{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T11:12:55Z","timestamp":1790075575774,"version":"4.0.1"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2011,11,1]],"date-time":"2011-11-01T00:00:00Z","timestamp":1320105600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Patients with heart failure (HF) and Cheyne-Stokes respiration or periodic breathing (PB) often demonstrate improved cardiac function when treatment with continuous positive airway pressure (CPAP) resolves PB. Unfortunately, CPAP is successful in only 50% of patients, and no known factor predicts responders to treatment. Because PB manifests from a hypersensitive ventilatory feedback loop (elevated loop gain [LG]), we hypothesized that PB persists on CPAP when LG far exceeds the critical threshold for stable ventilation (LG = 1).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To derive, validate, and test the clinical utility of a mathematically precise method that quantifies LG from the cyclic pattern of PB, where LG = 2\u03c0\/(2\u03c0DR \u2212 sin2\u03c0DR) and DR (i.e., duty ratio) = (ventilatory duration)\/(cycle duration) of PB.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>After validation in a mathematical model of HF, we tested whether our estimate of LG changes with CPAP (n = 6) and inspired oxygen (n = 5) as predicted by theory in an animal model of PB. As a first test in patients with HF (n = 14), we examined whether LG predicts the first-night CPAP suppression of PB.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>In lambs, as predicted by theory, LG fell as lung volume increased with CPAP (slope = 0.9 \u00b1 0.1; R2=0.82; P &amp;lt; 0.001) and as inspired\u2013arterial Po2 difference declined (slope = 1.05 \u00b1 0.12; R2=0.75; P &amp;lt; 0.001). In patients with HF, LG was markedly greater in 8 CPAP nonresponders versus 6 responders (1.29 \u00b1 0.04 versus 1.10 \u00b1 0.01; P &amp;lt; 0.001); LG predicted CPAP suppression of PB in 13\/14 patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our novel LG estimate enables quantification of the severity of ventilatory instability underlying PB, making possible a priori selection of patients whose PB is immediately treatable with CPAP therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.201103-0577oc","type":"journal-article","created":{"date-parts":[[2011,8,4]],"date-time":"2011-08-04T22:33:43Z","timestamp":1312497223000},"page":"1067-1075","source":"Crossref","is-referenced-by-count":115,"title":["Loop Gain As a Means to Predict a Positive Airway Pressure Suppression of Cheyne-Stokes Respiration in Patients with Heart Failure"],"prefix":"10.1093","volume":"184","author":[{"given":"Scott A.","family":"Sands","sequence":"first","affiliation":[{"name":"The Ritchie Centre, Monash Institute of Medical Research, Monash University, Melbourne, Victoria, Australia"},{"name":"Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bradley A.","family":"Edwards","sequence":"additional","affiliation":[{"name":"Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kirk","family":"Kee","sequence":"additional","affiliation":[{"name":"Department of Allergy, Immunology and Respiratory Medicine, The Alfred, Melbourne, Victoria, Australia"},{"name":"Faculty of Medicine, Monash University, Melbourne, Victoria, Australia; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony","family":"Turton","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Sleep Medicine, Monash Medical Centre, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth M.","family":"Skuza","sequence":"additional","affiliation":[{"name":"The Ritchie Centre, Monash Institute of Medical Research, Monash University, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teanau","family":"Roebuck","sequence":"additional","affiliation":[{"name":"Department of Allergy, Immunology and Respiratory Medicine, The Alfred, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denise M.","family":"O'Driscoll","sequence":"additional","affiliation":[{"name":"The Ritchie Centre, Monash Institute of Medical Research, Monash University, Melbourne, Victoria, 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