{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T12:46:05Z","timestamp":1789562765007,"version":"build-2803163510"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Heart Failure"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>There are limited data on the etiology, management, and outcomes of Society for Cardiovascular Angiography and Interventions (SCAI) stage B cardiogenic shock.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>From 2017 to 2022, adult patients (\u226518 years) admitted to the medical, intermediate, and critical care units in a 6-hospital system were evaluated. SCAI stage B cardiogenic shock was defined as hypotension (systolic \u226490\/mean \u226465 mm\u2009Hg) or hypoperfusion (lactate 2\u20135 mEq\/L). Cardiac arrest, use of circulatory support, and noncardiac etiologies were excluded. The composite primary end point included transfer to a higher level of care, SCAI stage escalation, or in-hospital mortality. Multivariable analysis and mixed-effects regression models were used.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      During this period, 500 patients (median age, 76 years; 56% men; 79% White) developed SCAI stage B cardiogenic shock (hypotension 18%, hypoperfusion 82%). The most common etiologies were heart failure (37%), arrhythmia (23%), and acute myocardial infarction (13%). The primary composite end point was noted in 135 patients (deterioration cohort). The deterioration cohort had comparable baseline characteristics to those who recovered, but before the primary outcome, had lower blood pressures, higher rates of renal (60% versus 33%) and hepatic (15% versus 4%) injury, less negative fluid balance (\u22120.30 versus \u22120.68 L), and greater diuretic resistance (21% versus 2%;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001). In a multivariable analysis, acute kidney injury\u2014adjusted odds ratio 2.17 (95% CI, 1.11\u20134.22);\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.02\u2014and diuretic resistance\u2014adjusted odds ratio 9.55 (95% CI, 2.61\u201334.89);\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.001\u2014were independently predictive of clinical deterioration. Patients with isolated hypotension had worse outcomes compared with those with isolated hypoperfusion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Among patients with SCAI stage B cardiogenic shock, a quarter of the population experienced clinical deterioration. Acute kidney injury and diuretic resistance in the preceding 24 hours were independently predictive of developing the primary end point.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circheartfailure.125.013814","type":"journal-article","created":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T10:00:32Z","timestamp":1771495232000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":4,"title":["Management and Outcomes of Society for Cardiovascular Angiography and Interventions Stage B Cardiogenic Shock"],"prefix":"10.1161","volume":"19","author":[{"given":"Chirag","family":"Mehta","sequence":"first","affiliation":[{"name":"Department of Medicine (C.M., I.V., B.O., A. Shin, V.C., S.C., D.D.P., A. Sweeting, R.T.), Warren Alpert Medical School of Brown University, Providence, RI."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4052-221X","authenticated-orcid":true,"given":"Phinnara","family":"Has","sequence":"additional","affiliation":[{"name":"Biostatistics, Epidemiology, Research Design, and Informatics, Brown University Health, Providence, RI (P.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3491-5503","authenticated-orcid":true,"given":"Aryan","family":"Mehta","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Connecticut School of Medicine, Farmington, CT (A.M.)."},{"name":"Brown University Health Cardiovascular Institute, Providence, RI (A.M., D.J.L., M.J.C., J.D.A., S.V.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irene","family":"Vargas","sequence":"additional","affiliation":[{"name":"Department of Medicine (C.M., I.V., B.O., A. Shin, V.C., S.C., D.D.P., A. Sweeting, R.T.), Warren Alpert Medical School of Brown University, Providence, RI."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Osorio","sequence":"additional","affiliation":[{"name":"Department of Medicine (C.M., I.V., B.O., A. Shin, V.C., S.C., D.D.P., A. Sweeting, R.T.), Warren Alpert Medical School of Brown University, Providence, RI."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abraham","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Medicine (C.M., I.V., B.O., A. Shin, V.C., S.C., D.D.P., A. Sweeting, R.T.), Warren Alpert Medical School of Brown University, Providence, RI."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vaisali","family":"Chilamkurthy","sequence":"additional","affiliation":[{"name":"Department of Medicine (C.M., I.V., B.O., A. Shin, V.C., S.C., D.D.P., A. 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