{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T12:33:47Z","timestamp":1792672427129,"version":"4.5.0"},"reference-count":28,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"17","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2006,5,2]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic>Background\u2014<\/jats:italic>\n                    <\/jats:bold>\n                    Right ventricular apical (RVA) pacing creates abnormal left ventricular contraction, hypertrophy, and reduced pump function. The adverse effects of ventricular desynchronization may explain the association of RVA pacing with an increased risk of heart failure hospitalization (HFH) in clinical trials.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>\n                      <jats:italic>Methods and Results\u2014<\/jats:italic>\n                    <\/jats:bold>\n                    Baseline and postimplantation variables were used to predict HFH in the Mode Selection Trial, a 2010-patient, 6-year trial of dual-chamber (DDDR) versus ventricular (VVIR) pacing in sinus node dysfunction. A Cox model showed that New York Heart Association (NYHA) class at baseline and follow-up predicted HFH (hazard ratio [HR], 3.99; 95% confidence interval [CI], 2.74\u20135.79 for NYHA class III\/IV and HR, 2.17; 95% CI, 1.54\u20133.04 for NYHA class II versus class I); other predictors were heart failure (HR, 2.30; 95% CI, 1.70\u20133.11), atrioventricular (AV) block (HR, 1.48; 95% CI, 1.11\u20131.97), and myocardial infarction (MI)(HR, 1.37; 95% CI, 1.00\u20131.86). Postimplantation predictors were VVIR cumulative percent ventricular pacing (Cum%VP) &gt;80 (HR, 3.58; 95% CI, 1.72\u20137.45), DDDR Cum%VP &gt;40 or VVIR Cum%VP \u226480 (HR, 1.81; 95% CI, 0.94\u20133.50) versus DDDR Cum%VP \u226440; whether QRS duration (QRSd) was paced or spontaneous (HR, 2.21; 95% CI, 1.39\u20133.54; spontaneous versus paced); and drugs for atrial fibrillation (HR, 1.60; 95% CI, 1.19\u20132.15). Low baseline ejection fraction (EF) and postimplantation RVA-paced or spontaneous QRSd predicted HFH; the increased risk with QRSd was steeper for normal versus low EF (HR, 1.18; 95% CI, 1.11\u20131.27; versus HR, 1.08; 95% CI, 1.01\u20131.15; for a 10-ms increase); at a QRSd of \u2248200 ms, normal- and low-EF patients had equivalent risk. HFH risk nearly doubled when VVIR Cum%VP was \u226480 or DDDR Cum%VP was &gt;40 versus DDDR Cum%VP \u226440 and was additive with other risk factors.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>\n                      <jats:italic>Conclusions\u2014<\/jats:italic>\n                    <\/jats:bold>\n                    Differences in HFH risk can be explained by interactions between substrate (atrial fibrillation, AV conduction, heart failure, MI, EF) and pacing promoters (ventricular desynchronization-paced QRSd and Cum%VP, and AV desynchronization-pacing mode). Management of RVA pacing is important for reducing the risk of HFH, particularly among patients with low EF and heart failure.\n                  <\/jats:p>","DOI":"10.1161\/circulationaha.105.608356","type":"journal-article","created":{"date-parts":[[2006,4,24]],"date-time":"2006-04-24T20:38:09Z","timestamp":1145911089000},"page":"2082-2088","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":216,"title":["Heart Failure During Cardiac Pacing"],"prefix":"10.1161","volume":"113","author":[{"given":"Michael O.","family":"Sweeney","sequence":"first","affiliation":[{"name":"From Brigham and Women\u2019s Hospital and Harvard Medical School (M.O.S.), Boston, Mass, and the Duke Clinical Research Institute and Duke University Medical Center (A.S.H.), Durham, NC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne S.","family":"Hellkamp","sequence":"additional","affiliation":[{"name":"From Brigham and Women\u2019s Hospital and Harvard Medical School (M.O.S.), Boston, Mass, and the Duke Clinical Research Institute and Duke University Medical Center (A.S.H.), Durham, NC."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0735-1097(86)80140-1"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1460-9592.2002.00484.x"},{"key":"e_1_3_2_3_2","first-page":"H300","volume":"259","year":"1990","unstructured":"Prinzen FW, Augustijn CH, Arts T, Allessi MA, Reneman RS. 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