Sex Difference in Outcomes Following Transcatheter Aortic Valve Replacement in Bicuspid Aortic Stenosis.

BACKGROUND: It is unknown whether the sex difference whereby female transcatheter aortic valve replacement (TAVR) candidates had a lower risk profile, a higher incidence of in-hospital complications, but more favorable short- and long-term survival observed in tricuspid cohorts undergoing TAVR would persist in patients with bicuspid aortic valves (BAVs). OBJECTIVES: The aim of this study was to reexamine the impact of sex on outcomes following TAVR in patients with BAVs. METHODS: In this single-center study, patients with BAVs undergoing TAVR for severe aortic stenosis from 2012 to 2021 were retrospectively included. Baseline characteristics, aortic root anatomy, and in-hospital and 1-year valve hemodynamic status and survival were compared between sexes. RESULTS: A total of 510 patients with BAVs were included. At baseline, women presented with fewer comorbidities. Men had a greater proportion of Sievers type 1 BAV, higher calcium volumes (549.2 ± 408.4 mm3 vs 920.8 ± 654.3 mm3; P < 0.001), and larger aortic root structures. Women experienced more vascular complications (12.9% vs 4.9%; P = 0.002) and bleeding (11.1% vs 5.3%; P = 0.019) and higher residual gradients (16.9 ± 7.7 mm Hg vs 13.2 ± 6.4 mm Hg; P < 0.001), while men were more likely to undergo second valve implantations during index TAVR (6.3% vs 15.9%; P = 0.001). Death at 1 year was not significantly different between sexes (HR: 1.15; 95% CI: 0.56-2.35; P = 0.70). Bleeding (adjusted HR: 4.62; 95% CI: 1.51-14.12; P = 0.007) was the single independent predictor of 1-year death for women. CONCLUSIONS: In patients with BAVs undergoing TAVR, women presented with fewer comorbidities, while men had a greater proportion of type 1 BAV, more calcification, and larger aortic roots. In-hospital outcomes favored men, with fewer complications except for the need for second valve implantation, but 1-year survival was comparable between sexes.

Decreased left atrial myocardial strain in patients with suboptimal blood pressure control.

BACKGROUND: Suboptimal blood pressure (BP) control is commonly observed in patients receiving antihypertensive agents, but the relationship between uncontrolled BP and left atrial (LA) impairment remains unknown. METHODS: This study enrolled 279 hypertensive patients who had been medicated, as well as 85 matched normal controls. The BP of systolic <140 mmHg and diastolic<90 mmHg was defined as optimal (HT1 group, n=146), otherwise as suboptimal BP control (HT2 group, n = 133). LA myocardial function was assessed by the systolic (SSa), early diastolic (SEa), and late diastolic (SAa) LA strains. RESULTS: Both the HT1 group and HT2 group had higher BP reading, thicker interventricular septum, larger LA volume index, and enhanced active atrial emptying fraction than the control group (all <0.05). When compared with normal subjects, hypertensive patients displayed obvious reduction in the SSa (50.0 ± 10.9 vs. 35.9 ± 8.0%), SEa (30.1 ± 7.7 vs. 18.5 ± 7.1%) and SAa (19.9 ± 6.4 vs. 17.8 ± 4.2%) (all p < 0.001). In addition to a further impaired SEa found in the HT2 group than in the HT1 group (17.2 ± 5.3 vs. 19.8 ± 8.3%, p = 0.002), the treated BP of >140/90 mmHg appeared an independent risk factor associated with the abnormal SEa (odds ratio, 2.957; interval of confidence, 1.614-5.415; p = 0.001). CONCLUSIONS: Suboptimal BP control status in hypertensive patients is related to a further reduction of LA myocardial function assessed by the novel 2DSTI free strain, and suboptimal BP might be regarded as a composite risk factor and therefore a simplified treatment target. However, the prognostic value of LA free strain in patients with inability to achieve the BP target needs to be evaluated in future prospective studies.

Uncontrolled blood pressure as an independent risk factor of early impaired left ventricular systolic function in treated hypertension.

