Oncology, Cross Cancer Institute University of Alberta  Edmonton Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naveen S.","family":"Basappa","sequence":"additional","affiliation":[{"name":"Department of Oncology, Division of Medical Oncology, Cross Cancer Institute University of Alberta  Edmonton Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Smylie","sequence":"additional","affiliation":[{"name":"Department of Oncology, Division of Medical Oncology, Cross Cancer Institute University of Alberta  Edmonton Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anil 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