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The toxicity of doxorubicin (DOX) limits its clinical application. Nevertheless, at present, there is no effective drug to prevent DOX-induced cardiac injury. miR-204 is a newly discovered miRNA with many protective effects on cardiovascular diseases. However, little research has been done on the effects of miR-204 on DOX-induced cardiac injury. Our study is aimed at investigating the effect of miR-204 on DOX-induced myocardial injury. An adenoassociated virus system was used to achieve cardiac-specific overexpression of miR-204. Two weeks later, the mice were intraperitoneally injected with DOX (15 mg/kg) to induce cardiac injury. H9c2 myocardial cells were used to validate the role of miR-204 in vitro. Our study showed that miR-204 expression was decreased in DOX-treated hearts. miR-204 overexpression improved cardiac function and alleviated cardiac inflammation, apoptosis, and autophagy induced by DOX. In addition, our results showed that miR-204 prevented DOX-induced injury in cardiomyocytes by directly decreasing HMGB1 expression. Moreover, the overexpression of HMGB1 could offset the protective effects of miR-204 against DOX-induced cardiac injury. In summary, our study showed that miR-204 protected against DOX-induced cardiac injury via the inhibition of HMGB1, and increasing miR-204 expression may be a new treatment option for patients with DOX-induced cardiac injury.

OBJECTIVE This study aimed to validate the fully automated Pangao PG-800B68 upper-arm device according to the European Society of Hypertension International Protocol (ESH-IP) revision 2010. MATERIALS AND METHODS Sequential measurements of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were obtained in 33 participants using the standard mercury sphygmomanometer and the test device. The ESH-IP revision 2010 was followed precisely and 99 pairings of test device and reference blood pressure measurements were obtained for analysis. RESULTS The number of blood pressure differences within 5, 10, and 15 mmHg was 76, 95, and 98, respectively, for SBP and 79, 96, and 99, respectively, for DBP. The device achieved all the required criteria of the ESH-IP revision 2010 with a device-observer difference of -0.03±4.64 mmHg for SBP and -0.64±4.50 mmHg for DBP. CONCLUSION According to the validation results on the basis of the ESH-IP revision 2010, the Pangao PG-800B68 can be recommended for clinical use and self-measurement in adults.

Objectives To investigate the relationship between serum plasma pregnancy-associated plasma protein A (PAPP-A) and coronary plaque characteristics, and their prognostic value for coronary no-reflow after percutaneous coronary intervention (PCI). Methods Patients with unstable angina undergoing PCI were divided into a normal reflow group and a no-reflow group after stent deployment. Coronary blood flow was measured angiographically; plaque components were detected by virtual histology intravascular ultrasound. Serum PAPP-A and high-sensitivity C-reactive protein (hsCRP) were measured before PCI. Cardiac troponin T (cTnT) was measured before and 24 h after PCI. Results A total of 166 patients with unstable angina undergoing PCI were included: normal reflow group ( n = 145) and no-reflow group ( n = 21), after stent deployment. Baseline coronary blood flow was similar in the two groups. The no-reflow group had plaques with less-fibrotic tissue and a larger necrotic core, more thin-cap fibroatheromas and plaque ruptures, and higher serum PAPP-A, hsCRP and post-PCI cTnT levels than the normal reflow group. Serum PAPP-A was correlated negatively with plaque fibrotic area and positively with necrotic core area. Conclusion High serum PAPP-A and plaque lesions with a large necrotic core are associated with the no-reflow phenomenon after PCI, in patients with unstable angina.

Purpose: Elevation of the levels of myocardial biomarkers after percutaneous coronary intervention (PCI) has prognostic value in patients with coronary heart disease. We explored the relationship between elevation of the serum level of cardiac troponin T (cTnT) after PCI and platelet aggregation rate and coronary plaque composition. Methods: Eighty patients with unstable angina pectoris underwent PCI and were divided into two groups according to serum cTnT level 24 hours after PCI: group I (cTnT ≥2 times the normal level) and group II (cTnT

Diabet. Med. 29, 359–365 (2012) Abstract Aims To observe the effects of pioglitazone on coronary plaque area, plaque burden, serum high-sensitivity C-reactive protein, adiponectin and plasma endothelin-1 levels in patients with impaired glucose tolerance and coronary borderline lesions. Methods Thirty patients were randomly divided into two groups: a pioglitazone group and a control group. The latter was administered placebo in addition to standard therapy; the former pioglitazone 15 mg/d in addition to standard therapy. Before treatment and 6 months later, left ventricular ejection fraction, serum lipid profile, high-sensitivity C-reactive protein, adiponectin and plasma endothelin-1 levels were detected. Coronary plaque area and plaque burden were examined using intravascular ultrasound. Results No significant differences were found in left ventricular ejection fraction and serum lipid levels pre- and post-trial. Compared with the control group, 6 months’ treatment with pioglitazone significantly decreased coronary plaque burden (50.7 ± 11.1 vs. 64.1 ± 10.3%, P