BACKGROUND: Uncontrolled blood pressure (BP) is commonly observed in patients receiving antihypertensive agents. However, its relationship with early left ventricular (LV) dysfunction has not been elucidated. METHODS: This study enrolled 276 patients with treated hypertension and 85 healthy controls. The 140/90 mm Hg was used to define controlled (HT1 group, n=145) or uncontrolled BP (HT2 group, n=131) according to the concurrent guidelines. LV myocardial function was assessed by two-dimensional speckle tracking imaging, and the circumferential end-systolic wall stress (cESS)-corrected mid-wall fraction shortening (MWFS), systolic longitudinal (εLs-18), circumferential (εCs-18), and radial (εRs-18) strain were measured. RESULTS: Despite similar ejection fraction, the HT1 and HT2 groups displayed an overall reduction in the cESS-corrected MWFS (13.4±2.7 vs 11.7±1.7 vs 15.5±1.2), εLs-18 (15.6±2.8 vs 13.0±2.2 vs 17.4±2.8), εCs-18 (17.3±3.4 vs 14.1±2.7 vs 18.9±3.3), and εRs-18 (18.4±4.0 vs 14.8±3.1 vs 20.5±4.5) %·cm2 /kdyne·10-2 when compared with the control group (all P<.001). The changes were more obvious in the HT2 group, regardless of LV hypertrophy. Reductions in the cESS-corrected MWFS and εLs-18 were seen in 68 (25%) and 52 (19%) patients, respectively. Uncontrolled BP were 4.365 times (95% CI 2.203-8.648, P<.001) and 3.928 times (1.851-8.337, P<.001) more likely to be associated with the changes. CONCLUSIONS: Uncontrolled BP in hypertensive patients is associated with further reduction in LV myocardial function detected by advanced echocardiographic techniques, which cannot be explained by the increase in afterload. It might be regarded as a composite risk factor for earlier and faster development of clinical heart failure, therefore, a simplified treatment target.

[Functional Analysis of DNA Damage Repair Factor WDR70 and Its Mutation in Ovarian Cancer].

OBJECTIVES: To analyze the cellular function of the newly discovered DNA damage repair factor WDR70, and investigate the mutation in ovarian cancer to verify if function loss of the WDR70gene was associated with ovarian cancer. METHODS: The WDR70 gene was silenced by using siRNA technique or overexpressed its wild and mutation type by with lentivirus and plasmid in hunman cells. The subcellular localization and biochemical function of WDR70 was analyzes by indirect immunofluorescence and immunoblotting. The expression level of WDR70 and the mutations of its cDNA was checked with RT-PCR sequencing for 1 normal ovarian tissue and 16 ovarian cancer specimen. RESULTS: We found gene silencing of WDR70 or overexpression of WDR70 mutation type disrupts the phosphorylation level of homologous recombination functional protein RPA32 and the ability of recruitment at DNA damage site of recombinase RAD51, the loss of function of WDR70 also causes the elevation of the chromosome breakage in metaphase. Meanwhile, we also noticed that the existence of multiple mutations in genomic WDR70 in ovarian cancer specimen. CONCLUSIONS: Our results defined that in vitro system, WDR70 is a DNA damage repair gene, silencing of WDR70 or overexpression of WDR70 mutation type disrupts homologous recombination and chromosomal instability; the frequent mutations of WDR70 gene in genome of ovarian cancer specimens could also lead to DNA repair defeat and gene instability. Consequently WDR70 gene could represent an anti-cancer mechanism for ovarian cancer.

Higher blood pressure control rate in a real life management program provided by the community health service center in China.

