Project description:Background: Cardiogenic unilateral pulmonary edema (UPE) has been reported as an unusual condition and to occur in association with severe mitral regurgitation (MR). However, the prevalence of UPE in patients with severe MR remains unknown. Methods and Results: Among 143 consecutive patients with chordal rupture and significant MR, 38 patients with acute severe MR were studied. The prevalence of UPE was 50% (19 patients); all these patients had right-sided UPE. Eight (21%) patients had bilateral pulmonary edema (BPE). All 8 patients with BPE and 18 of 19 patients with UPE had chordal rupture of the posterior leaflet. All patients with UPE and BPE had severe MR with similar left atrial size. Chest radiographs taken ≤48 h from symptom onset diagnosed UPE in 15 of 19 (79%) patients and BPE in 3 of 8 (38%) patients (P=0.037). Chest radiographs taken >48 h from symptom onset diagnosed UPE in 4 (21%) patients and BPE in 5 (62%) patients (P=0.037). Conclusions: The prevalence of UPE was estimated as 50%; it was most frequently right sided and almost always associated with chordal rupture of the posterior leaflet. UPE is not rare, but common, particularly shortly after the development of acute severe MR caused by chordal rupture.
Project description:An 81-year-old woman presented with acute pulmonary edema. Echocardiography revealed severe functional mitral regurgitation, the mechanism of which was unusual. An atypical bileaflet tethering caused by disharmonic annular remodeling, concomitant aortic dilatation, and reduced aorto-mitral angle without left ventricular dysfunction or dilatation was found. A transcatheter edge-to-edge repair was nonetheless successfully performed.
Project description:Development of transcatheter mitral valve interventions has ushered a significant need for large animal models of secondary mitral regurgitation. Though currently used heart failure models that chronically develop secondary mitral regurgitation are viable, the severity is lower than patients, the incubation time is long, and mortality is high. We sought to develop a swine model of acute secondary mitral regurgitation that uses image-guided placement of snares around the mitral chordae. Twenty-seven adult swine (n = 27) were assigned to secondary mitral regurgitation induced by valve tethering with image-guided chordal encircling snares (group 1, n = 7, tether MR (tMR)); secondary mitral regurgitation by percutaneous posterolateral myocardial infarction causing ventricular dysfunction and regurgitation (group 2, n = 6, functional MR (fMR)); and control animals (group 3, n = 14). Regurgitant fraction in tMR was 42.1 ± 14.2%, in fMR was 22 ± 9.6%, and in controls was 5.3 ± 3.8%. Mitral tenting height was 9.6 ± 1.3 mm in tMR, 10.1 ± 1.5 mm in fMR, and 5.8 ± 1.2 mm in controls. Chordal encircling tethers reproducibly induce clinically relevant levels of secondary mitral regurgitation, providing a new animal model for use in translational research.
Project description:BackgroundApical displacement of the coaptation point of the mitral valve (MV) in response to ischemic mitral regurgitation (IMR) represents remodeling of the MV apparatus. Whereas it implies chronicity, it lacks specificity in discriminating normal from a significantly remodeled MV apparatus. Regional aspects of MV remodeling have shown superior value over global remodeling in predicting recurrence after MV repair for IMR. Quite possibly, presence of specific regional changes in MV geometry that are unique to chronic IMR patients could also be used to diagnose the presence and track progression of remodeling. Knowledge of these changes in MV apparatus in patients with IMR can possibly be used to identify patients for surgical intervention before irreversible remodeling occurs.MethodsThree-dimensional transesophageal echocardiographic data were collected from patients who underwent MV surgery for IMR (IMR group, n = 66), and from patients with normal valvular and biventricular function (control group, n = 10). The acquired data of the MV were geometrically analyzed to make regional comparisons between the IMR and the control group to identify measurements that reliably differentiate normal from remodeled MVs.ResultsLengthening of the middle potion of the anterior annulus (A2 regional perimeter: 11.149 mm versus 9.798 mm, p = 0.0041), larger nonplanarity angle (147.985 versus 140.720 degrees, p = 0.0459), and increased tenting angle of the posteromedial scallop of the posterior leaflet (P3 tenting angle: 44.354 versus 40.461 degrees, p = 0.0435) were sufficient in differentiating between IMR and the control group.ConclusionsSpecific three-dimensional changes in MV geometry can be used to reliably identify a significantly remodeled valve apparatus.
Project description:This study sought to assess patterns and functional consequences of mitral apparatus infarction after acute myocardial infarction (AMI).The mitral apparatus contains 2 myocardial components: papillary muscles and the adjacent left ventricular (LV) wall. Delayed-enhancement cardiac magnetic resonance (DE-CMR) enables in vivo study of inter-relationships and potential contributions of LV wall and papillary muscle infarction (PMI) to mitral regurgitation (MR).Multimodality imaging was performed: CMR was used to assess mitral geometry and infarct pattern, including 3D DE-CMR for PMI. Echocardiography was used to measure MR. Imaging occurred 27 ± 8 days after AMI (CMR, echocardiography within 1 day).A total of 153 patients with first AMI were studied; PMI was present in 30% (n = 46 [72% posteromedial, 39% anterolateral]). When stratified by angiographic culprit vessel, PMI occurred in 65% of patients with left circumflex, 48% with right coronary, and only 14% of patients with left anterior descending infarctions (p <0.001). Patients with PMI had more advanced remodeling as measured by LV size and mitral annular diameter (p <0.05). Increased extent of PMI was accompanied by a stepwise increase in mean infarct transmurality within regional LV segments underlying each papillary muscle (p <0.001). Prevalence of lateral wall infarction was 3-fold higher among patients with PMI compared to patients without PMI (65% vs. 22%, p <0.001). Infarct distribution also impacted MR, with greater MR among patients with lateral wall infarction (p = 0.002). Conversely, MR severity did not differ on the basis of presence (p = 0.19) or extent (p = 0.12) of PMI, or by angiographic culprit vessel. In multivariable analysis, lateral wall infarct size (odds ratio 1.20/% LV myocardium [95% confidence interval: 1.05 to 1.39], p = 0.01) was independently associated with substantial (moderate or greater) MR even after controlling for mitral annular (odds ratio 1.22/mm [1.04 to 1.43], p = 0.01), and LV end-diastolic diameter (odds ratio 1.11/mm [0.99 to 1.23], p = 0.056).Papillary muscle infarction is common after AMI, affecting nearly one-third of patients. Extent of PMI parallels adjacent LV wall injury, with lateral infarction-rather than PMI-associated with increased severity of post-AMI MR.