One hundred patients (32 male) aged 5 months to 82 years (median 32 years) underwent 106 surgical procedures for 112 mechanical prosthetic valves obstructed by a thrombus (n = 61) or pannus (n = 7), or both (n = 44), between January 1, 1980 and December 31, 1989. The position of the obstructed prosthesis was aortic in 51 patients (48%), mitral in 49 (46%) and both aortic and mitral in 6 (6%). The types of obstructed prosthetic valves were Björk-Shiley (n = 51), St. Jude (n = 41) and Medtronic-Hall (n = 20). The time interval between valve replacement and obstruction ranged from 6 weeks to 13 years (median 4 years). Of 63% of patients in whom coagulation variables were available at the time of obstruction, 70% were receiving inadequate anticoagulant therapy. In 63% of the procedures the patient was in New York Heart Association functional class IV. Two patients underwent preoperative thrombolysis with incomplete results. Operative procedures included valve replacement (n = 81), valve declotting and excision of pannus (n = 23) and aortic valve replacement and mitral valve declotting (n = 2). The early mortality rate was 12.3% (13 patients), and there was no difference between surgery for mitral prostheses (12.2%) versus aortic prostheses (13.7%). The perioperative mortality rate was 17.5% (11 of 63 patients) in patients in functional class IV and 4.7% (2 of 43 patients) in those in functional classes I to III (p less than 0.05). For valve replacement, the mortality rate was 12% (10 of 81 patients) and for declotting of the prosthesis 13% (3 of 23 patients).(ABSTRACT TRUNCATED AT 250 WORDS)
It is not known if the favorable changes in preload and afterload that augment ejection performance in acute experimental aortic and mitral regurgitation are also present in patients with chronic regurgitation. Additionally, observations that patients with mitral versus aortic regurgitation respond differently to valve replacement suggest that differences exist preoperatively between these two types of volume overload. Therefore, ventricular mechanics were compared in nine patients with severe aortic regurgitation, eight patients with severe mitral regurgitation and seven normal subjects. The amount of volume overload was similar in both groups with regurgitation. In both aortic and mitral regurgitation, ejection performance was reduced compared with findings in normal subjects. Preload estimated as enddiastolic stress was comparably elevated above normal in both groups with regurgitation: 69 +/- 24 dynes X 10(3)/cm2 in mitral regurgitation compared with 81 +/- 34 dynes X 10(3)/cm2 in aortic regurgitation and 36 +/- 11 dynes X 10(3)/cm2 in normal subjects. However, afterload estimated as mean systolic stress was normal in mitral regurgitation (186 +/- 34 dynes X 10(3)/cm2) but markedly elevated in aortic regurgitation (260 +/- 41 dynes X 10(3)/cm2) (p less than 0.01). Contractile depression tended to be more severe in mitral regurgitation despite similar ejection performance in mitral and aortic regurgitation. Thus, in mitral regurgitation favorable loading conditions may mask contractile dysfunction, and in aortic regurgitation excessive afterload contributes to poor pump performance, possibly accounting for previously observed differences in the response to valve replacement.
When preoperative end-systolic diameter is more than 50 mm, a poor postoperative outcome is predicted despite chordal preservation in relatively young patients with rheumatic mitral regurgitation, and alternative strategies should therefore be considered. When preoperative end-systolic diameter is 40 mm or less, an excellent outcome is predicted, and close observation without surgery would appear to be reasonable in the absence of symptoms.
Nebivolol improved stroke volume, ejection fraction and left ventricular end-diastolic pressure, not through a measurable reduction in afterload or a lusitropic effect, but by improving systolic contractile performance.
Thus, severe new mitral regurgitation following MBV is due to noncommissural tearing of the mitral leaflet and confers an adverse long-term prognosis. A mild increase in mitral regurgitation following MBV is frequent and occurs at the site of commissural split or is associated with prolapse of the anterior leaflet. Furthermore, in this study, an increase in mitral regurgitation could not be predicted from any valvular or procedure-related factor.
From January 1982 to December 1988, 203 consecutive patients were selected for early valve replacement (mean 10 days from time of admission) if they had clinical evidence of native valve endocarditis with 1) vegetations on echocardiography, 2) severe valvular lesions, and 3) heart failure. Surgery was performed within 7 days of admission in 56% of patients and was done urgently because of hemodynamic deterioration in 108 (53%). All vegetations were identified by echocardiography and confirmed macroscopically at surgery. One hundred ten patients had isolated aortic valve infection, 50 had isolated mitral valve infection (p less than 0.05 for aortic vs. mitral) and 43 had double-valve infection. Mean aortic cross-clamp time was 57, 38 and 67 min, respectively. Sixty-four patients (32%) had extensive infection involving the anulus or adjacent tissues, or both; such infection more frequently involved the aortic than the mitral valve (p less than 0.05). Thirty-eight patients (35%) with aortic valve infection had abscess formation compared with 1 patient (2%) with mitral valve infection (p less than 0.05). Only eight patients (4%) died in the hospital. There were seven patients (3%) with a periprosthetic leak and five patients (3%) with early prosthetic valve endocarditis. Long-term follow-up, available in 174 hospital survivors (89%), revealed 10 deaths and two new ring leaks at 38 +/- 22 months. In conclusion, among patients with endocarditis who need surgery for heart failure, aortic valve infection is more prevalent than mitral valve infection and is more often associated with extensive infection, including abscess formation.(ABSTRACT TRUNCATED AT 250 WORDS)
Diminished left ventricular distensibility has been postulated as a cause of left ventricular failure in atrial septal defect. To evaluate this hypothesis the indexes of left ventricular compliance and stiffness were estimated in 15 patients with atrial septal defect and the results compared with those in 10 normal subjects. Age, peak left ventricular systolic pressure, end-diastolic pressure, ejection fraction and cardiac index did not differ significantly between groups. Left ventricular end-diastolic volume for the atrial septal defect group was significantly less than that for the control group (mean +/- SD, 61 +/- 9 ml/m2 versus 73 +/- 13, p less than 0.05) in keeping with previous studies. The slope of the log pressure-volume relation was significantly greater in the group with atrial septal defect than in the normal group (0.056 +/- 0.010 versus 0.044 +/- 0.008, p less than 0.01), consistent with increased chamber stiffness. For a group of six patients with atrial septal defect and elevated left ventricular end-diastolic pressure, normalized compliance was significantly less than that in the control group (0.017 +/- 0.001 versus 0.036 +/- 0.007, p less than 0.02). The slope k of the elastic stiffness-stress relation for the total group with atrial septal defect was significantly greater than that of the normal group (21.0 +/- 2.3 versus 18.1 +/- 2.3, p less than 0.01). An index of muscle fiber stretch (dV/VdP x end-diastolic stress x 100) was significantly less in the atrial septal defect group than in the control group (74 +/- 24 versus 106 +/- 22, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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