BACKGROUND: Community health service center (CHSC) in China is always regarded as a good facility of primary care, which plays an important role in chronic non-communicable disease management. This study aimed to investigate the blood pressure (BP) control rate in a real life CHSC-based management program and its determinants. METHODS: The study enrolled 3191 patients (mean age of 70 ± 10 years, 43% males) in a hypertension management program provided by the Yulin CHSC (Chengdu, China), which had been running for 9 years. Uncontrolled BP was defined as the systolic BP of ≥140 mmHg and/or the diastolic BP of ≥90 mmHg, and its associated factors were analyzed by using logistic regression. RESULTS: The duration of stay in the program was 33 ± 25 months. When compared with the BP at entry, the recent BP was significantly lowered (147 ± 17 vs. 133 ± 8 mmHg; 83 ± 11 vs. 75 ± 6 mmHg) and the BP control rate was dramatically increased (32 vs. 85%) (all p < 0.001). The age of >70 years [1.40 (odds ratio), 1.15-1.71 (95% confidence interval)], female gender (0.76, 0.63-0.93), longer stay of >33 months (0.77, 0.63-0.94), doctor in charge (0.97, 0.95-0.99), and the use of calcium channel blocker (1.35, 1.09-1.67) were significantly related to uncontrolled BP at the recent follow up (all p < 0.05). CONCLUSIONS: This CHSC-run hypertension program provides an ideal platform of multi-intervention management, which is effective in achieving higher BP control rate in community patient population. However, the BP control status could be affected by age, gender and adherence of the patients, as well as practice behavior of the doctors.

Comparison of left ventricular reverse remodeling induced by cardiac contractility modulation and cardiac resynchronization therapy in heart failure patients with different QRS durations.

BACKGROUND: Cardiac contractility modulation (CCM) is a new device-based therapy for advanced systolic heart failure with normal QRS duration and therefore not suitable for cardiac resynchronization therapy (CRT). Left ventricular (LV) reverse remodeling was reported in patients treated with CCM or CRT, however, the extent of response was not compared. METHODS: This observational study consisted of three groups of patients with symptomatic heart failure and LV ejection fraction <35% despite optimal medical therapy. Group 1 included those received CCM with a QRS duration <120 ms (n=33), Group 2 included those received CRT with a QRS duration of 120-150 ms (n=43), and Group 3 included those received CRT with a QRS duration >150 ms (n=56). LV end-systolic volume (LVESV) was measured at baseline and 3 months later. RESULTS: Age, gender, etiology of heart failure and baseline ejection fraction were comparable. A significant LV reverse remodeling was observed in each group. The degree of LVESV reduction was similar between Group 1 and Group 2 (-11.3 ± 1 1.8 vs. -13.6 ± 18.3%, p=0.833), however, it was greater in Group 3 (-25.0 ± 18.0%, both p<0.01). By using the reduction ≥ 15%, the responder rate was not different between Group 1 (39%) and Group 2 (42%), but significantly higher in Group 3 (68%) (χ(2)=9.514, p=0.009). CONCLUSION: CCM exhibited a similar LV reverse remodeling response to CRT for patients with a mildly prolonged QRS, though the effect was less strong when compared to CRT for patients with a very wide QRS.

Incremental value of global systolic dyssynchrony in determining the occurrence of functional mitral regurgitation in patients with left ventricular systolic dysfunction.

AIMS: The aim of this study was to assess the contribution of left ventricular (LV) systolic dyssynchrony to functional mitral regurgitation (MR). METHODS AND RESULTS: Patients (n = 136) with LV systolic dysfunction (ejection fraction <50%) and at least mild MR were prospectively recruited. The effective regurgitant orifice area (EROA) was assessed by the proximal isovelocity surface area method. Left ventricular global systolic dyssynchrony [the maximal difference in time to peak systolic velocity among the 12 LV segments (Ts-Dif)] and regional systolic dyssynchrony (the delay between the anterolateral and posteromedial papillary muscle attaching sites) were assessed by tissue Doppler imaging. Left ventricular global and regional remodelling, systolic function, indices of mitral valvular and annular deformation were also measured. The size of the EROA correlated with the degrees of mitral deformation, LV remodelling, systolic function, and systolic dyssynchrony. By multivariate logistic regression analysis, the mitral valve tenting area (OR = 1.020, P < 0.001) and the Ts-Dif (OR = 1.011, P = 0.034) were independent determinants of significant functional MR (defined by EROA ≥20 mm(2)). From the receiver-operating characteristic curve, the tenting area of 2.7 cm(2) (sensitivity 83%, specificity 82%, AUC 0.86, P < 0.001) and the Ts-Dif of 85 ms (sensitivity 66%, specificity 72%, AUC 0.74, P < 0.001) were associated with significant functional MR. The assessment of Ts-Dif showed an incremental value over the mitral valve tenting area for determining functional MR (χ(2) = 53.92 vs.49.11, P = 0.028). CONCLUSION: This cross-sectional study showed that LV global, but not regional systolic dyssynchrony, is a determinant of significant functional MR in patients with LV systolic dysfunction, and is incremental to the tenting area that is otherwise the strongest factor for mitral valve deformation.

