Effect of vitamin D on ventricular remodelling in heart failure: a meta-analysis of randomised controlled trials.

OBJECTIVES: The level of vitamin D is considered to be associated with the development and progression of heart failure (HF). However, it is still unclear whether supplementation of vitamin D could improve ventricular remodelling in patients with HF. This study aimed to systematically evaluate the influence and safety of additional vitamin D supplementation on ventricular remodelling in patients with HF. DESIGN: This study is a meta-analysis of randomised controlled trials (RCTs). SETTING: The PubMed, EMBASE, CNKI, Cochrane library, Web of Science databases and grey literature were searched for RCTs regarding the effect of vitamin D on ventricular remodelling in patients with HF (from database creation to October 2017). RevMan V.5.3 software was employed for data analysis. PARTICIPANTS: Seven RCTs with a total of 465 patients, including 235 cases in the vitamin D group and 230 cases in the control group, were included. PRIMARY AND SECONDARY OUTCOME MEASURES: Left ventricular end-diastolic dimension (LVEDD), left ventricular ejection fraction (LVEF) and the incidence of adverse reactions. RESULTS: Compared with the control group, a decrease in the LVEDD (mean difference (MD)=-2.31 mm, 95% CI -4.15 to -0.47, p=0.01) and an increase in the LVEF (MD=4.18%, 95% CI 0.36 to 7.99, p=0.03) were observed in the vitamin D group. Subgroup analysis also revealed a reduced LVEDD in adults (>18 years) and adolescents (<18 years) of the vitamin D group relative to that in those of the control group. High-dose vitamin D (>4000 IU/day) was more effective at reducing the LVEDD than low-dose vitamin D (<4000 IU/day). Moreover, vitamin D supplementation was more effective at reducing the LVEDD and increasing the LVEF in patients with reduced ejection fraction than in patients without reduced ejection fraction. CONCLUSION: Vitamin D supplementation inhibits ventricular remodelling and improves cardiac function in patients with HF. TRIAL REGISTRATION NUMBER: CRD42017073893.

Impact of Physician-Coordinated Intensive Follow-Up on Long-Term Medical Costs in Patients with Unstable Angina Undergoing Percutaneous Coronary Intervention.

BACKGROUND: To investigate the impact of professional physician-coordinated intensive follow-up on long-term expenditures after percutaneous coronary intervention (PCI) in unstable angina (UA) patients. METHODS: In this study, there were 669 UA patients who underwent successful PCI and followed up for 3 years, then divided into the intensive follow-up group (N = 337), and the usual follow-up group (N = 332). Patients were provided with detailed discharge information and individualized follow-up schedules. The intensive group received the extra follow-up times and medical consultations, and all patients were followed up for approximately 3 years. RESULTS: At the 3-year mark after PCI, the cumulative major adverse cardiac events (MACE), recurrence of myocardial ischemia, cardiac death, all-cause death and revascularization in the intensive group were lower than in the usual group. Additionally, the proportion of good medication adherence was significantly higher than in the usual group (56.4% vs. 46.1%, p < 0.001). The hospitalization daytime, total hospitalization cost and total medical cost in the intensive group were lower. Multiple linear regression showed that diabetes, hypertension, intensive follow-up and good medication adherence were associated with emergency and regular clinical cost (p < 0.05), the re-hospitalization cost (p < 0.05) and the total medical cost (p < 0.05) of patient care. Intensive follow-up and good adherence were negatively correlated with the cost of re-hospitalization (standardized coefficients = -0.132, -0.128, p < 0.05) and total medical costs (standardized coefficients = -0.072, -0.086, p < 0.05). CONCLUSIONS: Intensive follow-up can reduce MACE, improve medication adherence and save long-term total medical costs, just by increasing the emergency and regular clinical visits cost in UA patients after PCI.

Pathological observation of acute myocardial infarction in Chinese miniswine.