Background: Chronic right ventricular apex (RVA) pacing can induce negative clinical effects. The aim of the present study was to compare RVA pacing with para-right bundle branch (para-RBB) pacing in terms of electrocardiogram (ECG) and echocardiographic (ECHO) features. Methods: Forty-one consecutive persistent atrial fibrillation patients with an indication for permanent pacing treatment due to complete atrioventricular block were randomly assigned to receive a screw-in lead either in the RVA (n = 22) or at the para-RBB (n = 19). Para-RBB pacing leads were located according to the RBB potential recorded by electrophysiology catheter. ECG was recorded before and after implantation. All patients underwent the pacemaker pro­gramming at 1 day, 6 months, 12 months and 24 months after implantation. ECHO examina­tion was performed during follow-up at 6, 12 and 24 months after implantation to assess the heart function and synchronism. Results: There was no significant difference in pacing lead parameters between para-RBB pacing group and RVA pacing group. Compared with RVA pacing group, the para-RBB pacing group obtained a narrower QRS complex, more synchronic ventricular systole, and less nega­tive effect on heart function (p < 0.05). Conclusions: Para-RBB pacing has potential clinical benefits and may be a physiological pacing site.

BACKGROUND: Previous studies suggest the higher the red blood cell distribution width (RDW) the greater the risk of mortality in patients with coronary artery disease (CAD). However, the relationship between RDW and long-term outcome in CAD patients undergoing percutaneous coronary intervention (PCI) with a drug-eluting stent (DES) remains unclear. This study was designed to evaluate the long-term effect of RDW in patients treated with drug-eluting stent for CAD. METHODS: In total of 2169 non-anemic patients (1468 men, mean age 60.2 ± 10.9 years) with CAD who had undergone successful PCI and had at least one drug-eluting stent were included in this study. Patients were grouped according to their baseline RDW: Quartile 1 (RDW

Elevation of the levels of myocardial biomarkers after percutaneous coronary intervention (PCI) has prognostic value in patients with coronary heart disease. We explored the relationship between elevation of the serum level of cardiac troponin T (cTnT) after PCI and platelet aggregation rate and coronary plaque composition.Eighty patients with unstable angina pectoris underwent PCI and were divided into two groups according to serum cTnT level 24 hours after PCI: group I (cTnT ≥2 times the normal level) and group II (cTnT2 times the normal level). Coronary plaque composition was measured with virtual histology-intravascular ultrasound. Platelet aggregation rate was detected immediately before and 24 hours after PCI.Compared with the patients in group II, patients in group I showed more unstable plaques, a larger necrotic core area (20.88 ± 8.04% vs. 15.31 ± 5.48%, P0.05), higher platelet aggregation rate (51.47 ± 12.72% vs. 44.78 ± 13.29%, P0.05), and longer stents. The serum cTnT level 24 hours after PCI was positively correlated with the necrotic core area.In patients with unstable angina pectoris, a large necrotic core, high rate of platelet aggregation, and stent length are predictors of cTnT elevation after PCI.

To investigate the modulation effects of mesenchymal stem cells (MSCs) implantation on the collagen remodeling in myocardial infarction.Acute myocardial infarction (AMI) was induced in SD rats by left anterior descending coronary artery ligation, and the animals were assigned randomly into the Sham group, MI + PBS group and MI + MSCs group. Echocardiography and hemodynamic examinations were performed to evaluate the cardiac function. HE staining and Masson trichrome staining were used to evaluate the myocardial infarction size. Infarcted area and infarcted expansion index were calculated. The expression of collagens in infarcted hearts was evaluated by immunohistochemistry, RT-PCR and Western blot.(1) Infarct area was significantly reduced post MSCs transplantation [MI + MSCs vs. MI + PBS: (38.27 ± 2.70)% vs. (46.20 ± 3.17)%, P0.001]. (2) Cardiac function was significantly improved post MSCs transplantation [MI + MSCs vs. MI + PBS: FS(%): 29.98 ± 4.50 vs. 23.43 ± 3.34, P = 0.005; LVSP (mm Hg, 1 mm Hg = 0.133 kPa): 113.63 ± 10.81 vs. 99.25 ± 16.76, P0.05; LVEDP (mm Hg): 12.10 ± 4.28 vs. 20.08 ± 4.26, P0.05; +dp/dtmax (mm Hg/s): 4616.63 ± 363.34 vs. 3912.75 ± 248.79, P0.05; -dp/dtmax (mm Hg/s): 4254.63 ± 324.34 vs. 3530.88 ± 309.71, P0.05]. (3) Collagen synthesis was enhanced in infarcted area and decreased in non-infarcted area post MSCs transplantation (P0.05).MSCs transplantation could enhance the collagen synthesis in infarcted area while decrease the deposition of collagen in non-infarcted area in this MI model. This may be one of the mechanisms by which ventricular remodeling is attenuated post MSCs transplantation.