[Visualization of right atrial flow patterns and quantification of pulmonary to systemic flow ratio in patients with atrial septal defect by vector flow mapping].

OBJECTIVE: To evaluate the ability of vector flow mapping (VFM) in visualizing right atrial flow and quantifying pulmonary to systemic flow ratio in patients with atrial septal defect (ASD). METHODS: VFM was performed on 30 patients with ASD and 50 healthy volunteers. The pulmonary to systemic flow ratio (Qp/Qs) was calculated using VFM and spectral doppler compared with that obtained through oximetric data derived from cardiac catheterization. RESULTS: Blood streams from superior and inferior caval veins did not collide but turned forward, contributing to a forward clockwise vortex during systole on the subcostal bi-atrial plane in the healthy volunteers. The vortex was disrupted continuously by a left to right shunt in the patients with ASD during the hole cardiac cycle. The Qp/Qs measured by VFM was less angle-dependent in all the cases than the other methods. The mean value of Qp/Qs of the healthy volunteers calculated by apical three-chamber view and apical five-chamber view ranged from 0.84:1 to 1.15:1, which is consistent with the theoretical value 1 of no left to right shunts. The values of Qp/Qs of patients with ASD measured by VFM and spectral doppler showed no significant differences with those obtained through oximetric data [(2.18 +/- 0.48) vs. (2.29 +/- 0.76), P = 0.29; (2.30 +/- 0.91) vs. (2.29 +/- 0.76), P = 0.86]. However, the Qp/Qs value measured by VFM had a better correlation with the oximetric data than that measured by spectral doppler (r = 0.71, P < 0.001 vs. r = 0.38, P < 0.05). The inter-observer and intraobserver variability of Qp/Qs measured by VFM was 9.84% and 9.86% respectively. CONCLUSION: VFM can visualize right atrial flow field in patients with ASD and quantify Qp/Qs in a more accurate way than spectral dopler.

Impact of a dedicated training program on the reproducibility of systolic dyssynchrony measures using tissue Doppler imaging.

BACKGROUND: The reproducibility of the measurement of mechanical dyssynchrony by echocardiography including Doppler tissue imaging has recently been questioned. The aim of this study was to ascertain the role of a dedicated training program to improve skills and the reproducibility of dyssynchrony assessment. METHODS: In 70 patients with heart failure, color Doppler tissue images were acquired, and the time to peak systolic velocity of each segment and several dyssynchrony indices, including the standard deviation of time to peak systolic velocity, were measured by an expert to constitute a reference standard. The same images were then assessed by two beginners, who had only basic knowledge of dyssynchrony analysis after a 1-hour lecture, and two graduates, who had received a structured hands-on training program. Both sets of results were compared with the standard. RESULTS: For the standard deviation of time to peak systolic velocity, the linear correlations between the standard and beginner 1 (r = 0.643) and beginner 2 (r = 0.532) were only modest (P < .001 for both). When referenced to the standard, interobserver variability was 18% for beginner 1 and 19% for beginner 2. Measurements with differences of ≥10 msec were found in 24% and 22% of cases by beginners 1 and 2, respectively. In contrast, the assessments made by graduates 1 and 2 were significantly improved. The correlation coefficients were 0.935 and 0.929 (P < .001 for both), and interobserver variability values were 8% and 7%. The prevalence rates of measurements with differences ≥ 10 msec were 1.5% and 3%, respectively. CONCLUSIONS: There is a learning curve for the measurement of systolic dyssynchrony using Doppler tissue imaging, but good reproducibility can be achieved by the use of a dedicated training program.

