Impact of left atrium plication on chronic heart failure with atrial functional mitral regurgitation.

Purpose: We hypothesized that a giant left atrium may oppress  the posterior left ventricle and aggravate diastolic dysfunction and heart failure. We evaluated the effect of left atrial plication (LAP) on atrial functional mitral regurgitation. Methods: We retrospectively reviewed patients who underwent LAP for atrial functional mitral regurgitation at our institution between January 2017 and December 2021. Early outcomes, follow-up echocardiography data, and heart failure indicators were compared. Results: Eighteen patients were divided into two groups: LAP + (n = 9) or LAP- (n = 9). There were no significant differences in patient characteristics and preoperative echocardiographic parameters, except for the preoperative New York Heart Association classification. Operative (505.7 [standard deviation: 100.0] minutes vs. 382.9 [standard deviation: 58.1] minutes, P = .0055) and cardiopulmonary bypass times (335.6 [standard deviation: 50.4] minutes vs. 246.9 [standard deviation: 62.7] minutes, P = .0044) were significantly longer in the LAP + group. No in-hospital mortalities were observed in both groups. The postoperative left atrial volume was significantly reduced in the LAP + group, and mitral regurgitation was controlled at less than mild levels in both groups. At follow-up, the left ventricular end-diastolic volume was reduced significantly in the LAP + group. Brain natriuretic peptide, cardiothoracic ratio, and the New York Heart Association classification were improved in the LAP + group. Conclusions: Additional left atrial plication contributes to the control of atrial functional mitral regurgitation and heart failure at a later stage. A careful long-term follow-up is needed as re-expansion of the left atrium is possible. Supplementary Information: The online version contains supplementary material available at 10.1007/s12055-023-01569-6.

Long-term outcomes of left ventricular posterior wall plication for ischemic mitral regurgitation.

Purpose: To evaluate the early and long-term outcomes of left ventricular posterior wall plication for ischemic mitral regurgitation. Methods: Patients with ischemic mitral regurgitation who underwent left ventricular posterior wall plication via right-sided left atriotomy at our institution between 2010 and 2020 were retrospectively reviewed. Cases with normal cardiac function, left ventricular end-systolic diameter < 50 mm, and left ventriculotomy approach were excluded. Results: The mean follow-up period was 5.3 years [standard deviation (SD) = 3.5], with a maximum of 10 years. Among the 21 patients enrolled, 9 had New York Heart Association (NYHA) class ≥ III. Three patients required preoperative inotrope support, while two preoperative ventilator support. The mean left ventricular ejection fraction was 31.4% (SD: 8.6), and 16 patients had mitral regurgitation grade ≥ III. All patients underwent coronary artery bypass grafting and mitral annuloplasty. Concomitant surgeries included 11 chordae cutting and 3 tricuspid annuloplasties. One in-hospital death occurred due to sepsis. At the follow-up, echocardiographic data showed significant improvement in cardiac dilation and function and good control of mitral regurgitation. The serum brain natriuretic peptide level was significantly reduced, and 85% of patients improved to NYHA class I. Four deaths occurred later due to sudden, unknown causes. The 5- and 8-year survival rates were 60.2% and 46.8%, respectively, and the 5- and 8-year hospitalization rates due to heart failure were 14.9% and 21.3%, respectively. Conclusion: The long-term outcomes of left ventricular posterior wall plication were satisfactory for controlling heart failure and improving survival rate and patient prognosis. Supplementary Information: The online version contains supplementary material available at 10.1007/s12055-023-01527-2.

Noncommunicating acute type A aortic dissection in elderly patients: Surgery versus medical management.

OBJECTIVES: Our goal was to evaluate the surgical and conservative outcomes of acute type A aortic dissection with a thrombosed false lumen of the ascending aorta in elderly patients. METHODS: Patients older than 75 years with acute type A aortic dissection admitted to our hospital from October 2011 to December 2020 were reviewed retrospectively, including those with the noncommunicating type without malperfusion and low physical capacity prehospitalization. RESULTS: Sixty-six patients were enrolled consecutively in the medical (M, n = 30) and surgical (S, n = 36) groups. The ascending aorta was the most replaced section in the S group (78%). Groups did not differ significantly in hospital deaths and in intensive care unit and hospital stays. Two patients (7%) underwent surgery and 3 (10%) underwent redissection in the M group. No significant difference existed between the groups in the decline of physical performance during hospitalization. Seven patients in the M group (24%) had aorta-related events in the late period as opposed to none in the S group (P=0.003). Survival rates after 4 years were 78.3% and 71.4% in the S and M groups, respectively (P=0.154). The cumulative incidence of overall reintervention due to an aortic event was significantly higher in the M group; however, the 2 groups did not differ significantly in overall aorta-related deaths. CONCLUSIONS: Surgical outcomes of noncommunicating acute type A aortic dissection in elderly patients were favorable. There was no significant difference in maintaining physical function at discharge, and the medical group had a significantly higher overall aortic event rate than the surgical group.

[Successful Surgical Management for Ischemic Heart Failure with Fractional Flow Reserve Derived from Computed Tomography:Report of a Case].