The acute myocardial infarction (AMI) model in Chinese miniswine was built by percutaneous coronary artery occlusion. Pathological observation of AMI was performed, and the expression of tumor necrosis factor alpha (TNF-α) in the infarct sites was detected at different days after modeling in Chinese miniswine. The experimental findings may be used as the basis for blood flow reconstruction and intervention after AMI. Seven experimental Chinese miniswine were subjected to general anesthesia and Seldinger right femoral artery puncture. After coronary angiography, the gelfoam was injected via the microtube to occlude the obtuse marginal branch (OM branch). At 1 d, 3 d, 5 d, 7 d, 10 d, 14 d and 17 d after modeling, hetatoxylin-eosin (HE) staining was performed to observe the pathological changes and to detect the expression of TNF-α in the myocardial tissues. Cytoplasmic acidophilia of the necrotic myocardial tissues at 1 d after modeling was enhanced, and cytoplasmic granules were formed; at 3 d, the margins of the necrotic myocardial tissues were infiltrated by a large number of inflammatory cells; at 5 d, the nuclei of the necrotic myocardial cells were fragmented; at 7 d, extensive granulation tissues were formed at the margin of the necrotic myocardial tissues; at 10 d, part of the granulation tissues were replaced by fibrous scar tissues; at 14-17 d, all granulation tissues were replaced by fibrous scar tissues. Immunohistochemical detection indicated that no TNF-α expression in normal myocardial tissues. The TNF-α expression was first detected at 3 d in the necrotic myocardial tissues and then increased at 5 d and 7 d. After reaching the peak at 10 d, the expression began to decrease at 14 d and the decrease continued at 17 d. Coronary angiography showed the disappearance of blood flow at the distal end of OM branch occluded by gelfoam, indicating that AMI model was constructed successfully. The repair of the infarcted myocardium began at 10-17 d after modeling with safe blood flow reconstruction. TNF-α expression in the infarcted myocardium was the highest at 10 d, which can be explained by inflammation and repair of the infarcted myocardium.

Association between left ventricular end-diastolic pressure and coronary artery disease as well as its extent and severity.

Patients with myocardial ischemia exhibit increased left ventricular end-diastolic pressure (LVEDP). The study was to evaluate the relationship between LVEDP measured by left cardiac catheterization and coronary artery disease (CAD) as well as its extent and severity evaluated by coronary angiography (CAG). 912 patients who underwent CAG and left cardiac catheterization were enrolled. There were 313 patients without CAD and 599 with CAD according to CAG. The extent and severity of coronary artery was evaluated by number of vessels and Gensini score. Analyze the correlation of LVEDP and CAD as well as its extent and severity. LVEDP was significantly higher in CAD patients than non-CAD (9.58±5.78 mmHg vs 10.9±5.46 mmHg, P<0.001), and was correlated independently with the presence of CAD (OR = 0.11, per 5 mmHg increase, 95% CI 1.02-1.29, P = 0.02). LVEDP was increased with an increase of number of vessels. By linear regression analysis, LVEDP was significantly associated with Gensini score (standardized ß = 0.034, P = 0.001). In non-CAD group, LVEDP was only correlated with age (r = 0.123, P = 0.030). In conclusion, our findings suggest that elevated LVEDP was significantly associated with CAD as well as its extent and severity. LVEDP was only correlated with age in non-CAD patients. LVEDP measurement provides incremental clinical value for CAD and non-CAD patients.

Application of Intravascular Ultrasound in the Emergency Diagnosis and Treatment of Patients with ST-Segment Elevation Myocardial Infarction.

PURPOSE: This study aimed to examine the application of intravascular ultrasound (IVUS) in ST-segment elevation myocardial infarction (STEMI) patients with high thrombus burden (thrombus grade ≥3) undergoing emergency diagnosis and primary percutaneous coronary intervention. METHODS: Eighty STEMI patients were enrolled and randomly assigned to the IVUS-guided group (38 patients) or non-IVUS group (42 patients). Stent implantation was performed in non-IVUS group patients. IVUS group patients were further divided into low-risk and high-risk patients on the basis of IVUS evaluation for determining whether stenting should be performed. Major adverse cardiac event (MACE) rates, changes in the left ventricular end-diastolic diameter (LVEDD) and ejection fraction (EF) values, and stent numbers were examined during hospitalization, and follow-up was performed at 1, 3, 6, and 12 months postoperatively. RESULTS: During hospitalization, there were no significant differences in the MACE rates, LVEDD, and EF values and in the follow-up outcomes at 1, 3, 6, and 12 months postoperatively among the patients in the 2 groups (P > 0.05). A significantly lower number of stents were implanted in the IVUS group than in the non-IVUS group patients (P < 0.05). CONCLUSION: During the IVUS-guided emergency intervention, enhanced antithrombotic therapy and best medical care for low-risk STEMI patients may be feasible.

[Effects of docosahexaenoic acid on ion channels of rat coronary artery smooth muscle cells].