LV mechanical dyssynchrony in heart failure with preserved ejection fraction complicating acute coronary syndrome.

OBJECTIVES: The aim of this study was to evaluate the role of left ventricular (LV) mechanical dyssynchrony in heart failure with preserved ejection fraction (HFPEF) complicating acute coronary syndrome (ACS). BACKGROUND: In systolic heart failure, LV mechanical dyssynchrony worsens cardiac function and cardiac resynchronization therapy improves clinical outcome. The role of LV mechanical dyssynchrony in HFPEF complicating ACS is unknown. METHODS: One hundred two patients presenting with ACS (ejection fraction ≥50%) and 104 healthy controls were studied using tissue Doppler imaging: group 1 (n = 55) had HFPEF on presentation and group 2 (n = 47) had no clinical HFPEF. The SD of time to peak systolic myocardial velocity and the SD of early diastolic (Te-SD) myocardial velocity of 12 LV segments were obtained for evaluation of dyssynchrony. Longitudinal mean myocardial ejection systolic velocity (mean Sm) and mean early diastolic velocity (mean Em) were measured. RESULTS: Te-SD was greater in group 1 (33 ± 13 ms) than group 2 (21 ± 9 ms) (p < 0.001), and diastolic mechanical dyssynchrony was evident in 35% of patients in group 1 but in only 9% in group 2 (p < 0.001). Conversely, the SD of time to peak systolic myocardial velocity was similar in the 2 ACS groups (34 ± 16 ms vs. 32 ± 18 ms; p = NS), showing a similar prevalence of systolic mechanical dyssynchrony (47% vs. 43%; p = NS). Worsening of the diastolic dysfunction grade was associated with a parallel increase in Te-SD (grades 0, 1, 2, and 3: 16 ± 3 ms, 21 ± 5 ms, 28 ± 9 ms, and 41 ± 17 ms, respectively; p < 0.001). Te-SD correlated negatively with mean Em (r = -0.56, p < 0.001) and positively with peak mitral inflow velocity of the early rapid-filling wave/Em (r = 0.69, p < 0.001); mean myocardial ejection systolic velocity correlated significantly with mean Em (r = 0.56, p < 0.001), SD of time to peak systolic myocardial velocity (r = -0.42, p < 0.001) and Te-SD (r = -0.23, p = 0.001). Multivariate analysis identified peak mitral inflow velocity of the early rapid-filling wave/Em as the only variable independently associated with HFPEF (odds ratio: 1.48, p = 0.001). When peak mitral inflow velocity of the early rapid-filling wave/Em was excluded from the model, Te-SD (odds ratio: 1.13, p < 0.001) and mean Em (odds ratio: 0.37, p < 0.001) became independently associated with HFPEF. CONCLUSIONS: LV diastolic mechanical dyssynchrony may impair diastolic function and contribute to the pathophysiology of HFPEF, complicating ACS.

Resting global and regional left ventricular contractility in patients with heart failure and normal ejection fraction: insights from speckle-tracking echocardiography.

