Concept: Mitral valve
Mitral annulus morphologic and functional analysis using real time tridimensional echocardiography in patients submitted to unsupported mitral valve repair
- Revista brasileira de cirurgia cardiovascular : órgão oficial da Sociedade Brasileira de Cirurgia Cardiovascular
- Published over 2 years ago
Mitral valve repair is the treatment of choice to correct mitral insufficiency, although the literature related to mitral valve annulus behavior after mitral repair without use of prosthetic rings is scarce.
Patients with chronic heart failure (HF) secondary to left ventricular systolic dysfunction (LVSD) are frequently deficient in vitamin D. Low vitamin D levels are associated with a worse prognosis.
The diagnosis of heart failure may be challenging because symptoms are rather nonspecific. Elevated left ventricular (LV) filling pressure may be used to confirm the diagnosis, but cardiac catheterization is often not practical. Echocardiographic indexes are therefore used as markers of filling pressure.
Background Ischemic mitral regurgitation is associated with a substantial risk of death. Practice guidelines recommend surgery for patients with a severe form of this condition but acknowledge that the supporting evidence for repair or replacement is limited. Methods We randomly assigned 251 patients with severe ischemic mitral regurgitation to undergo either mitral-valve repair or chordal-sparing replacement in order to evaluate efficacy and safety. The primary end point was the left ventricular end-systolic volume index (LVESVI) at 12 months, as assessed with the use of a Wilcoxon rank-sum test in which deaths were categorized below the lowest LVESVI rank. Results At 12 months, the mean LVESVI among surviving patients was 54.6±25.0 ml per square meter of body-surface area in the repair group and 60.7±31.5 ml per square meter in the replacement group (mean change from baseline, -6.6 and -6.8 ml per square meter, respectively). The rate of death was 14.3% in the repair group and 17.6% in the replacement group (hazard ratio with repair, 0.79; 95% confidence interval, 0.42 to 1.47; P=0.45 by the log-rank test). There was no significant between-group difference in LVESVI after adjustment for death (z score, 1.33; P=0.18). The rate of moderate or severe recurrence of mitral regurgitation at 12 months was higher in the repair group than in the replacement group (32.6% vs. 2.3%, P<0.001). There were no significant between-group differences in the rate of a composite of major adverse cardiac or cerebrovascular events, in functional status, or in quality of life at 12 months. Conclusions We observed no significant difference in left ventricular reverse remodeling or survival at 12 months between patients who underwent mitral-valve repair and those who underwent mitral-valve replacement. Replacement provided a more durable correction of mitral regurgitation, but there was no significant between-group difference in clinical outcomes. (Funded by the National Institutes of Health and the Canadian Institutes of Health; ClinicalTrials.gov number, NCT00807040 .).
Background In a randomized trial comparing mitral-valve repair with mitral-valve replacement in patients with severe ischemic mitral regurgitation, we found no significant difference in the left ventricular end-systolic volume index (LVESVI), survival, or adverse events at 1 year after surgery. However, patients in the repair group had significantly more recurrences of moderate or severe mitral regurgitation. We now report the 2-year outcomes of this trial. Methods We randomly assigned 251 patients to mitral-valve repair or replacement. Patients were followed for 2 years, and clinical and echocardiographic outcomes were assessed. Results Among surviving patients, the mean (±SD) 2-year LVESVI was 52.6±27.7 ml per square meter of body-surface area with mitral-valve repair and 60.6±39.0 ml per square meter with mitral-valve replacement (mean changes from baseline, -9.0 ml per square meter and -6.5 ml per square meter, respectively). Two-year mortality was 19.0% in the repair group and 23.2% in the replacement group (hazard ratio in the repair group, 0.79; 95% confidence interval, 0.46 to 1.35; P=0.39). The rank-based assessment of LVESVI at 2 years (incorporating deaths) showed no significant between-group difference (z score=-1.32, P=0.19). The rate of recurrence of moderate or severe mitral regurgitation over 2 years was higher in the repair group than in the replacement group (58.8% vs. 3.8%, P<0.001). There were no significant between-group differences in rates of serious adverse events and overall readmissions, but patients in the repair group had more serious adverse events related to heart failure (P=0.05) and cardiovascular readmissions (P=0.01). On the Minnesota Living with Heart Failure questionnaire, there was a trend toward greater improvement in the replacement group (P=0.07). Conclusions In patients undergoing mitral-valve repair or replacement for severe ischemic mitral regurgitation, we observed no significant between-group difference in left ventricular reverse remodeling or survival at 2 years. Mitral regurgitation recurred more frequently in the repair group, resulting in more heart-failure-related adverse events and cardiovascular admissions. (Funded by the National Institutes of Health and Canadian Institutes of Health Research; ClinicalTrials.gov number, NCT00807040 .).
Interstitial fibrosis plays a key role in the development and progression of heart failure. Here, we show that an enzyme that crosslinks collagen-Lysyl oxidase-like 2 (Loxl2)-is essential for interstitial fibrosis and mechanical dysfunction of pathologically stressed hearts. In mice, cardiac stress activates fibroblasts to express and secrete Loxl2 into the interstitium, triggering fibrosis, systolic and diastolic dysfunction of stressed hearts. Antibody-mediated inhibition or genetic disruption of Loxl2 greatly reduces stress-induced cardiac fibrosis and chamber dilatation, improving systolic and diastolic functions. Loxl2 stimulates cardiac fibroblasts through PI3K/AKT to produce TGF-β2, promoting fibroblast-to-myofibroblast transformation; Loxl2 also acts downstream of TGF-β2 to stimulate myofibroblast migration. In diseased human hearts, LOXL2 is upregulated in cardiac interstitium; its levels correlate with collagen crosslinking and cardiac dysfunction. LOXL2 is also elevated in the serum of heart failure (HF) patients, correlating with other HF biomarkers, suggesting a conserved LOXL2-mediated mechanism of human HF.