OBJECTIVE: To investigate the effects of docosahexaenoic acid (DHA) on large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels and voltage-dependent K(+) (K(V)) channels in rat coronary artery smooth muscle cells (CASMCs), and evaluate the vasorelaxation mechanisms of DHA. METHODS: BK(Ca) and K(V) currents in individual CASMC were recorded by patch-clamp technique in whole-cell configuration. Effects of DHA at various concentrations (0, 10, 20, 40, 60 and 80 µmol/L) on BK(Ca) and K(V) channels were observed. RESULTS: (1) DHA enhanced IBK(Ca) and BK(Ca) tail currents in a concentration-dependent manner while did not affect the stably activated curves of IBK(Ca). IBK(Ca) current densities were (68.2 ± 22.8), (72.4 ± 24.5), (120.4 ± 37.9), (237.5 ± 53.2), (323.6 ± 74.8) and (370.6 ± 88.2)pA/pF respectively (P < 0.05, n = 30) with the addition of 0, 10, 20, 40, 60 and 80 µmol/L DHA concentration, and half-effect concentration (EC(50)) of DHA was (36.22 ± 2.17)µmol/L. (2) IK(V) and K(V) tail currents were gradually reduced, stably activated curves of IK(V) were shift to the right, and stably inactivated curves were shifted to the left in the presence of DHA. IK(V) current densities were (43.9 ± 2.3), (43.8 ± 2.3), (42.9 ± 2.0), (32.3 ± 1.9), (11.7 ± 1.5) and (9.6 ± 1.2)pA/pF respectively(P < 0.05, n = 30)post treatment with 0, 10, 20, 40, 60 and 80 µmol/L DHA under manding potential equal to +50 mV, and EC(50) of DHA was (44.19 ± 0.63)µmol/L. CONCLUSION: DHA can activate BK(Ca) channels and block K(V) channels in rat CASMCs, the combined effects on BK(Ca) and K(V) channels lead to the vasodilation effects of DHA on vascular smooth muscle cells.

[Effects of docosahexaenoic acid on sodium channel current and transient outward potassium channel current in rat ventricular myocytes].

OBJECTIVE: To investigate the effects of docosahexaenoic acid (DHA) on sodium channel current (I(Na)) and transient outward potassium channel current (I(to)) in rat ventricular myocytes and to evaluate potential anti-arrhythmic mechanisms of DHA. METHODS: I(Na) and I(to) of individual ventricular myocytes were recorded by patch-clamp technique in whole-cell configuration at room temperature. Effects of DHA at various concentrations (0, 20, 40, 60, 80, 100 and 120 micromol/L) on I(Na) and I(to) were observed. RESULTS: (1) I(Na) was blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged while stably activated curves were not affected by DHA. At -30 mV, I(Na) was blocked to (1.51 ± 1.32)%, (21.13 ± 4.62)%, (51.61 ± 5.73)%, (67.62 ± 6.52)%, (73.49 ± 7.59)% and (79.95 ± 7.62)% in the presence of above DHA concentrations (all P < 0.05, n = 20), and half-effect concentration (EC(50)) of DHA on I(Na) was (47.91 ± 1.57)micromol/L. (2) I(to) were also blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged with increasing concentrations of DHA, and stably activated curves were not affected by DHA. At +70 mV, I(to) was blocked to (2.61 ± 0.26)%, (21.79 ± 4.85)%, (63.11 ± 6.57)%, (75.52 ± 7.26)%, (81.82 ± 7.63)% and (84.33 ± 8.25)%, respectively, in the presence of above DHA concentrations (all P < 0.05, n = 20), and the EC(50) of DHA on I(to) was (49.11 ± 2.68)micromol/L. CONCLUSION: The blocking effects of DHA on APD and I(to) may serve as one of the anti-arrhythmia mechanisms of DHA.

[Echocardiographic standardized myocardial segmentation features in patients with left ventricular noncompaction].

OBJECTIVE: To analyze the echocardiographic standardized myocardial segmentation features in patients with left ventricular noncompaction (LVNC). METHODS: Echocardiographic characteristics of 9 patients with LVNC were analyzed and the localization of lesions were determined according to the standardized myocardial segmentation (SMS) recommended by American Heart Association (AHA). RESULTS: Loose trabeculation in the myocardial lesions were evidenced in all LVNC patients. Communication between deep intertrabecular recess and LV cavity was evident with color flow imaging. According to SMS of AHA, noncompaction of ventricular myocardium was localized in apical segment in all 9 patients, in apical segment of the inferior wall (IW) in 9 patients, in apical segment of the lateral wall (LW) in 7 patients, in middle segment (MS) of IW in 7 patients, in MS of LW in 6 patients. One NC segment was also evidenced in apical segment and MS of septal ventricular wall, basal segment of IW and LW and right ventricular apex, respectively. NC was not found in left ventricular anterior wall. CONCLUSION: Echocardiographic standardized myocardial segmentation is helpful to diagnose LVNC and NC was mostly localized in the apical segments of LVNC patients.