UNLABELLED: OBEJCTIVE: To compare left ventricular (LV) systolic performance and contractility in patients with heart failure and normal ejection fraction (HFNEF), compared with patients with heart failure and reduced ejection fraction (HFREF) and healthy subjects using newer echocardiographic techniques. DESIGN: A case-control trial. SETTING: University teaching hospital (tertiary referral centre). PATIENTS: Sixty healthy control subjects (53 ± 10 years), 112 patients with HFNEF (74 ± 12 years) and 175 patients with HFREF (67 ± 13 years). INTERVENTIONS: All underwent standard two-dimensional, Doppler and speckle-tracking echocardiography. MAIN OUTCOME MEASURES: Effective arterial (Ea) and LV end-systolic elastance (Ees), stress-corrected mid-wall shortening, preload recruitable stroke work, two-dimensional strain and torsion. Comparisons were adjusted for age, gender and body size. RESULTS: Besides diastolic dysfunction, patients with HFNEF had impaired load-independent ventricular contractility with a progressive decrease of the corrected Ees from controls (2.9 ± 0.8 mm Hg/g) to HFNEF (2.2 ± 0.9 mm Hg/g) followed by HFREF (0.8 ± 0.3 mm Hg/g; all p<0.001). Ventricular-arterial coupling ratio was preserved in the HFNEF subgroup (normal 0.48 ± 0.09 vs 0.65 ± 0.16; p = NS) at the expense of both increased LV systolic stiffness and Ea. In addition, there was progressive decrease of global 2D circumferential, radial and longitudinal strain as well as torsion from normal, HFNEF to HFREF groups, even after adjustment for LV end-systolic wall stress or end-diastolic volume (all p<0.01). About 50% of patients with HFNEF had ≥ 1 global strain or torsion parameter depressed below normal after correction for LV end-systolic wall stress, with >85% falling below their corresponding stress-corrected mean. CONCLUSIONS: Impaired myocardial contractility is evident in many patients with HFNEF and this may contribute towards pathophysiology of HFNEF more than previously thought.

A novel multi-layer approach of measuring myocardial strain and torsion by 2D speckle tracking imaging in normal subjects and patients with heart diseases.

BACKGROUND: This study adopted a new multi-layer approach of measuring myocardial deformation by two-dimensional (2D) speckle tracking imaging to examine whether a transmural gradient exists in normal subjects and cardiac diseases. METHODS: Eighty patients were included with 20 in each group: (1) normal control; (2) acute coronary syndrome (ACS) with ejection fraction (EF) >45%; (3) right ventricular apical (RVA) pacing with EF>45%; (4) systolic heart failure (SHF) with EF<45%. Circumferential strain (ε-circum), torsion (Tor) and systolic dyssynchrony defined as the maximal difference in the time to peak circumferential strain were measured in the subendocardial and subepicardial myocardium layers (QLab 6.0, Philips). RESULTS: In all the 4 groups, a subendocardial to subepicardial gradient was present in both ε-circum (-20.7 ± 7.6 vs. -14.9 ± 5.6%, p<0.001) and Tor (12.0 ± 6.0 vs. 9.3 ± 4.7°, p<0.05), with higher values in the subendocardial layer. However, it was significantly narrowed for ε-circum (2.7 ± 1.2%) and Tor (0.8 ± 0.9°) in SHF patients (all p ≤ 0.001 vs. other groups). On the contrary, systolic dyssynchrony measured in the 2 layers showed no difference (264 ± 107 vs. 273 ± 110 ms, p = NS) and a homogenous distribution in ε-circum was observed from basal to apical planes (-17.0 ± 6.8 vs. -18.1 ± 7.4 vs. -18.1 ± 7.8%, all p = NS). CONCLUSIONS: A transmural gradient exists in circumferential strain and torsion, with higher values in the subendocardial layer. It might be reduced when systolic function is impaired. Therefore, the multi-layer approach of 2D speckle tracking imaging provides further information on assessment of myocardial diseases.

Different determinants of improvement of early and late systolic mitral regurgitation contributed after cardiac resynchronization therapy.

BACKGROUND: Functional mitral regurgitation (MR) at different phases of the regurgitant period may respond differently to cardiac resynchronization therapy (CRT). The aims of this study were to examine the impact of CRT on the phasic changes of MR (early vs late systole) and to explore the mechanisms of such changes. METHODS: Instantaneous MR flow rate and total MR volume were evaluated in 60 patients who had more than mild functional MR before and 3 months after CRT. In addition, indices of global left ventricular (LV) remodeling, mitral deformation, and LV systolic dyssynchrony were assessed. RESULTS: CRT diminished MR volume (38 ± 18 vs 32 ± 20 mL) by reducing both the early (72 ± 47 vs 58 ± 48 mL/sec) and late (48 ± 42 vs 40 ± 42 mL/sec) systolic components (all p values < .01). In patients with ≥10% reductions in total MR volume but not in patients without this improvement, there were significant reductions in LV end-systolic volume, increases in LV +dP/dt, decreases in mitral valvular tenting, and improvements of systolic dyssynchrony at 3 months (all P values < .05). By multivariate regression, the reductions in LV end-systolic volume and tenting area were independent determinants of a reduction in total MR volume: the reductions in LV end-systolic volume and global dyssynchrony determined the reduction in early systolic MR, and the reductions in tenting area and global dyssynchrony determined reduction in late systolic MR. CONCLUSIONS: CRT decreases MR volume by reducing both early and late systolic MR. The determinants of the phasic improvement in functional MR are different.

