{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T22:45:30Z","timestamp":1792709130256,"version":"4.5.0"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1991,2]]},"abstract":"<jats:p>Chronic supraventricular tachycardia causes a dilated cardiomyopathy in man. Terminating this tachycardia appears to result in symptomatic improvement; however, its effects on left ventricular (LV) volume, mass, and function have not been fully examined. Accordingly, hemodynamic studies using simultaneous echocardiography and catheterization were performed in three groups of pigs: 1) those subjected to rapid left atrial pacing (240 beats\/min) for 3 weeks (SVT, n = 8), 2) those subjected to supraventricular tachycardia for 3 weeks followed by termination of pacing and a 4-week recovery period (PSVT, n = 9), and 3) sham-operated controls (CTR, n = 10). Systolic pump function was assessed using fractional shortening (FS), peak ejection rate [peak (-)dD\/dt], and maximum rate of pressure development [peak (+)dP\/dt]. Diastolic function was assessed using the time constant of isovolumic pressure decline (tau), peak early diastolic filling rate [peak (+)dD\/dt], the chamber stiffness constant (Kc), and the myocardial stiffness constant (Km). Supraventricular tachycardia caused LV dilation (end-diastolic dimension [EDD] increased from 3.5 +\/- 0.4 cm in CTR to 4.9 +\/- 0.5 cm in SVT, p less than 0.05) but no change in LV mass (LV weight-to-body weight ratio [LV\/BW]) was 2.58 +\/- 0.3 g\/kg in CTR and 2.66 +\/- 0.4 g\/kg in SVT), all indexes of systolic function became abnormal (FS fell from 30 +\/- 4% in CTR to 13 +\/- 5% in SVT, p less than 0.05), and the indexes of relaxation and filling were slowed (tau increased from 36 +\/- 3 msec in CTR to 51 +\/- 13 msec in SVT, p less than 0.05). There were no significant changes in Kc or Km. After terminating the supraventricular tachycardia, LV volume fell but remained greater than that in CTR (EDD was 4.2 +\/- 0.4 cm in PSVT, p less than 0.05 versus CTR) and substantial LV hypertrophy developed (LV\/BW was 3.48 +\/- 0.5 g\/kg in PSVT, p less than 0.05 versus CTR). Systolic function returned to normal (FS was 31 +\/- 5% in PSVT) but diastolic function remained abnormal. In PSVT, tau remained prolonged (49 +\/- 12 msec, p less than 0.05 versus CTR), Kc increased from 3.7 +\/- 1.0 in CTR to 7.4 +\/- 1.2 (p less than 0.05), and Km increased from 4.4 +\/- 1.5 in CTR to 13.9 +\/- 9.7 (p less than 0.05). Thus, the improvement in systolic function that occurs after the termination of supraventricular tachycardia is associated with the development of LV hypertrophy and persistent diastolic dysfunction.<\/jats:p>","DOI":"10.1161\/01.cir.83.2.635","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:01:09Z","timestamp":1339459269000},"page":"635-644","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":127,"title":["Changes in left ventricular volume, mass, and function during the development and regression of supraventricular tachycardia-induced cardiomyopathy. Disparity between recovery of systolic versus diastolic function."],"prefix":"10.1161","volume":"83","author":[{"given":"M","family":"Tomita","sequence":"first","affiliation":[{"name":"Department of Medicine, Cardiology Division, F.A.C., Medical University of South Carolina, Charleston 29425."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F G","family":"Spinale","sequence":"additional","affiliation":[{"name":"Department of Medicine, Cardiology Division, F.A.C., Medical University of South Carolina, Charleston 29425."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F A","family":"Crawford","sequence":"additional","affiliation":[{"name":"Department of Medicine, Cardiology Division, F.A.C., Medical University of South Carolina, Charleston 29425."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M R","family":"Zile","sequence":"additional","affiliation":[{"name":"Department of Medicine, Cardiology Division, F.A.C., Medical University of South Carolina, Charleston 29425."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","container-title":["Circulation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/pdf\/10.1161\/01.CIR.83.2.635","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T15:40:46Z","timestamp":1715528446000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.CIR.83.2.635"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1991,2]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1991,2]]}},"alternative-id":["10.1161\/01.CIR.83.2.635"],"URL":"https:\/\/doi.org\/10.1161\/01.cir.83.2.635","relation":{},"ISSN":["0009-7322","1524-4539"],"issn-type":[{"value":"0009-7322","type":"print"},{"value":"1524-4539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1991,2]]},"assertion":[{"value":"1991-02-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}