Whereas both leaflets tethering is related to preoperative ischemic MR, both leaflets tethering but with predominant contribution from augmented and progressive PML tethering is related to recurrent/persistent ischemic/functional MR late after surgical annuloplasty.
Objective
Diastolic subvalvular mitral leaflet tethering by left ventricular remodeling that restricts leaflet opening in the presence of annular size reduction by surgery for ischemic mitral regurgitation potentially causes functional mitral stenosis in the absence of organic leaflet lesions. Exercise, known to worsen systolic tethering and ischemic mitral regurgitation, might also dynamically exacerbate such mitral stenosis by increasing tethering. This study evaluates the mechanism and response of such mitral stenosis to exercise.
Methods
We measured the diastolic mitral valve area, annular area, and peak and mean transmitral pressure gradient by echocardiography in 20 healthy individuals and 31 patients who underwent surgical annuloplasty for ischemic mitral regurgitation.
Results
Although the mitral valve area and annular area did not significantly differ in healthy individuals (4.7 ± 0.6 cm2 vs 5.2 ± 0.6 cm2, not significant), mitral valve area was significantly smaller than the annular area in patients after annuloplasty (1.6 ± 0.2 cm2 vs 3.3 ± 0.5 cm2, P < .01). The mitral valve area was less than 1.5 cm2 only after the surgery (P < .01) and was significantly correlated with restricted leaflet opening (r2 = 0.74, P <.001), left ventricular dilatation (r2 = 0.17, P <.05), and New York Heart Association functional class (P <. 05). Exercise stress echocardiography of 12 patients demonstrated dynamic worsening in functional mitral stenosis (mitral valve area: 2.0 ± 0.5 cm2 to 1.4 ± 0.2 cm2, P < .01; mean pressure gradient: 1.5 ± 0.9 mm Hg to 6.0 ± 2.2 mm Hg, P < .01).
Conclusions
Persistent subvalvular leaflet tethering in the presence of annular size reduction by surgery in ischemic mitral regurgitation frequently causes functional mitral stenosis at the leaflet tip level, which is related to heart failure symptoms and can be dynamic with significant exercise-induced worsening.
Pulmonary tumor thrombotic microangiopathy (PTTM) is a fatal cancer-related complication with rapid progression. Although the underlying molecular mechanisms of PTTM remain unclear, platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) may play important roles in the pathogenesis of PTTM. We herein report a case of PTTM that was diagnosed antemortem by pathology using pulmonary wedge aspiration. The patient was treated with a combination therapy of imatinib (PDGF receptor antagonist), bevacizumab (VEGF receptor inhibitor), S-1, and cisplatin. These findings suggest that molecular-target drugs are effective for the treatment of PTTM.
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