Impact of reduction in early- and late-systolic functional mitral regurgitation on reverse remodelling after cardiac resynchronization therapy.

AIMS: To examine whether the presence of pre-pacing functional mitral regurgitation (MR) and its improvement would affect the extent of left ventricular (LV) reverse remodelling after cardiac resynchronization therapy (CRT). METHODS AND RESULTS: Echocardiographic assessment was performed in 83 patients before and 3 months after CRT. Total MR volume and the early- and late-systolic MR flow rate were assessed. At 3 months, there was reduction in total MR volume (38 ± 20 vs. 33 ± 21 mL) with decrease in both early- (71 ± 52 vs. 60 ± 51 mL/s) and late-systolic (49 ± 46 vs. 42 ± 46 mL/s) MR flow rate (all P < 0.05). Receiver-operating characteristic curve found that an 11% decrease in total MR volume was associated with LV reverse remodelling [defined by the reduction in LV end-systolic volume (LVESV) of ≥15%] [sensitivity, 90%; specificity, 80%; area under the curve (AUC), 0.85; P < 0.001]. The improvement in early- and late-systolic MR was also associated with LV reverse remodelling, in which improvement in early-systolic MR had higher sensitivity, specificity, and AUC than late-systolic MR. The extent of reverse remodelling with gain in LV ejection fraction and forward stroke volume was greatest in patients with improvement in total MR, intermediate in those with mild or no MR at baseline, and the least in those without improvement in total MR (LVESV, -29.8 ± 12.0 vs. -18.6 ± 16.6 vs. -5.5 ± 8.6%; ejection fraction, 11.8 ± 6.2 vs. 7.0 ± 6.8 vs. 3.0 ± 5.0%; forward stroke volume, 43.1 ± 37.9 vs. 21.1 ± 26.1 vs. 6.8 ± 34.6%; all P < 0.05). CONCLUSION: Improvement of functional MR contributes to LV reverse remodelling after CRT, whereas reduction of early-systolic MR is more powerful than late-systolic MR.

Difference in prevalence and pattern of mechanical dyssynchrony in left bundle branch block occurring in right ventricular apical pacing versus systolic heart failure.

BACKGROUND: This study compared the prevalence and pattern of mechanical dyssynchrony in patients with normal heart and right ventricular apical (RVA) pacing versus patients with systolic heart failure (SHF) and spontaneous left bundle branch block (LBBB). METHODS: A total of 112 patients having LBBB pattern on surface electrocardiogram were included (57 with ejection fraction>50% received RVA pacing; 55 had SHF with ejection fraction<35%). Using tissue Doppler imaging, systolic and diastolic dyssynchrony was defined by the standard deviation of the time to peak systolic and peak early diastolic velocity, respectively. RESULTS: Despite comparable QRS duration and LBBB pattern, the prevalence of electromechanical dyssynchrony was significantly lower in the patients with RVA pacing (systolic: 54% vs 73%, chi2=4.058, P=.044; diastolic: 32% vs 61%, chi2=9.738, P=.002). The presence of coexisting systolic and diastolic dyssynchrony, isolated systolic dyssynchrony, isolated diastolic dyssynchrony, and no dyssynchrony also showed a different distribution between the 2 groups (RVA pacing: 14%, 40%, 18%, and 28%; SHF: 51%, 22%, 11%, and 16%; chi2=17.498, P=.001). Furthermore, the SHF group had a higher prevalence of medial wall (ie, septal, anteroseptal, and inferior) delay (56% vs 30%), whereas RVA pacing resulted in more free wall (ie, lateral, posterior and anterior) delay (44% vs 70%) (chi2=8.050, P=.005). CONCLUSIONS: The prevalence of mechanical dyssynchrony is lower in patients with normal ejection fraction and RVA pacing when compared with patients with SHF and spontaneous LBBB. The pattern of delay in contraction also appears to be different between the 2 groups.