Background: The purpose of the study was to evaluate the acute and chronic effect of smoking on left ventricular function in healthy heavy smokers by conventional Doppler flow, tissue Doppler, and two-dimensional speckle tracking echocardiography (2D-STE). Methods: Echocardiograms were performed in 42 healthy heavy (>20 cigarettes/day) smokers (age 34 ± 5 years), before (group SM-1), 15 minutes (SM-2) and 30 minutes (SM-3) after starting smoking 2 cigarettes. Nonsmokers (n = 41, age 33 ± 4 years) served as controls. Transmitral flow, isovolumetric relaxation time (IVRT), and myocardial performance index (MPI) were measured. Tissue velocity measurements were averaged from lateral and septal mitral annulus. Longitudinal strain (GS), systolic (SRs), early diastolic (SRe), late diastolic (SRa), and isovolumetric relaxation (SRivr) strain rate were measured. The percent change in strain from end-systole to the first one-third of diastole (SI-DI = [(GS - strain at one-third diastole)/GS] × 100) was also measured. Results: IVRT and MPI were increased and early diastolic mitral annular velocity was decreased in SM-2; they returned to baseline in SM-3. There was no difference in GS and SRs. SRe and SRivr were reduced in SM-1 (P < 0.05), and remained significantly reduced in SM-2 and SM-3. SI-DI was lower in SM-1 (P = 0.011) and was further reduced in SM-2 and SM-3 (P < 0.001). Conclusion: Acute and chronic smoking inhalation has adverse effects on myocardial function in healthy heavy smokers. 2D-STE is able to detect both baseline differences and late acute effects of smoking.
Prolapse of mitral valve leaflets is a frequent disorder and the most common cause of severe mitral regurgitation in western countries. However, little is known about the effects of altitude on mitral valve prolapse. We studied the prevalence and echocardiographic characteristics of mitral valve prolapse at moderately high altitude and sea level.
Percutaneous transcatheter mitral valvuloplasty is the indicated treatment of choice for symptomatic native mitral valve stenosis, but there have been limited reports of successful procedures of balloon valvuloplasty for bioprosthetic mitral valve stenosis. We present the case of a 62-year-old woman suffering from progressive dyspnea due to bioprosthetic mitral valve stenosis. The measured mean pressure gradient across the mitral valve was 30 mmHg and the mitral valve area was 0.73 cm(2). Redoing mitral replacement was considered high risk and was refused by the patient. Percutaneous balloon valvuloplasty was performed with an Inoue balloon catheter inflated to 20 mm. The patient’s symptoms immediately improved after the procedure, with no procedure-related complications. The mean pressure gradient across the valve decreased to 19 mmHg, and the mitral valve area increased to 1.21 cm(2) in postprocedural echocardiography. We conducted a literature search and identified 26 cases of balloon valvuloplasty for degenerated bioprosthetic valves. Of these, 14 cases were bioprosthetic mitral valves, and the results were favorable. However, more case reports are required to establish an evidence base for future expert recommendation of balloon valvuloplasty of prosthetic mitral valve. Meanwhile, balloon valvuloplasty will serve a niche role in highly selected patients with prosthetic mitral valve stenosis.
Histopathological characteristics and oxidative injury secondary to atrial fibrillation in the left atrial appendages of patients with different forms of mitral valve disease.
- Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
- Published over 5 years ago
BACKGROUND: The prevalence of atrial fibrillation (AF) and the frequency cardioversion of AF postoperatively are different in different forms of mitral valve disease. We hypothesized that these differences would relate to different extent of histopathological characteristics and oxidative injury in different forms of mitral valve diseases. METHODS: Left atrial appendages were obtained from 24 patients of mitral valve disease with or without AF undergoing mitral valve surgery. Control data were obtained from left appendages of 4 persons in normal sinus rhythm (SR) died of traffic accident. Histopathology, immunohistochemistry, Western blotting and enzyme kinetics examination were performed to assess the extent of histopathological characteristics and oxidative injury. RESULTS: The average cross-sectional diameter of atrial myocyte of mitral stenosis (MS)+AF, MS+SR, mitral regurgitation (MR)+AF, MR+SR and control was 25.62±7.56 μm, 20.20±9.34 μm, 21.69±7.00 μm, 13.93±4.32 μm and 9.81±2.34 μm, respectively. Significantly statistical difference was found between each group (P<.05). Increased degree of atrial interstitial fibrosis was seen both in MS and MR with AF patients compared to other groups (P<.05), and the extent of fibrosis was more remarkable in MR patients compared to MS patients (P<.05). The extent of 3-nitrotyrosine (3-NT) immunoreactivity significantly increased in the patients with MS and AF compared to those of MR and AF (P<.05), and the immunoprevalence of 3-NT was significantly increased in patients of MS and SR compared to those of MR and SR (P<.05). Correlation analysis demonstrated a negative correlation between creatine kinase (CK) activity and extent of 3-NT immunoreactivity in atrial tissues (r=-0.382, P<.05). Significant decreases in CK activity were observed in myocardium from all patients of mitral valve disease with or without AF compared to controls (P<.05). Western blotting demonstrating an increased prevalence of 3-NT formation in CK-MM was detected compared to control group (P<.05). Correlation analysis demonstrated a negative correlation between CK-MM activity and extent of CK-MM tyrosine nitration (r=-0.446, P<.05). CONCLUSIONS: In different forms of mitral valve disease with different cardiac rhythm, the extent of histopathological characteristics and oxidative injury are different. Histopathological characteristics and oxidative injury not only relate to mitral valve disease but also relate to the development and sustain of AF.