ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Craver, J. M.
Right arrow Articles by Hatcher, C. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Craver, J. M.
Right arrow Articles by Hatcher, C. R., Jr

The Annals of Thoracic Surgery, Vol 40, 163-171, Copyright © 1985 by The Society of Thoracic Surgeons


ARTICLES

Avoidance of transverse midventricular disruption following mitral valve replacement

JM Craver, EL Jones, RA Guyton, BW Cobbs Jr and CR Hatcher Jr

From 1974 through 1977 when our hospital mortality for aortic valve replacement and myocardial revascularization was 3.5% and 1.1%, respectively, hospital mortality for mitral valve replacement (MVR) was 8.3% (13/156)--as high as 14.9% in 1976. Transverse midventricular disruption (TMD) was present in 7 of 10 patients on whom an autopsy was done and was clinically diagnosed in 3 others without postmortem examination. Transverse midventricular disruption presented as refractory myocardial failure immediately on termination of bypass or later (1 to 5 days) after an initial period of good hemodynamics. It appeared to result when volume loading or afterload pressure was returned to the untethered ventricle after MVR performed with potassium- induced, cold cardioplegia and ischemic arrest. Operative techniques were modified to preserve a portion of the mitral suspensory mechanism, to extend the reperfusion interval following cardioplegia and ischemic arrest, and to control strictly ventricular volume and pressure loading following bypass. By utilizing these methods, TMD was avoided from 1978 through 1982, and hospital mortality for MVR was 3.7% (9/241). The improved hospital mortality and avoidance of TMD did not result from patient selection. Allowing adequate time for recovery of the myocardium after cardioplegia plus ischemic arrest prior to ventricular loading, preservation of mitral suspensory function, and strict control of preload and afterload pressures have been effective in lowering hospital mortality for MVR and have eliminated TMD in a 5-year period.


This article has been cited by other articles:


Home page
Card Surg AdultHome page
H. V. Schaff and R. M. Suri
Multiple Valve Disease
Card. Surg. Adult, January 1, 2008; 3(2008): 1129 - 1158.
[Full Text]


Home page
Card Surg AdultHome page
H. V. Schaff and D. H. Marsh
Multiple Valve Disease
Card. Surg. Adult, January 1, 2003; 2(2003): 1017 - 1045.
[Full Text]


Home page
Ann. Thorac. Surg.Home page
G. Victorino, J. N. Young, W. M. DeCampli, and C. L. Ennix Jr
Left Thoracotomy for Emergent Repair of Ventricular Rupture During Mitral Valve Replacement
Ann. Thorac. Surg., April 1, 1995; 59(4): 1011 - 1013.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1985 by The Society of Thoracic Surgeons.