[The inhibitive effect of sodium tanshinone II A sulfonic acid on intimal hyperplasia in rabbit iliac artery ballon injury model].

OBJECTIVE: To study the preventive effect of Sodium Tanshinone II A sulfonic acid on intimal hyperplasia in rabbit iliac artery balloon injury model and explore the possible mechanism. METHODS: Thirty male pure hreed New Zealand white rabbits were undertaken experimental balloon injury in left iliac artery. Then the rabbits were assigned into treatment group (n=15) and control group (n=15), paired with weights. Sodium Tanshinone II A sulfonic acid had been injected intravenously with 7.5 - 9 mg/day for 6 days in treatment group. Saline of equivalence was given in contol group. The balloon injured arteries were harvested in the 7th, 14th, and 28th days after balloon injuy, and Paraffin sections were made. At last, HE staining, apoptosis TUNEL assay were undertaken. RESULTS: (1) HE staining analysis: Media and intimal areas in treatment group at 14th day post-operation were larger than that in the 7th day (P = 0.003 and < 0.001, respectively). Media and intimal areas in treatment group decreased at the 28th day post-operation, while increased in control. Both media and intimal areas were significantly different (P < 0.001 respectively. (2) Tunel analysis discovered that, apoptosis reached peak in both treatment and control groups at the 28th post-operation. Differences of apoptosis cells counts in media and intimal between treatment and control groups were non-significant at the 7th, and 28th days, while differences at the 14th day were significant(p = 0.031 and 0.029 respectively). Apoptosis cells counting in treatment group at the 14th day increased more dramatically than that in the control. CONCLUSION: Intravenous Sodium Tanshinone II A sulfonic acid inhibites intimal proliferation after arterial balloon injury in rabits. The effect can e partially explaineArte by the induction of apoptosis in injured artery. Clinical effect of tanshinone II A still needs further evaluation. Sodium TA-II A sulfonic acid may be of potential therapeutic value in the prevention of OBJECTIVE: To study the preventive effect of Sodium Tanshinone II A sulfonic acid on intimal by perplasia in rabbit iliac artery balloon injury model and explore the possible mechanism. METHODS: Thirty male pure breed Nexw Zealand white rabbits were un-dertaken experimental balloon injury in left iliac artery. Then the rabbits were assigned into treatment group (n=15) and control group (n=15), paired with weights. Sodium Tanshinone II A sulfonie acid had been injected intraxenously with 7.5 - 9 mg/day for 6 days in treatment group. Saline of equivalence was given in contol group. The balloon injured arteries were harvested in the 7th, 14th, and 28th days after balloon injury, and Paraffin sections were made. At last, HE staining, apoptosis TUNEL assay were undertaken. RESULTS: (1) HE staining analysis: Media and intimal areas in treatment group at 14th day post-operation were larger than that in the 7th day (P = 0.003 and < 0.001, respectively). Media and intimal areas in treatment group decreased at the 28th day post-operation, while increased in control. Both media and intimal areas were significantly different (P < 0.001 respectively. (2) Tunel analysis discovered that, apoptosis reached peak in both treatment and control groups at the 28th post-operation. Differences of apoptosis cells counts in media and intimal between treatment and control groups were non-significant at the 7th, and 28th days, while differences at the 14th day were significant (p = 0.031 and 0.029 respectively). Apoptosis cells counting in treatment group at the 14th day increased more dramatically than that in the control. CONCLUSION: Intravenous Sodium Tanshinone II A sulfonic acid inhibites intimal proliferation after arterial balloon injury in rabbits. The effect can he partially explained by the induction of apoptosis in injured artery. Clinical effect of tanshinone II A still needs further evaluation. Sodium TA-II A sulfonic acid may be of potential therapeutic value in the prevention of restenosis after angioplasty.