Kayoko Kubota

Mechanism of Recurrent/Persistent Ischemic/Functional Mitral Regurgitation in the Chronic Phase After Surgical Annuloplasty Importance of Augmented Posterior Leaflet Tethering

Background— Surgical annuloplasty can potentially hoist the posterior annulus anteriorly, exaggerate posterior leaflet (PML) tethering, and lead to recurrent ischemic/functional mitral regurgitation (MR). Characteristics of leaflet configurations in late postoperative MR were investigated. Methods and Results— In 30 patients with surgical annuloplasty for ischemic MR and 20 controls, the anterior leaflet (AML) and PML tethering angles relative to the line connecting annuli, posterior and apical displacement of the coaptation and the MR grade were measured by echocardiography before, early after, and late after surgery. Early after surgery, grade of MR and AML tethering generally decreased (P<0.01), whereas PML tethering significantly worsened (P<0.01). Nine of the 30 patients showed recurrent/persistent MR late after surgery. Compared with patients without late MR, those with the MR showed similar reduction in the annular area, significant re-increase in posterior displacement of the coaptation, and progressive worsening in PML tethering (P<0.05) late after surgery in comparison to the early phase. Both preoperative MR and late postoperative MR were significantly correlated with all tethering variables in univariate analysis. Although apical displacement of the coaptation was the primary determinant of preoperative MR (r2=0.60, P<0.0001), increased PML tethering was the primary determinant of late MR (r2=0.75, P<0.0001). Conclusions— 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.

Functional mitral stenosis after surgical annuloplasty for ischemic mitral regurgitation: Importance of subvalvular tethering in the mechanism and dynamic deterioration during exertion

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 cm(2) vs 5.2 +/- 0.6 cm(2), not significant), mitral valve area was significantly smaller than the annular area in patients after annuloplasty (1.6 +/- 0.2 cm(2) vs 3.3 +/- 0.5 cm(2), P < .01). The mitral valve area was less than 1.5 cm(2) only after the surgery (P < .01) and was significantly correlated with restricted leaflet opening (r(2) = 0.74, P < .001), left ventricular dilatation (r(2) = 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 cm(2) to 1.4 +/- 0.2 cm(2), 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.

Left ventricular global systolic dysfunction has a significant role in the development of diastolic heart failure in patients with systemic hypertension

Regional left ventricular (LV) systolic dysfunction has been identified in diastolic heart failure (DHF). However, the relationship between regional or global LV systolic function and heart failure symptoms in DHF has not been evaluated in detail. The present study evaluates such relationships in patients with systemic hypertension (HT) and DHF. We assessed LV systolic and diastolic function in 220 consecutive patients with systemic HT and in 30 normal individuals (Control) using Doppler echocardiography. Patients with HT were assigned to groups with DHF, asymptomatic diastolic dysfunction (ADD) and no diastolic dysfunction (Simple HT). Ejection fraction in DHF was significantly decreased (63±8%) compared with the Control, Simple HT and ADD groups (67±5, 66±7 and 68±8%, respectively). Isovolumetric contraction time in DHF (70±30 msec) was significantly increased compared with those in the ADD, Simple HT and Control groups (31±17, 31±15 and 30±19 msec, respectively). Mitral annular systolic velocities were significantly decreased in the DHF and ADD groups (6.4±1.5 and 7.2±1.3 cm sec−1, respectively) compared with those in the Simple HT and Control groups (8.5±1.8 and 8.4±3.0 cm sec−1, respectively), and in the DHF group compared with the ADD group. LV global systolic dysfunction has a significant role in the development of heart failure symptoms associated with DHF in patients with systemic HT.

Prosthetic tricuspid valve dysfunction assessed by three-dimensional transthoracic and transesophageal echocardiography

A 39-year-old male who had undergone tricuspid valve replacement for severe tricuspid regurgitation was admitted with palpitation and general edema. Two-dimensional (2D) echocardiography showed tricuspid prosthetic valve dysfunction. Additional three-dimensional (3D) transthoracic and transesophageal echocardiography (TEE) could clearly demonstrate the disabilities of the mechanical tricuspid valve. Particularly, 3D TEE demonstrated a mass located on the right ventricular side of the tricuspid prosthesis, which may have caused the stuck disk. This observation was confirmed by intra-operative findings.

Impairment of Iodine-123-Metaiodobenzylguanidine ( 123 I-MIBG) Uptake in Patients with Pulmonary Artery Hypertension

According to recent studies, lung uptake of iodine-123-metaiodobenzylguanidine (123I-MIBG) is impaired in many lung diseases and low lung uptake of 123I-MIBG suggests endothelial dysfunction of the pulmonary artery. 123I-MIBG scintigraphy in patients with pulmonary hypertension (PH) has not yet been clinically evaluated. We hypothesized that the lung uptake of 123I-MIBG is reduced in patients with PH and differs among PH subtypes. The purpose of the present study was to analyze the lung uptake of 123I-MIBG in patients with PH and compare it with the data obtained by echocardiography or right heart catheterization. 123I-MIBG scintigraphy was performed in 286 consecutive patients from 2003 to 2014. We enrolled 21 patients with PH and 8 control patients. The 21 patients with PH were categorized into those with pulmonary artery hypertension (PAH, n = 12) and those with chronic thromboembolic pulmonary hypertension (CTEPH, n = 9). The mean pulmonary artery pressure was not significantly different between patients with CTEPH and PAH (37.7 ± 6.8 versus 32.3 ± 5.3 mmHg respectively; P = 0.054). There were no significant differences in any other hemodynamic parameters between the two groups. The lung uptake of 123I-MIBG in PAH patients (early image: 1.54 ± 0.18, delayed image: 1.41 ± 0.16) was significantly lower than that of CTEPH patients (early image: 2.17 ± 0.25, P < 0.0001; delayed image: 1.99 ± 0.20, P = 0.0001, adjusted for age and World Health Organization classification) and controls (early image: 2.32 ± 0.27, P = 0.0007; delayed image: 1.92 ± 0.19, P = 0.0007). In conclusion, we found for the first time that the lung uptake of 123I-MIBG in patients with PAH is lower than that in patients with CTEPH and controls.

NOVEL DIAGNOSTIC TOOL OF PAH: LUNG 123I-MIBG SCINTIGRAPHY

Recent studies reported that lung 123I-MIBG uptake was impaired in many lung diseases and low uptake of lung 123I-MIBG is suggested to indicate the pulmonary endothelial dysfunction of pulmonary artery (PA). However, the clinical validation of 123I-MIBG scintigraphy for patients with pulmonary