A 71-year-old woman was referred to our hospital for mitral valve repair and coronary artery bypass grafting (CABG). Conventional coronary artery angiography showed stenosis in the right coronary artery (RCA) and two diagonal branches, whereas transthoracic echocardiography (TTE) showed diffuse hypokinesis and mild-to-moderate mitral valve regurgitation. Fractional flow reserve derived from computed tomography (FFRct) demonstrated two additional lesions in the coronary artery at the left anterior descending artery (LAD) and the high lateral (HL) branch. Thus, we decided to perform CABG to RCA, LAD, the second diagonal branch, and HL as well as mitral valve repair. TTE one year after surgery showed trivial mitral regurgitation and progressive improvements in the left ventricular wall motion and the ejection fraction. FFRct is a usuful non-invasive method to identify coronary lesions that cause ischemia.

A modified Piehler technique for aberrant origin of left coronary arteries.

A bicuspid aortic valve sometimes coincides with a sinus of Valsalva aneurysm having a coronary artery anomaly. A meticulous aortic root replacement strategy is needed in these cases. In a 64-year-old man, the left coronary arteries (LCA) with an aberrant origin were excised together and reattached to the side hole of a valved conduit via a short Dacron graft. To prevent the formation of an aneurysm at the site, a strip of Dacron graft was sutured from outside between the LCA. The procedure for aortic root replacement with a coronary anomaly needs a case-by-case surgical strategy.

Expression of DMP1 in the developing mouse tongue embryo.

Dentin matrix protein 1 (DMP-1) is an important factor in the mineralization of hard tissues. However, it has many other functions in addition to the regulation of mineralized tissues. We analyzed the expression and localization of DMP-1 by immunohistochemical staining and in situ hybridization in the developing mouse tongue during embryonic days 12.5 (E12.5), E14.5, E17.5, and E18.5. We also detected the mRNA abundance of tongue morphogenesis markers such as FGF6, TGF-ß1, Collagen I, osteocalcin, chondromodulin 1, tenomodulin, Vascular endothelial growth factor (VEGF), caspase-3, and Aifm from embryonic stages by real-time RT-PCR. The antisense probe for DMP-1 was detected in a few mesenchymal cells surrounding blood vessels at E12.5, and faint localization was seen at E18.5 in the embryonic mouse tongue by in situ hybridization. The DMP-1 and osteocalcin abundance levels gradually increased compared with the other tongue markers from E12.5 to E18.5 (p<0.001). Cluster analyses identified the following distinct clusters for mRNA abundance in the tongue: cluster 1, E12.5; cluster 2, E14.5 and E17.5; and cluster 3, E18.5. The positive correlation between DMP-1 and osteocalcin (Pearson's r=0.685; p<0.05) and negative correlation between DMP-1 and Caspase-3 (Pearson's r=-0.632; p<0.05) were analyzed. These data suggested that DMP-1 potentially influences osteocalcin and Caspase-3 during mouse tongue development and morphogenesis. DMP-1 also affects the angiogenic marker VEGF in specific stages and areas, terminating the differentiation of the tongue from other developing tissues. We conclude that DMP-1 may be involved in regulating the temporal expression at embryonic stages in the mouse tongue.

PKC plays a crucial roles in c-mpl gene expression in megakaryoblastic cells.

Thrombopoietin is the cytokine involved in megakaryopoiesis and its receptor (c-Mpl) is considered to regulate development of megakaryocyte. In this research, to elucidate the underlying mechanisms of c-mpl gene expression in megakaryoblastic cells, we investigated the effect of a protein kinase C (PKC) on c-mpl promoter activity in a time-dependent manner. PKC is a member of a family of serine/threonine protein kinases in the cytosol involved in cell growth and differentiation. Phorbol 12-myristate 13-acetate (PMA) is known as PKC activator, significantly enhanced the c-mpl promoter activity and PKC inhibitor, 2-methylpiperazine dihydrochloride (H-7) suppressed the up-regulation of PMA-induced promoter activity and this effect decreased in a time-dependent manner. These results clearly suggest that in megakaryoblastic cells, PKC plays the crucial role in the initiation of up-regulation of PMA-induced c-mpl promoter activity.

Modulation mechanism of c-Mpl promoter activity in megakaryoblastic cells.

Thrombopoietin receptor (c-Mpl) is considered to regulate megakaryocytopoiesis. In this study, we investigated an effect of activation of a protein kinase C (PKC) on c-mpl promoter activity to elucidate the underlying mechanisms of c-mpl gene expression in megakaryoblastic cells. PKC is a member of a family of serine/threonine protein kinases in the cytosol involved in cell growth and differentiation. Phorbol 12-myristate 13-acetate (PMA) is known as PKC activator, significantly enhanced the c-mpl promoter activity and PKC inhibitors (H7, GF109203) suppressed the up-regulation of PMA-induced promoter activity and reduced the steady level of its activity. These results strongly suggest that PKC plays the essential role in the modulation of c-mpl promoter activity of megakaryoblastic cells.